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TATA box gene transcriptions

2026-05-20T19:33:08Z

TATA boxes (Carninci 2006) samplings

← Older revision		Revision as of 19:33, 20 May 2026
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	==TATA boxes (Carninci 2006) samplings==		==TATA boxes (Carninci 2006) samplings==
			[[TATA box gene transcriptions#TATA boxes (Carninci 2006) samplings\|TATA boxes (Carninci 2006) samplings]]

	For the Basic programs testing consensus sequence TATAAAA (starting with SuccessablesTATACA--.bas.bas) written to compare nucleotide sequences with the sequences on either the template strand (-), or coding strand (+), of the DNA, in the negative direction (-), or the positive direction (+), the programs are, are looking for, and found:		For the Basic programs testing consensus sequence TATAAAA (starting with SuccessablesTATACA--.bas.bas) written to compare nucleotide sequences with the sequences on either the template strand (-), or coding strand (+), of the DNA, in the negative direction (-), or the positive direction (+), the programs are, are looking for, and found:

Motif ten element gene transcriptions

2026-05-20T18:48:34Z

Samplings

← Older revision		Revision as of 18:48, 20 May 2026
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	==Samplings==		==Samplings==
			[[Motif ten element gene transcriptions#Samplings\|Samplings]]

	For the Basic programs (starting with SuccessablesMTE.bas) written to compare nucleotide sequences with the sequences on either the template strand (-), or coding strand (+), of the DNA, in the negative direction (-), or the positive direction (+), including extension of nts from 958 to 4445, the programs are, are looking for, and found:		For the Basic programs (starting with SuccessablesMTE.bas) written to compare nucleotide sequences with the sequences on either the template strand (-), or coding strand (+), of the DNA, in the negative direction (-), or the positive direction (+), including extension of nts from 958 to 4445, the programs are, are looking for, and found:

Vimseltinib

2026-05-20T18:18:27Z

Created page with "{{DrugProjectFormSinglePage |aOrAn=a |drugClass=kinase inhibitor |indicationType=treatment |indication=adult patients with symptomatic tenosynovial giant cell tumor (TGCT) for which surgical resection will potentially cause worsening functional limitation or severe morbidity. |adverseReactions=laboratory abnormalities are increased AST, periorbital edema, fatigue, rash, increased cholesterol, peripheral edema, face edema, decreased neutr..."

New page

{{DrugProjectFormSinglePage
|aOrAn=a
|drugClass=kinase inhibitor
|indicationType=treatment
|indication=adult patients with symptomatic [[tenosynovial]] [[giant cell tumor]] (TGCT) for which surgical resection will potentially cause worsening functional limitation or severe morbidity.
|adverseReactions=laboratory abnormalities are increased [[AST]], [[periorbital edema]], [[fatigue]], [[rash]], increased [[cholesterol]], [[peripheral edema]], face edema, decreased [[neutrophils]], decreased [[leukocytes]], [[pruritus]], and increased [[ALT]].
|blackBoxWarningTitle='''<span style="color:#FF0000;">TITLE</span>'''
|blackBoxWarningBody=''<span style="color:#FF0000;">Condition Name:</span>'' (Content)
|fdaLIADAdult=====FDA-labeled Indications====
ROMVIMZA is indicated for treatment of adult patients with symptomatic tenosynovial giant cell tumor (TGCT) for which surgical resection will potentially cause worsening functional limitation or severe morbidity.

====Dosage====
The recommended dosage of ROMVIMZA is 30 mg orally taken twice weekly, with a minimum of 72 hours between doses, as directed on the blister package.

'''Dosage Forms and Strengths'''
* 14 mg capsule
Orange cap, white body size 4 capsule imprinted with “DCV14” in black ink.

* 20 mg capsule
Yellow cap, white body size 2 capsule imprinted with “DCV20” in black ink.

* 30 mg capsule
Light blue cap, white body size 1 capsule imprinted with “DCV30” in black ink.

''''Dose Modifications for Adverse Reactions''''
The recommended dose reductions for adverse reactions are provided in the table on the right.

Add table for dose reductions and hepatotoxicity

''''Doasage Modifications for P-glycoprotein (P-gp)Substrates'''
Avoid concomitant use of ROMVIMZA with P-gp substrates. If concomitant use of a P-gp substrate is unavoidable, administer ROMVIMZA at least 4 hours before taking the P-gp substrate unless otherwise recommended in the substrate Prescribing Information.
|offLabelAdultGuideSupport=There is limited information regarding ''Off-Label Guideline-Supported Use'' of Vimseltinib in adult patients.
|offLabelAdultNoGuideSupport=There is limited information regarding ''Off-Label Non–Guideline-Supported Use'' of Vimseltinib in adult patients.
|offLabelPedGuideSupport=There is limited information regarding ''Off-Label Guideline-Supported Use'' of Vimseltinib in pediatric patients.
|offLabelPedNoGuideSupport=There is limited information regarding ''Off-Label Non–Guideline-Supported Use'' of Vimseltinib in pediatric patients.
|contraindications=None.
|warnings='''Hepatotoxicity'''
* Cases of serious and fatal liver injury have occurred with the use of another kinase inhibitor that targets CSF1R.Serious and fatal liver injury have not been observed with ROMVIMZA.
* Avoid ROMVIMZA in patients with pre-existing increased serum transaminases; total bilirubin or direct bilirubin (>ULN); or active liver or biliary tract disease, including ALP.
* Monitor liver tests, including AST, ALT, total bilirubin, direct bilirubin, ALP and gamma-glutamyl transferase (GGT), prior to initiation of ROMVIMZA, twice a month for the first two months and once every 3 months for the first year of therapy and as clinically indicated thereafter.
* Withhold and reduce the dose, or permanently discontinue ROMVIMZA based on the severity of the hepatotoxicity.

'''Embryo-Fetal Toxicity'''
* Based on data from animal studies and its mechanism of action, ROMVIMZA can cause fetal harm when administered to pregnant women.
* In female rats administered vimseltinib, fetal structural abnormalities occurred at exposures that were at least 3 times the recommended dose based on area under the curve (AUC). Advise pregnant women on the potential risk to the fetus.
* Advise females of reproductive potential and males with female partners of reproductive potential to use effective contraception during treatment with ROMVIMZA and for 1 month after the last dose.

'''Allergic Reactions to FD&C Yellow No.5 (Tartrazine) and No. 6 (Sunset Yellow FCF)'''
* ROMVIMZA 20 mg capsule contains FD&C Yellow No. 5 (tartrazine) which may cause allergic reactions (including bronchial asthma) in certain susceptible patients.
* Although the overall incidence of FD&C Yellow No. 5 (tartrazine) sensitivity in the general population is low, it is frequently seen in patients who also have aspirin sensitivity.
* ROMVIMZA 14 mg and 20 mg capsules contain FD&C Yellow No.6 (Sunset Yellow FCF), which may cause allergic reactions.

''' Increased Creatinine without Affecting Renal Function'''
* In MOTION, serum creatinine increased (mean increase of 19 μmol/L) and reached a maximum mean increase by 10.4 weeks compared to baseline.
* These increases in serum creatinine may not be associated with changes in renal function. Increases in creatinine reversed upon ROMVIMZA discontinuation.
* The increases in serum creatinine may be due to inhibition of renal tubular secretion transporters.
* During ROMVIMZA treatment, use alternative measures that are not based on serum creatinine to assess renal function.
|clinicalTrials=====Clinical Trials Experience====
* Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.
* The pooled safety population described in the Warnings and Precautions reflects exposure to ROMVIMZA in 83 patients with TGCT enrolled in the double-blind portion and in 35 patients with TGCT in the open-label portion who crossed over to ROMVIMZA in MOTION, and in 135 patients with TGCT or solid tumors in other clinical trials.
* MOTION excluded patients with bilirubin, AST, or ALT >ULN. All patients received ROMVIMZA twice weekly until disease progression or unacceptable toxicity. Among these patients, 82% were exposed for 6 months or longer and 30% were exposed for greater than one year.
* Serious adverse reactions occurred in 2.4% of patients who received ROMVIMZA. Serious adverse reactions in ≥1% included subcutaneous abscess (1.2%) and cellulitis (1.2%).
* Permanent discontinuation due to an adverse reaction occurred in 4.8% of patients who received ROMVIMZA. Adverse reactions leading to permanent discontinuation in one patient each included periorbital edema, neuropathy, rash, and hypertension.
* Dose reductions due to an adverse reaction or laboratory abnormality occurred in 39% of patients who received ROMVIMZA. Adverse reactions leading to dose reductions in ≥2% of patients receiving ROMVIMZA were rash, periorbital edema, peripheral edema, fatigue, pruritus, face edema, increased CPK, neuropathy, and hypertension.
* Dose interruptions due to an adverse reaction or laboratory abnormality occurred in 40% of patients who received ROMVIMZA. Adverse reactions leading to interruptions in ≥2% of patients included rash, fatigue, peripheral edema, increased CPK, periorbital edema, face edema, pruritus, neuropathy, and hypertension.
* The most common (≥20%) adverse reactions, including laboratory abnormalities that occurred in patients receiving ROMVIMZA were increased AST, periorbital edema, fatigue, rash, increased cholesterol, peripheral edema, face edema, decreased neutrophils, decreased leukocytes, pruritus, and increased ALT.
|drugInteractions='''P-glycoprotein (P-gp)substrates'''
* Avoid concomitant use with P-gp substrates while taking ROMVIMZA.
If concomitant use cannot be avoided, take ROMVIMZA at least 4 hours prior to P-gp substrates unless otherwise recommended in the substrate Prescribing Information.
* This recommendation is based upon a mechanistic understanding of vimseltinib pharmacokinetics and it being a P-gp inhibitor in vitro. Concomitant use of ROMVIMZA with P-gp substrates may increase exposure of these substrates; however, this has not been studied clinically.

'''Breast Cancer Resistance Protein (BCRP) substrates'''
* Avoid concomitant use with BCRP substrates while taking ROMVIMZA.
Refer to the Prescribing Information of the BCRP substrate for dose modifications if concomitant use cannot be avoided.
* This recommendation is based upon a mechanistic understanding of vimseltinib pharmacokinetics and it being a BCRP inhibitor in vitro. Concomitant use of ROMVIMZA with BCRP substrates may increase exposure of these substrates; however, this has not been studied clinically.

'''Organic Cation Transporter 2 (OCT2) substrates'''
* Avoid concomitant use with OCT2 substrates while taking ROMVIMZA.
Refer to the Prescribing Information of the OCT2 substrate for dose modifications if concomitant use cannot be avoided.
* This recommendation is based upon a mechanistic understanding of vimseltinib pharmacokinetics and it being an OCT2 inhibitor in vitro. Concomitant use of ROMVIMZA with OCT2 substrates may increase exposure of these substrates; however, this has not been studied clinically.
|useInPregnancyFDA='''Risk Summary'''
* Based on data from animal studies and its mechanism of action, ROMVIMZA can cause fetal harm when administered to a pregnant woman.
* There are no available data on vimseltinib use in pregnant women to evaluate for a drug-associated risk of major birth defects, miscarriage, or adverse maternal or fetal outcomes.
* In female rats administered vimseltinib during the period of organogenesis, fetal structural abnormalities occurred at exposures that were at least 3 times the recommended dose based on AUC.Advise pregnant women of the potential risk to a fetus.
* The background risk of major birth defects and miscarriage for the indicated population is unknown. All pregnancies have a background risk of birth defect, loss, or other adverse outcomes.
* In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively.
|useInNursing='''Risk Summary'''
There are no data on the presence of vimseltinib or its metabolites in either human or animal milk or its effects on a breastfed child or on milk production. Because of the potential for serious adverse reactions in the breastfed child, advise women not to breastfeed during treatment with ROMVIMZA and for 1 month after the last dose.
|useInPed=The safety and effectiveness of ROMVIMZA in pediatric patients have not been established.
|useInGeri=Clinical studies of ROMVIMZA did not include a sufficient number of patients aged 65 years and older to determine whether they respond differently from younger patients.
|useInHepaticImpair=No dose adjustment is recommended for patients with mild (bilirubin ≤upper limit of normal (ULN) and aspartate aminotransferase (AST) >ULN or bilirubin >1x to 1.5x ULN and any AST) hepatic impairment. ROMVIMZA has not been studied in patients with moderate (bilirubin >1.5x to 3x ULN and any AST) or severe (bilirubin >3x ULN and any AST) hepatic impairment.
|useInReproPotential=ROMVIMZA can cause fetal harm when administered to a pregnant woman [see Use in Specific Populations.

* '''Pregnancy Testing'''
Verify pregnancy status in females of reproductive potential prior to the initiation of ROMVIMZA [see Use in Specific Populations (8.1)].

* '''Contraception'''

Females
Advise females of reproductive potential to use effective contraception during treatment with ROMVIMZA and for 1 month after the last dose.

Males
Advise males that are partnered with females of reproductive potential to use effective contraception during treatment with ROMVIMZA and for 1 month after the last dose.

* '''Infertility'''

Females and Males
Based on findings from animal studies, ROMVIMZA may impair fertility.
|administration=Instruct patients to follow the schedule on the blister package and to take ROMVIMZA on the same days each week.

* ROMVIMZA may be taken with or without food.
* Swallow ROMVIMZA capsules whole. Do not open, break, or chew the capsules.
* If a dose is missed by 48 hours or less, take the missed dose as soon as possible and take the next dose on its regularly scheduled day.
* If a dose is missed by more than 48 hours, skip the missed dose, and take the next dose on its regularly scheduled day.
* If vomiting occurs within 30 minutes of taking a dose, repeat that dose. Otherwise, take the next dose on its regularly scheduled day.
|mechAction=Vimseltinib is a kinase inhibitor that inhibits colony-stimulating factor 1 receptor (CSF1R). In vitro, vimseltinib inhibited CSF1R autophosphorylation, signaling induced by CSF1 ligand binding, and proliferation of cells expressing CSF1R.
|structure=Vimseltinib is a white to off-white crystalline solid. Vimseltinib is a weak base, very slightly soluble in water. The molecular formula for vimseltinib dihydrate is C23H25N7O2 • 2 H2O, and the molecular weight is 467.52 g/mol. The chemical structure is:

Add structure image
|PD='''Exposure-Response Relationship'''

* Higher vimseltinib exposure is associated with an increased risk of all grades of edema, rash, increased AST, and increased ALT.
* Vimseltinib exposure-response relationship for efficacy and time course of pharmacodynamic response have not been fully characterized.

'''Cardiac Elecrophysiology'''
* The maximum recommended dose of ROMVIMZA, clinically significant QTc interval prolongation was not observed. However, the largest mean increase in QTc interval was 8.2 ms (upper confidence internal = 12.3 ms) after administration of vimseltinib 40 mg once daily for 5 days (3.3 times the maximum recommended weekly dose). The increase in QTc interval was concentration-dependent.
|PK=* Vimseltinib pharmacokinetic parameters were determined following a single oral dose of 30 mg or at steady state following multiple doses of 30 mg twice weekly and are provided as mean (CV%) unless otherwise specified.
* Vimseltinib peak plasma concentration (Cmax) is 283 ng/mL (36%) or 747 ng/mL (39%) after a single dose or at steady state, respectively, and area under the time concentration curve (AUC0-inf) is 46,900 ng•h/mL (45%) after a single dose and AUC0-24hr is 13,400 ng•h/mL (45%) at steady state.
* Vimseltinib pharmacokinetics are dose-proportional.
* Vimseltinib median time to Cmax (Tmax) is 1 hour (0.5 to 4 hours).
* No clinically significant differences in vimseltinib pharmacokinetics were observed following administration of a high-fat meal (800 to 1000 kcal, 50% fat), compared to fasted conditions.
* Vimseltinib volume of distribution (V/F) is 90 L (16%). Vimseltinib is 96.5% bound to human plasma proteins.
* Vimseltinib elimination half-life (t1/2) is approximately 6 days (32%) with a clearance (CL/F) of 0.5 L/h (23%).
* Vimseltinib is primarily metabolized by oxidation, N-demethylation, and N-dealkylation; secondary biotransformation pathways included N-demethylation, dehydrogenation, and oxidation. CYP450 enzymes are not anticipated to play a major role in the metabolism of vimseltinib.
* Approximately 43% of the dose was recovered in feces (9.1% unchanged) and 38% in urine (5.1% unchanged) after a single radiolabeled dose.
* No clinically significant differences in the pharmacokinetics of vimseltinib were observed based on age (20 to 91 years), sex, race (Asian, Black or African American, White), body weight (43 to 150 kg), tumor (TGCT or other malignant solid tumors), and mild to moderate renal impairment (estimated glomerular filtration rate [eGFR] ≥30 mL/min calculated by CKD-EPI equation). The effect of severe renal impairment (eGFR <30 mL/min) or moderate to severe hepatic impairment (total bilirubin >1.5 x ULN with any AST) on vimseltinib pharmacokinetics is unknown.
* Clinical Studies and Model-Informed Approaches

P-glycoprotein (P-gp) inhibitors: Dabigatran (a P-gp substrate) AUC0-inf and Cmax are predicted to increase 2- to 3-fold with concomitant use with vimseltinib 30 mg twice weekly.

Dabigatran Cmax and AUC0-inf are predicted to increase up to 1.3-fold if administered 4 hours after administration of vimseltinib 30 mg twice weekly.
* Other Drugs: No clinically significant differences in vimseltinib pharmacokinetics were observed when used concomitantly with itraconazole (a P-gp inhibitor) or rabeprazole (a proton pump inhibitor).
* In Vitro Studies

CYP 450 enzymes: Vimseltinib is not a substrate of CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, and CYP3A.

Vimseltinib is not an inhibitor of CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, and CYP3A4.

Vimseltinib is not an inducer of CYP1A2, CYP2B6, or CYP3A4.
* Transporter systems: Vimseltinib is a P-gp substrate but is not a substrate of BCRP, BSEP, OATP1B1, OATP1B3, OAT1, OAT3, OCT2, MATE1, and MATE2-K.

Vimseltinib inhibits P-gp, BCRP, BSEP, OATP1B1, OATP1B3, OCT2, BSEP, MATE1, and MATE2-K. Vimseltinib does not inhibit OAT1 and OAT3. Vimseltinib may increase serum creatinine by decreasing renal tubular secretion of creatinine; this may occur due to inhibition of renal transporters OCT2 and MATE1 and may not affect renal function.
|nonClinToxic=====Carcinogenesis, Mutagenesis, Impairment of Fertility====
* In a 6-month transgenic mouse carcinogenicity study at doses up to 12.5 mg/kg/day, vimseltinib was negative for carcinogenic findings.
* In a 2-year rat carcinogenicity study, female rats were orally administered vimseltinib at doses of 0.15, 0.45, or 1.5 mg/kg/day.
* There was no evidence of vimseltinib-related neoplasms in female rats. Male rats were orally administered vimseltinib at doses of 0.1, 0.3, or 1.0 mg/kg/day.
* There was a statistically significant increase in the combined incidence of benign and malignant pheochromocytomas in the adrenal gland of male rats administered 1.0 mg/kg/day (approximately 1.4 times the exposure at the recommended dose based on AUC).
* The relevance of this finding to human carcinogenic risk is not known. In male rats receiving 1.0 mg/kg/day, two out of sixty rats were identified as having sarcomas in the synovium of the femorotibial joint. The sarcoma finding was not statistically significant and its relevance to human carcinogenic risk is not known.
* Vimseltinib was not mutagenic in the bacterial reverse mutation assay (Ames). In an in vitro micronucleus assay, vimseltinib increased micronuclei after a 24 -hour incubation in the absence of metabolic activation.
* In vivo, vimseltinib administered to rats at doses up to 200 mg/kg/day did not increase bone marrow micronucleated polychromatic erythrocytes, nor did vimseltinib increase liver DNA strand breaks.
* In a fertility and early embryonic development study, male rats were administered 1, 2.5, or 5 mg/kg/day of vimseltinib starting 10 weeks before cohabitation, during cohabitation with untreated females, and at least 2 weeks post-cohabitation. Lower epididymal and testes weights were observed at 5 mg/kg/day (approximately 12 times the exposure at the recommended dose based on AUC).
* There were no treatment-related effects on mating, fertility, or sperm parameters at any dose tested. Female rats were administered 2.5, 5, or 10 mg/kg/day of vimseltinib 2 weeks prior to cohabitation with untreated males and during cohabitation until gestational day 7.
* Although there were no treatment-related effects on mating or estrous cycles, vimseltinib administered daily resulted in post-implantation loss at 10 mg/kg/day in female rats (approximately 20 times the exposure at the recommended dose based on AUC).
* In a 26-week repeat-dose general toxicology study, recovery male rats that were administered 2.5 or 5 mg/kg/day had moderate to marked reductions in sperm and marked testicular atrophy (1 of 5 and 2 of 5 animals, respectively) corresponding to approximately 6 and 12 times the exposure at the recommended dose based on AUC, respectively.
* In a 39-week repeat-dose general toxicology study, minimal to moderate epididymal mineralization occurred in male dogs administered ≥4 mg/kg/day corresponding to exposures lower than the exposure at the recommended dose based on AUC.
|clinicalStudies=* The efficacy of ROMVIMZA was evaluated in MOTION (NCT05059262), a phase 3, double-blind, multicenter, randomized (2:1), placebo-controlled study in patients with TGCT for whom surgical resection may cause worsening functional limitation or severe morbidity. Eligible patients had a confirmed diagnosis of TGCT with measurable disease per the Response Evaluation Criteria in Solid Tumors (RECIST v1.1) with at least one lesion having a minimum size of 2 cm.
* Patients were randomized to placebo or ROMVIMZA 30 mg twice weekly for 24 weeks. Randomization was stratified by tumor location (lower limb versus all other) and region (United States [US] versus non-US). At Week 25, patients who completed the double-blind, randomized part of the trial were eligible to advance to an ongoing, open-label extension study in which all patients received ROMVIMZA.
* The major efficacy outcome measure was overall response rate (ORR) as assessed by blinded independent radiological review (IRR) per RECIST v1.1 at Week 25.
* Additional efficacy outcomes measured at Week 25 included ORR as assessed using tumor volume score (TVS), mean change from baseline in active range of motion of the affected joint at Week 25 measured by goniometry assessments, change from baseline in the Patient-Reported Outcomes Measurement Information System-Physical Function (PROMIS-PF) 15-item score (upper and lower extremity items), and response of at least a 30% improvement in the mean Brief Pain Inventory (BPI) Worst Pain numeric rating scale (NRS) score without a 30% or greater increase in narcotic analgesic use.
* A total of 123 patients were randomized: 83 to ROMVIMZA and 40 to placebo during the double-blind period of the study. The median age was 44 years (range 20 to 78 years); 59% of patients were female; 65% were White, 4% were Asian, 3% were Black or African American, and 28% were not reported or unknown; 69% were not Hispanic or Latino, 3% were Hispanic or Latino, and 28% were not reported or unknown; 74% of patients had prior surgery; 69% of patients had diffuse TGCT; and 23% of patients were previously treated with systemic therapy. Disease locations were knee (67%), ankle (12%), hip (10%), other (5%), foot (3.3%), and wrist (2.4%).

Add graph
|howSupplied=* Store at controlled room temperature 20°C to 25°C (68°F to 77°F); excursions permitted to 15°C to 30°C (59°F to 86°F) [See USP Controlled Room Temperature].
* Store capsules in their original blister packs until ready to be taken. Do not store ROMVIMZA in another container.

Add supply table
|fdaPatientInfo=* Advise the patient to read the FDA approved patient labeling (Medication Guide).

* '''Hepatotoxicity'''
Advise patients there may be a potential risk of hepatotoxicity and that they will need to undergo laboratory tests to monitor liver function and to immediately report any signs or symptoms of severe liver injury to their healthcare provider.

* '''Embryo-Fetal Toxicity'''
Advise pregnant women and females of reproductive potential of the potential risk to the fetus. Advise females of reproductive potential to inform their healthcare provider of a known or suspected pregnancy.
Advise females of reproductive potential to avoid pregnancy and to use effective contraception during treatment with ROMVIMZA and for 1 month after the last dose.
Advise males with female partners of reproductive potential to use effective contraception during treatment and for 1 month after the last dose of ROMVIMZA.

* '''Lactation'''
Advise females not to breastfeed during treatment with ROMVIMZA and for 1 month after the final dose.

* '''Infertility''
Advise patients that ROMVIMZA may impair fertility.

Allergic Reactions to FD&C Yellow No. 5 (Tartrazine) and No. 6 (Sunset Yellow FCF)

Advise patients that ROMVIMZA 20 mg contains FD&C Yellow No. 5 (tartrazine), which may cause allergic-type reactions (including bronchial asthma) in certain susceptible persons or in patients who also have aspirin hypersensitivity [see Warnings and Precautions (5.3)]. Advise patients ROMVIMZA 14 mg and ROMVIMZA 20 mg contains FD&C Yellow No. 6 (Sunset Yellow FCF) which may cause allergic-type reactions [see Warnings and Precautions (5.3)].

* '''Administration'''
Instruct patients that doses should be taken twice weekly at least 72 hours apart [see Dosage and Administration (2.1)].
Instruct patients to swallow capsules whole (do not open, break, or chew)

* '''Drug Interactions'''
Advise patients to inform their healthcare providers of all concomitant products, including over-the-counter products and supplements.
|alcohol=Alcohol-Vimseltinib interaction has not been established. Talk to your doctor about the effects of taking alcohol with this medication.
}}

Enhancer box gene transcriptions

2026-05-20T18:13:27Z

MITF E-box (CAYRTG) samplings

← Older revision		Revision as of 18:13, 20 May 2026
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	==MITF E-box (CAYRTG) samplings==		==MITF E-box (CAYRTG) samplings==
			[[Enhancer box gene transcriptions#MITF E-box (CAYRTG) samplings\|MITF E-box (CAYRTG) samplings]]

	(CAYRTG) = CA(C/T)(A/G)TG.		(CAYRTG) = CA(C/T)(A/G)TG.

Middle sporulation element gene transcriptions

2026-05-20T17:43:23Z

MSE (Ozsarac) samplings

← Older revision		Revision as of 17:43, 20 May 2026
(One intermediate revision by the same user not shown)
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	==MSE (Branco) samplings==		==MSE (Branco) samplings==
			[[Middle sporulation element gene transcriptions#MSE (Branco) samplings\|MSE (Branco) samplings]]

	Copying apparent core consensus sequences for the MSEs of ACACAAA and putting it in "⌘F" finds none located between ZSCAN22 and none between ZNF497 and A1BG as can be found by the computer programs.		Copying apparent core consensus sequences for the MSEs of ACACAAA and putting it in "⌘F" finds none located between ZSCAN22 and none between ZNF497 and A1BG as can be found by the computer programs.
Line 219:		Line 220:

	==MSE (Ozsarac) samplings==		==MSE (Ozsarac) samplings==
			[[Middle sporulation element gene transcriptions#MSE (Ozsarac) samplings\|MSE (Ozsarac) samplings]]

	Copying a responsive elements consensus sequence C(A/G)CAAA(A/T) and putting the sequence in "⌘F" finds none between ZNF497 and A1BG or none between ZSCAN22 and A1BG as can be found by the computer programs.		Copying a responsive elements consensus sequence C(A/G)CAAA(A/T) and putting the sequence in "⌘F" finds none between ZNF497 and A1BG or none between ZSCAN22 and A1BG as can be found by the computer programs.

Metal responsive element gene transcriptions

2026-05-20T17:19:30Z

MRE samplings

← Older revision		Revision as of 17:19, 20 May 2026
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	==MRE samplings==		==MRE samplings==
	{{main\|Model samplings\|Samplings}}		{{main\|Model samplings\|Samplings}}
	Copying a responsive elements consensus sequence ~~TGCGCCC~~ and putting the sequence in "⌘F" finds none between ZNF497 and A1BG or none between ZSCAN22 and A1BG as can be found by the computer programs.		[[Metal responsive element gene transcriptions#MRE samplings\|MRE samplings]]

			Copying a responsive elements consensus sequence TGCRCNC and putting the sequence in "⌘F" finds none between ZNF497 and A1BG or none between ZSCAN22 and A1BG as can be found by the computer programs.

	For the Basic programs (starting with SuccessablesMRE.bas) written to compare nucleotide sequences with the sequences on either the template strand (-), or coding strand (+), of the DNA, in the negative direction (-), or the positive direction (+), including extending the number of nts from 958 to 4445, the programs are, are looking for, and found:		For the Basic programs (starting with SuccessablesMRE.bas) written to compare nucleotide sequences with the sequences on either the template strand (-), or coding strand (+), of the DNA, in the negative direction (-), or the positive direction (+), including extending the number of nts from 958 to 4445, the programs are, are looking for, and found:

User:Khizar Hayat

2026-05-20T15:31:50Z

User account Khizar Hayat was created by Alberto Castro Molina

User:Asad Farooq

2026-05-20T15:25:24Z

User account Asad Farooq was created by Alberto Castro Molina

Ischemic stroke medical therapy

2026-05-20T14:25:13Z

← Older revision		Revision as of 14:25, 20 May 2026
(6 intermediate revisions by the same user not shown)
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	*The dose of [[aspirin]] is usually between 160-300mg daily.<ref name="pmid9174558">{{cite journal \|vauthors= \|title=The International Stroke Trial (IST): a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19435 patients with acute ischaemic stroke. International Stroke Trial Collaborative Group \|journal=Lancet \|volume=349 \|issue=9065 \|pages=1569–81 \|date=May 1997 \|pmid=9174558 \|doi= \|url=}}</ref>		*The dose of [[aspirin]] is usually between 160-300mg daily.<ref name="pmid9174558">{{cite journal \|vauthors= \|title=The International Stroke Trial (IST): a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19435 patients with acute ischaemic stroke. International Stroke Trial Collaborative Group \|journal=Lancet \|volume=349 \|issue=9065 \|pages=1569–81 \|date=May 1997 \|pmid=9174558 \|doi= \|url=}}</ref>
	*[[Aspirin\|IV aspirin]] administration within 90 minutes after the start of [[Alteplase\|IV alteplase]] is associated with symptomatic intracranial hemorrhage, for which co administration is discouraged but benefits should be assessed in each individual case.<ref name="PowersRabinstein2019" /><ref name="ZinkstokRoos2012">{{cite journal\|last1=Zinkstok\|first1=Sanne M\|last2=Roos\|first2=Yvo B\|title=Early administration of aspirin in patients treated with alteplase for acute ischaemic stroke: a randomised controlled trial\|journal=The Lancet\|volume=380\|issue=9843\|year=2012\|pages=731–737\|issn=01406736\|doi=10.1016/S0140-6736(12)60949-0}}</ref>		*[[Aspirin\|IV aspirin]] administration within 90 minutes after the start of [[Alteplase\|IV alteplase]] is associated with symptomatic intracranial hemorrhage, for which co administration is discouraged but benefits should be assessed in each individual case.<ref name="PowersRabinstein2019" /><ref name="ZinkstokRoos2012">{{cite journal\|last1=Zinkstok\|first1=Sanne M\|last2=Roos\|first2=Yvo B\|title=Early administration of aspirin in patients treated with alteplase for acute ischaemic stroke: a randomised controlled trial\|journal=The Lancet\|volume=380\|issue=9843\|year=2012\|pages=731–737\|issn=01406736\|doi=10.1016/S0140-6736(12)60949-0}}</ref>
	*[[Dual antiplatelet therapy]] with [[aspirin~~]] and [[~~clopidogrel~~]] (75 mg/d, with a loading dose of 600mg) may~~ be started within 24 hours ~~after [[symptom]] onset~~ and continued ~~for~~ 21 days in patients with ~~no cardioembolic [[~~ischemic stroke]].<ref name="~~JohnstonEaston2018~~">{{cite journal\|~~last1~~=Johnston\|~~first1~~=~~S. Claiborne~~\|~~last2~~=~~Easton~~\|~~first2~~=~~J. Donald~~\|~~last3~~=~~Farrant~~\|~~first3~~=~~Mary~~\|~~last4~~=~~Barsan~~\|~~first4~~=~~William~~\|~~last5~~=~~Conwit~~\|~~first5~~=~~Robin~~ A.\|~~last6~~=~~Elm~~\|~~first6~~=~~Jordan J.~~\|~~last7~~=~~Kim~~\|~~first7~~=~~Anthony S.~~\|~~last8~~=~~Lindblad~~\|~~first8~~=~~Anne S~~.\|~~last9~~=~~Palesch~~\|~~first9~~=~~Yuko Y.~~\|title=~~Clopidogrel and Aspirin in~~ Acute Ischemic Stroke ~~and High-Risk TIA~~\|journal=~~New England Journal of Medicine~~\|volume=~~379~~\|issue=3\|~~year~~=~~2018~~\|~~pages~~=~~215–225~~\|~~issn~~=~~0028-4793~~\|doi=10.~~1056~~/~~NEJMoa1800410~~}}</ref>		*[[Dual antiplatelet therapy]] (DAPT) with aspirin plus clopidogrel should be started early (ideally within 24 hours) and continued short term (commonly ~21 days) in patients with minor noncardioembolic ischemic stroke or high-risk TIA who did not receive IV thrombolysis, followed by single antiplatelet therapy.<ref name="pmid41582814">{{cite journal \|vauthors=Prabhakaran S, Gonzalez NR, Zachrison KS, Adeoye O, Alexandrov AW, Ansari SA, Chapman S, Czap AL, Dumitrascu OM, Ishida K, Jadhav AP, Johnson B, Johnston KC, Khatri P, Kimberly WT, Lee VH, Leslie-Mazwi TM, Mac Grory B, Madsen TE, Menon B, Mistry EA, Park S, Parker S, Pérez de la Ossa N, Reeves M, Saiz T, Scott PA, Schwartzberg D, Sheth SA, Sporns PB, Times S, Tjoumakaris S, Wolfe SQ, Yaghi S \|title=2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association \|journal=Stroke \|volume= \|issue= \|pages= \|date=January 2026 \|pmid=41582814 \|doi=10.1161/STR.0000000000000513 \|url=}}</ref><ref name="pmid33724327">{{cite journal \|vauthors=Mendelson SJ, Prabhakaran S \|title=Diagnosis and Management of Transient Ischemic Attack and Acute Ischemic Stroke: A Review \|journal=JAMA \|volume=325 \|issue=11 \|pages=1088–1098 \|date=March 2021 \|pmid=33724327 \|doi=10.1001/jama.2020.26867 \|url=}}</ref>.
			*In patients with recent stroke/TIA attributable to severe symptomatic intracranial stenosis (Intracranial athrosclerotic diseas i.e ICAD), DAPT for up to 90 days is reasonable<ref name="pmid41582814">{{cite journal \|vauthors=Prabhakaran S, Gonzalez NR, Zachrison KS, Adeoye O, Alexandrov AW, Ansari SA, Chapman S, Czap AL, Dumitrascu OM, Ishida K, Jadhav AP, Johnson B, Johnston KC, Khatri P, Kimberly WT, Lee VH, Leslie-Mazwi TM, Mac Grory B, Madsen TE, Menon B, Mistry EA, Park S, Parker S, Pérez de la Ossa N, Reeves M, Saiz T, Scott PA, Schwartzberg D, Sheth SA, Sporns PB, Times S, Tjoumakaris S, Wolfe SQ, Yaghi S \|title=2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association \|journal=Stroke \|volume= \|issue= \|pages= \|date=January 2026 \|pmid=41582814 \|doi=10.1161/STR.0000000000000513 \|url=}}</ref>.
	*[[Aspirin]] should not substitute [[Alteplase\|IV alteplase]] or mechanical thrombectomy in patients eligible for these therapies.<ref name="PowersRabinstein2019" />		*[[Aspirin]] should not substitute [[Alteplase\|IV alteplase]] or mechanical thrombectomy in patients eligible for these therapies.<ref name="PowersRabinstein2019" />

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	\|-		\|-
	\| style="padding: 5px 5px; background: #F5F5F5;" \|'''Reperfusion therapy'''		\| style="padding: 5px 5px; background: #F5F5F5;" \|'''Reperfusion therapy'''
	\| style="padding: 5px 5px; background: #F5F5F5;" \|~~[[Tissue plasminogen activator\|'''Tissue plasminogen activator''']] '''~~(~~t-PA~~)~~'''~~		\| style="padding: 5px 5px; background: #F5F5F5;" \|IV thrombolysis (alteplase or tenecteplase); Endovascular thrombectomy (EVT)
	\| style="padding: 5px 5px; background: #F5F5F5;" \|		\| style="padding: 5px 5px; background: #F5F5F5;" \|
	* Recommended within 3-4.5 hours of onset of ischemic stroke in eligible patients by guidelines<ref name="pmid23370205">{{cite journal\| author=Jauch EC, Saver JL, Adams HP, Bruno A, Connors JJ, Demaerschalk BM et al.\| title=Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. \| journal=Stroke \| year= 2013 \| volume= 44 \| issue= 3 \| pages= 870-947 \| pmid=23370205 \| doi=10.1161/STR.0b013e318284056a \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23370205 }} </ref><ref name="pmid 22315273">{{cite journal\| author=Lansberg MG, O'Donnell MJ, Khatri P, Lang ES, Nguyen-Huynh MN, Schwartz NE et al.\| title=Antithrombotic and thrombolytic therapy for ischemic stroke: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. \| journal=Chest \| year= 2012 \| volume= 141 \| issue= 2 Suppl \| pages= e601S-36S \| pmid= 22315273 \| doi=10.1378/chest.11-2302 \| pmc=3278065 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22315273 }} </ref><ref>{{cite web\|url=http://www.aaem.org/em-resources/position-statements/clinical-practice/thrombolytic-therapy \|title=Position Statement on the Use of Intravenous Thrombolytic Therapy in the Treatment of Stroke \|publisher=American Academy of Emergency Medicine \|accessdate=2008-01-25}}</ref> and [[systematic review]]s<ref name="pmid25871671">{{cite journal\| author=Prabhakaran S, Ruff I, Bernstein RA\| title=Acute stroke intervention: a systematic review. \| journal=JAMA \| year= 2015 \| volume= 313 \| issue= 14 \| pages= 1451-62 \| pmid=25871671 \| doi=10.1001/jama.2015.3058 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25871671 }} </ref><ref name="pmid25072528">{{cite journal\| author=Wardlaw JM, Murray V, Berge E, del Zoppo GJ\| title=Thrombolysis for acute ischaemic stroke. \| journal=Cochrane Database Syst Rev \| year= 2014 \| volume= 7 \| issue= \| pages= CD000213 \| pmid=25072528 \| doi=10.1002/14651858.CD000213.pub3 \| pmc=4153726 \| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25072528 }} </ref><ref name="pmid25106063">{{cite journal\| author=Emberson J, Lees KR, Lyden P, Blackwell L, Albers G, Bluhmki E et al.\| title=Effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials. \| journal=Lancet \| year= 2014 \| volume= \| issue= \| pages= \| pmid=25106063 \| doi=10.1016/S0140-6736(14)60584-5 \| pmc= \| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25106063 }} </ref>		* Recommended within 3-4.5 hours of onset of ischemic stroke in eligible patients by guidelines<ref name="pmid23370205">{{cite journal\| author=Jauch EC, Saver JL, Adams HP, Bruno A, Connors JJ, Demaerschalk BM et al.\| title=Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. \| journal=Stroke \| year= 2013 \| volume= 44 \| issue= 3 \| pages= 870-947 \| pmid=23370205 \| doi=10.1161/STR.0b013e318284056a \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23370205 }} </ref><ref name="pmid 22315273">{{cite journal\| author=Lansberg MG, O'Donnell MJ, Khatri P, Lang ES, Nguyen-Huynh MN, Schwartz NE et al.\| title=Antithrombotic and thrombolytic therapy for ischemic stroke: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. \| journal=Chest \| year= 2012 \| volume= 141 \| issue= 2 Suppl \| pages= e601S-36S \| pmid= 22315273 \| doi=10.1378/chest.11-2302 \| pmc=3278065 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22315273 }} </ref><ref>{{cite web\|url=http://www.aaem.org/em-resources/position-statements/clinical-practice/thrombolytic-therapy \|title=Position Statement on the Use of Intravenous Thrombolytic Therapy in the Treatment of Stroke \|publisher=American Academy of Emergency Medicine \|accessdate=2008-01-25}}</ref> and [[systematic review]]s<ref name="pmid25871671">{{cite journal\| author=Prabhakaran S, Ruff I, Bernstein RA\| title=Acute stroke intervention: a systematic review. \| journal=JAMA \| year= 2015 \| volume= 313 \| issue= 14 \| pages= 1451-62 \| pmid=25871671 \| doi=10.1001/jama.2015.3058 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25871671 }} </ref><ref name="pmid25072528">{{cite journal\| author=Wardlaw JM, Murray V, Berge E, del Zoppo GJ\| title=Thrombolysis for acute ischaemic stroke. \| journal=Cochrane Database Syst Rev \| year= 2014 \| volume= 7 \| issue= \| pages= CD000213 \| pmid=25072528 \| doi=10.1002/14651858.CD000213.pub3 \| pmc=4153726 \| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25072528 }} </ref><ref name="pmid25106063">{{cite journal\| author=Emberson J, Lees KR, Lyden P, Blackwell L, Albers G, Bluhmki E et al.\| title=Effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials. \| journal=Lancet \| year= 2014 \| volume= \| issue= \| pages= \| pmid=25106063 \| doi=10.1016/S0140-6736(14)60584-5 \| pmc= \| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25106063 }} </ref>
			* IV alteplase in eligible patients within ≤4.5 h; tenecteplase 0.25 mg/kg IV bolus may be used as an alternative per protocol <ref name="pmid38884324">{{cite journal \|vauthors=Xiong Y, Campbell BC, Schwamm LH, Meng X, Jin A, Parsons MW, Fisher M, Jiang Y, Che F, Wang L, Zhou L, Dai H, Liu X, Pan Y, Duan C, Xu Y, Xu A, Zong L, Tan Z, Ye W, Wang H, Wang Z, Hao M, Cao Z, Wang L, Wu S, Li H, Li Z, Zhao X, Wang Y \|title=Tenecteplase for Ischemic Stroke at 4.5 to 24 Hours without Thrombectomy \|journal=N Engl J Med \|volume=391 \|issue=3 \|pages=203–212 \|date=July 2024 \|pmid=38884324 \|doi=10.1056/NEJMoa2402980 \|url=}}</ref>; evaluate urgently for EVT in eligible large-vessel occlusion (LVO).
	\| style="padding: 5px 5px; background: #F5F5F5;" \|		\| style="padding: 5px 5px; background: #F5F5F5;" \|
	* None		* None
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	*Oral administration of [[aspirin]] (initial dose is 325 mg) is recommended within 24 to 48 hours after stroke onset in most patients<ref name="pmid23370205">{{cite journal\| author=Jauch EC, Saver JL, Adams HP, Bruno A, Connors JJ, Demaerschalk BM et al.\| title=Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. \| journal=Stroke \| year= 2013 \| volume= 44 \| issue= 3 \| pages= 870-947 \| pmid=23370205 \| doi=10.1161/STR.0b013e318284056a \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23370205 }} </ref>		*Oral administration of [[aspirin]] (initial dose is 325 mg) is recommended within 24 to 48 hours after stroke onset in most patients<ref name="pmid23370205">{{cite journal\| author=Jauch EC, Saver JL, Adams HP, Bruno A, Connors JJ, Demaerschalk BM et al.\| title=Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. \| journal=Stroke \| year= 2013 \| volume= 44 \| issue= 3 \| pages= 870-947 \| pmid=23370205 \| doi=10.1161/STR.0b013e318284056a \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23370205 }} </ref>
	*Aspirin is contraindicated in patients with ischemic stroke within 24 hours of t-PA administration<ref name="pmid23370205">{{cite journal\| author=Jauch EC, Saver JL, Adams HP, Bruno A, Connors JJ, Demaerschalk BM et al.\| title=Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. \| journal=Stroke \| year= 2013 \| volume= 44 \| issue= 3 \| pages= 870-947 \| pmid=23370205 \| doi=10.1161/STR.0b013e318284056a \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23370205 }} </ref>		*Aspirin is contraindicated in patients with ischemic stroke within 24 hours of t-PA administration<ref name="pmid23370205">{{cite journal\| author=Jauch EC, Saver JL, Adams HP, Bruno A, Connors JJ, Demaerschalk BM et al.\| title=Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. \| journal=Stroke \| year= 2013 \| volume= 44 \| issue= 3 \| pages= 870-947 \| pmid=23370205 \| doi=10.1161/STR.0b013e318284056a \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23370205 }} </ref>
	*DAPT ~~therapy~~ (aspirin ~~and~~ clopidogrel) ~~is recommended~~ for 90 days in patients with symptomatic intracranial ~~large artery disease~~		*DAPT (aspirin + clopidogrel) for up to 90 days is reasonable only for selected patients with recent stroke/TIA attributable to severe symptomatic intracranial stenosis; routine minor stroke/high-risk TIA DAPT is generally shorter (~21 days) followed by SAPT <ref name="pmid41582814">{{cite journal \|vauthors=Prabhakaran S, Gonzalez NR, Zachrison KS, Adeoye O, Alexandrov AW, Ansari SA, Chapman S, Czap AL, Dumitrascu OM, Ishida K, Jadhav AP, Johnson B, Johnston KC, Khatri P, Kimberly WT, Lee VH, Leslie-Mazwi TM, Mac Grory B, Madsen TE, Menon B, Mistry EA, Park S, Parker S, Pérez de la Ossa N, Reeves M, Saiz T, Scott PA, Schwartzberg D, Sheth SA, Sporns PB, Times S, Tjoumakaris S, Wolfe SQ, Yaghi S \|title=2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association \|journal=Stroke \|volume= \|issue= \|pages= \|date=January 2026 \|pmid=41582814 \|doi=10.1161/STR.0000000000000513 \|url=}}</ref> <ref name="pmid33724327">{{cite journal \|vauthors=Mendelson SJ, Prabhakaran S \|title=Diagnosis and Management of Transient Ischemic Attack and Acute Ischemic Stroke: A Review \|journal=JAMA \|volume=325 \|issue=11 \|pages=1088–1098 \|date=March 2021 \|pmid=33724327 \|doi=10.1001/jama.2020.26867 \|url=}}</ref>.
	\| style="padding: 5px 5px; background: #F5F5F5;" \|		\| style="padding: 5px 5px; background: #F5F5F5;" \|
	* Long term therapy with [[clopidogrel]] or aspirin extended release [[dipyridamole]] may be used for secondary prevention of non cardioembolic stroke		* Long term therapy with [[clopidogrel]] or aspirin extended release [[dipyridamole]] may be used for secondary prevention of non cardioembolic stroke

User:Anthony Gallo

2026-05-20T12:28:08Z

← Older revision		Revision as of 12:28, 20 May 2026
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	__NOTOC__		__NOTOC__
	[[Image:Gallo.png\|right]]		[[Image:Gallo.png\|right]]
	==Anthony Gallo, B.S.==		==Anthony Gallo, D.O.==
	'''Anthony Gallo, B.S.'''		'''Anthony Gallo, D.O.'''

	~~Email: [mailto:galloa53@rowan.edu galloa53@rowan.edu]~~

	~~==Current Position==~~
	~~Rowan University School of Osteopathic Medicine, Student: Class of 2022~~

	==Past Positions==		==Past Positions==
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	==Professional Background==		==Professional Background==
	Anthony Gallo is a medical ~~student at~~ Rowan University School of Osteopathic Medicine. He has served as Chair of the Medical Society of New Jersey and is a member of the Gold Humanism Honor Society. ~~Anthony~~ is ~~excited to pursue a career~~ in ~~internal medicine; he hopes to pursue a fellowship following residency~~.		Anthony Gallo was a member of the PERFUSE Study Group from 2014-2017. He is currently a gastroenterology fellow at Penn State Medical Center. Prior to that, he was Chief Resident at the Cleveland Clinic Foundation and the Louis Stokes Cleveland VA Medical Center. He completed his residency in Internal Medicine at the Cleveland Clinic Foundation. He graduated medical school from Rowan University School of Osteopathic Medicine. He has served as Chair of the Medical Society of New Jersey and is a member of the Gold Humanism Honor Society. He is board certified in Internal Medicine.

	Previously, he was an undergraduate research student at the PERFUSE Study Group at Beth Israel Deaconess Medical Center. He graduated from Boston College in Chestnut Hill, MA with a bachelor of science degree in Biology; he was also a member in the College of Arts and Sciences Honors Program. Anthony is an associate editor-in-chief at WikiDoc.org where he authors content in infectious disease. He has also trained new domestic and international postdoctoral fellows.		Previously, he was an undergraduate research student at the PERFUSE Study Group at Beth Israel Deaconess Medical Center. He graduated from Boston College in Chestnut Hill, MA with a bachelor of science degree in Biology; he was also a member in the College of Arts and Sciences Honors Program. Anthony was an associate editor-in-chief at WikiDoc.org where he authors content in infectious disease. He has also trained new domestic and international postdoctoral fellows.

	==Education==		==Education==

Met31p box gene transcriptions

2026-05-20T11:27:27Z

Met31 samplings

← Older revision		Revision as of 11:27, 20 May 2026
(One intermediate revision by the same user not shown)
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	==Met31 samplings==		==Met31 samplings==
	{{main\|Model samplings}}		{{main\|Model samplings}}
			[[Met31p box gene transcriptions#Met31 samplings\|Met31 samplings]]

	Copying a responsive elements consensus sequence AAACTGTG and putting the sequence in "⌘F" finds none between ZNF497 and A1BG or none between ZSCAN22 and A1BG as can be found by the computer programs.		Copying a responsive elements consensus sequence AAACTGTG and putting the sequence in "⌘F" finds none between ZNF497 and A1BG or none between ZSCAN22 and A1BG as can be found by the computer programs.

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	==Met3 samplings==		==Met3 samplings==
			[[Met31p box gene transcriptions#Met3 samplings\|Met3 samplings]]

	Copying a responsive elements consensus sequence TCACGTG and putting the sequence in "⌘F" finds none between ZNF497 and A1BG or none between ZSCAN22 and A1BG as can be found by the computer programs.		Copying a responsive elements consensus sequence TCACGTG and putting the sequence in "⌘F" finds none between ZNF497 and A1BG or none between ZSCAN22 and A1BG as can be found by the computer programs.

Mcm1 regulatory factor gene transcriptions

2026-05-20T06:03:00Z

Rossi samplings

← Older revision		Revision as of 06:03, 20 May 2026
(One intermediate revision by the same user not shown)
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	==Samplings==		==Samplings==
			[[Mcm1 regulatory factor gene transcriptions#Samplings\|Samplings]]

	Copying a consensus regulatory element: TT(A/T)CCNN(A/T)TNGG(A/T)AA and putting the sequence in "⌘F" finds no locations for this sequence in any A1BG direction as can be found by the computer programs.		Copying a consensus regulatory element: TT(A/T)CCNN(A/T)TNGG(A/T)AA and putting the sequence in "⌘F" finds no locations for this sequence in any A1BG direction as can be found by the computer programs.
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	==Rossi samplings==		==Rossi samplings==
	{{main\|Model samplings}}		{{main\|Model samplings}}
			[[Mcm1 regulatory factor gene transcriptions#Rossi samplings\|Rossi samplings]]

	Copying a responsive elements consensus sequence TTnCCnnnTnnGGnAA and putting the sequence in "⌘F" finds none between ZNF497 and A1BG or none between ZSCAN22 and A1BG as can be found by the computer programs.		Copying a responsive elements consensus sequence TTnCCnnnTnnGGnAA and putting the sequence in "⌘F" finds none between ZNF497 and A1BG or none between ZSCAN22 and A1BG as can be found by the computer programs.

User:Parth Vikram Singh

2026-05-20T02:29:42Z

← Older revision		Revision as of 02:29, 20 May 2026
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	# Gibson CM, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease other imaging findings.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease other imaging findings\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_other_imaging_findings]]		# Gibson CM, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease other imaging findings.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease other imaging findings\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_other_imaging_findings]]
	# Gibson CM, Ganti A V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease other diagnostic studies.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease other diagnostic studies\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_other_diagnostic_studies]]		# Gibson CM, Ganti A V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease other diagnostic studies.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease other diagnostic studies\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_other_diagnostic_studies]]
	# Gibson CM, ~~Gunnam V~~, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ~~overview~~.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ~~overview~~\|https://www.wikidoc.org/index.php/Non-~~alcoholic_fatty_liver_disease_overview~~]]		# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease medical therapy.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease medical therapy\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_medical_therapy]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ~~overview~~.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ~~overview~~\|https://www.wikidoc.org/index.php/Non-~~alcoholic_fatty_liver_disease_overview~~]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease surgery.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease surgery\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_surgery]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ~~overview~~.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ~~overview~~\|https://www.wikidoc.org/index.php/Non-~~alcoholic_fatty_liver_disease_overview~~]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease primary prevention.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease primary prevention\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_primary_prevention]]
	#		#Gibson CM, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease future or investigational therapies.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease future or investigational therapies\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_future_or_investigational_therapies]]

	==[[Imam Ali Shah Professional Experience\|Professional Experience]]==		==[[Imam Ali Shah Professional Experience\|Professional Experience]]==

Non-alcoholic fatty liver disease future or investigational therapies

2026-05-20T02:28:10Z

← Older revision		Revision as of 02:28, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}}		{{CMG}}; {{AE}}[[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]]

	{{PleaseHelp}}		{{PleaseHelp}}

	==Overview==		==Overview==
			Future investigational therapies for MASH include tirzepatide and other dual- or triple-incretin receptor agonists, gliflozins, pan-peroxisome proliferator-activated receptor agonists such as lanifibranor, fibroblast growth factor 21 analogs, fatty acid synthase inhibitors, and genetic target-based therapies such as antisense oligonucleotides targeting PNPLA3.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>

			Blood-based biomarkers of fibrosis and vibration-controlled transient elastography are expected to be used more frequently to monitor disease progression and regression, predict long-term liver-related events, and assess treatment response. Polygenic risk scores, metabolic signatures, and microbiome signatures may help identify patients with distinct MASLD trajectories and treatment responses.

	==Future or Investigational Therapies==		==Future or Investigational Therapies==

Non-alcoholic fatty liver disease primary prevention

2026-05-20T02:26:19Z

JAMA article updates

← Older revision		Revision as of 02:26, 20 May 2026
Line 1:		Line 1:
	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
	~~Effective measures for the primary prevention of non-alcoholic fatty liver disease~~ include ~~eating~~ a healthy ~~diet~~ and regular ~~exercise~~.		Measures that may reduce MASLD development or progression include maintaining a healthy weight, reducing excess caloric intake, limiting ultraprocessed foods, saturated fats, refined sugars, and sugar-sweetened beverages, engaging in regular physical activity, avoiding alcohol intake, and effectively managing type 2 diabetes, obesity, dyslipidemia, and hypertension.

	==Primary Prevention==		==Primary Prevention==
	Effective measures for the primary prevention of non-alcoholic fatty liver disease include:		Effective measures for the primary prevention of non-alcoholic fatty liver disease include:
	*Eating a healthy [[diet]] that is rich in vegetables, fruits and healthy fats is the first and very important step.<ref name="pmid28573067">{{cite journal \|vauthors=Patil R, Sood GK \|title=Non-alcoholic fatty liver disease and cardiovascular risk \|journal=World J Gastrointest Pathophysiol \|volume=8 \|issue=2 \|pages=51–58 \|year=2017 \|pmid=28573067 \|pmc=5437502 \|doi=10.4291/wjgp.v8.i2.51 \|url=}}</ref>		*Eating a healthy [[diet]] that is rich in vegetables, fruits and healthy fats is the first and very important step.<ref name="pmid28573067">{{cite journal \|vauthors=Patil R, Sood GK \|title=Non-alcoholic fatty liver disease and cardiovascular risk \|journal=World J Gastrointest Pathophysiol \|volume=8 \|issue=2 \|pages=51–58 \|year=2017 \|pmid=28573067 \|pmc=5437502 \|doi=10.4291/wjgp.v8.i2.51 \|url=}}</ref><ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
	*Regular [[Physical exercise\|exercise]]		*Regular [[Physical exercise\|exercise]]
	*Maintaining a healthy weight		*Maintaining a healthy weight

Non-alcoholic fatty liver disease surgery

2026-05-20T02:24:40Z

JAMA article updates

← Older revision		Revision as of 02:24, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}}[[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
	Surgery is not the first-line treatment option for patients with non- Alcoholic fatty liver disease (NAFLD). However, [[gastric bypass surgery]] is recommended in patients with non-alcoholic fatty liver disease whose [[Body mass index\|BMI]] is greater than ~~40 who psychologically stable and failed medical~~ therapy.		Surgery is not the first-line treatment option for patients with non- Alcoholic fatty liver disease (NAFLD). However, [[gastric bypass surgery]] is recommended in patients with non-alcoholic fatty liver disease whose [[Body mass index\|BMI]] is greater than 35 particularly in those without improvement in imaging-detected hepatic steatosis or fibrosis after behavioral modification or medication therapy.

	== Surgery ==		== Surgery ==

	==== Indications ====		==== Indications ====
	* Patients with NAFLD and [[BMI]] greater than 40 who psychologically stable		* Patients with NAFLD and [[BMI]] greater than 35 who psychologically stable<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
	* In patients who failed medical therapy.		* In patients who failed medical therapy.

Non-alcoholic fatty liver disease medical therapy

2026-05-20T02:21:36Z

JAMA article updates

Show changes

User:Parth Vikram Singh

2026-05-20T01:53:04Z

← Older revision		Revision as of 01:53, 20 May 2026
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	# Gibson CM, Marketkar S, Singh PV. Contribution to: '''Neuralgia.''' In WikiDoc. 30 June 2025. [[Neuralgia\|https://www.wikidoc.org/index.php'''/Neuralgia''']]		# Gibson CM, Marketkar S, Singh PV. Contribution to: '''Neuralgia.''' In WikiDoc. 30 June 2025. [[Neuralgia\|https://www.wikidoc.org/index.php'''/Neuralgia''']]
	# Gibson CM, Singh PV. Contribution to: '''Neuralgia medical therapy.''' In WikiDoc. 30 June 2025. [[Neuralgia medical therapy\|https://www.wikidoc.org/index.php/Neuralgia_medical_therapy]]		# Gibson CM, Singh PV. Contribution to: '''Neuralgia medical therapy.''' In WikiDoc. 30 June 2025. [[Neuralgia medical therapy\|https://www.wikidoc.org/index.php/Neuralgia_medical_therapy]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
	# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease pathophysiology.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease pathophysiology\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_pathophysiology]]		# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease pathophysiology.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease pathophysiology\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_pathophysiology]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease causes.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease causes\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_causes]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease causes.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease causes\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_causes]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease differential diagnosis.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease differential diagnosis\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_differential_diagnosis]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease differential diagnosis.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease differential diagnosis\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_differential_diagnosis]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease epidemiology and demographics.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease epidemiology and demographics\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_epidemiology_and_demographics]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease epidemiology and demographics.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease epidemiology and demographics\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_epidemiology_and_demographics]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease risk factors.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease risk factors\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_risk_factors]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease risk factors.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease risk factors\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_risk_factors]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease disease screening.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease screening\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_screening]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease disease screening.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease screening\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_screening]]
	# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease natural history, complications and prognosis.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease natural history, complications and prognosis\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_natural_history,_complications_and_prognosis]]		# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease natural history, complications and prognosis.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease natural history, complications and prognosis\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_natural_history,_complications_and_prognosis]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]		# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease history and symptoms.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease history and symptoms\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_history_and_symptoms]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease physical examination.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease physical examination\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_physical_examination]]
			# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease laboratory findings.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease laboratory findings\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_laboratory_findings]]
			# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ultrasound.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ultrasound\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_ultrasound]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease MRI.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease MRI\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_MRI]]
			# Gibson CM, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease other imaging findings.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease other imaging findings\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_other_imaging_findings]]
			# Gibson CM, Ganti A V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease other diagnostic studies.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease other diagnostic studies\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_other_diagnostic_studies]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
			#

	==[[Imam Ali Shah Professional Experience\|Professional Experience]]==		==[[Imam Ali Shah Professional Experience\|Professional Experience]]==

Non-alcoholic fatty liver disease other diagnostic studies

2026-05-20T01:52:18Z

JAMA article updates

← Older revision		Revision as of 01:52, 20 May 2026
Line 1:		Line 1:
	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}} ; {{AE}} {{ADG}}		{{CMG}} ; {{AE}} {{ADG}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
	Liver biopsy may be helpful in the diagnosis of non-alcoholic fatty liver disease. Findings on biopsy include [[Steatosis\|macrovesicular steatosis]], [[inflammation]], ballooning degeneration, zone 3 perivenular/periportal/perisinusoidal fibrosis and, finally, [[mallory bodies]].		Liver biopsy may be helpful in the diagnosis of non-alcoholic fatty liver disease. Findings on biopsy include [[Steatosis\|macrovesicular steatosis]], [[inflammation]], ballooning degeneration, zone 3 perivenular/periportal/perisinusoidal fibrosis and, finally, [[mallory bodies]].
	==Other Diagnostic Studies==		==Other Diagnostic Studies==
	*Liver biopsy is considered as a gold-standard for diagnosing, grading, and staging NAFLD.		*Liver biopsy is considered as a gold-standard for diagnosing, grading, and staging NAFLD, but it is invasive, costly, and associated with rare acute bleeding. Liver biopsy is not typically required to diagnose MASLD, but may be useful when the etiology of liver disease is uncertain, when noninvasive tests are inconclusive, or when MASLD coexists with other liver diseases such as autoimmune hepatitis or viral hepatitis.
	*Invasive test		*Invasive test
	*Associated with significant bleeding risk in patients with [[Clotting\|clotting abnormalities]] due to hepatic disease.		*Associated with significant bleeding risk in patients with [[Clotting\|clotting abnormalities]] due to hepatic disease.
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	\|}		\|}
	===Staging===		===Staging===
	Based on the degree of fibrosis on biospy NASH can be classified into 4 stages.		Based on the degree of fibrosis on biospy NASH can be classified into '''5''' stages.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
	{\| ~~border~~=~~"1" cellpadding~~=~~"5" cellspacing~~=~~"0" align~~=~~"center"~~ \|class="wikitable"		{\| class="wikitable"
	~~! colspan="2" style="background:#efefef;"~~ \|~~Staging~~		\|'''Stage'''
			\|'''Histologic description'''
			\|-
			\|F0
			\|Absence of fibrosis
	\|-		\|-
	\|~~Stage 1~~		\|F1
	\|		\|Perisinusoidal or portal fibrosis
	~~Zone 3 [[fibrosis]]<br>~~
	Perisinusoidal ~~fibrosis<br>~~
	~~Portal/ periportal~~ fibrosis
	\|-		\|-
	\|~~Stage 2~~		\|F2
	\|Perisinusoidal and portal/periportal [[fibrosis]]		\|Perisinusoidal and portal or periportal fibrosis
	\|-		\|-
	\|~~Stage 3~~		\|F3
	\|~~Bridging [[~~fibrosis]]		\|Septal and bridging fibrosis
	\|-		\|-
	\|~~Stage 4~~		\|F4
	\|[[Cirrhosis]]		\|Cirrhosis
	\|}		\|}

Non-alcoholic fatty liver disease other imaging findings

2026-05-20T01:47:59Z

JAMA article updates

← Older revision		Revision as of 01:47, 20 May 2026
(One intermediate revision by the same user not shown)
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}}		{{CMG}}; {{AE}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]]

	==Overview==		==Overview==
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	==Liver stiffness measurement (LSM) by elastography ==		==Liver stiffness measurement (LSM) by elastography ==

			Vibration-controlled transient elastography is used to noninvasively measure liver stiffness and is commonly used after FIB-4 testing in patients at increased risk for advanced fibrosis. A liver stiffness measurement greater than 8.0 kPa should prompt referral to a hepatologist for further evaluation.

	Two-dimensional shear wave elastography [SWE]) can estimate liver stiffness measurements: "LS of 8 and 12.5 kPa represent generally accepted cut-off values for F3 and F4 fibrosis. LS highly correlates with portal pressure, and esophageal varices are likely at values >20 kPa."<ref name="pmid24367208">{{cite journal\| author=Mueller S, Sandrin L\| title=Liver stiffness: a novel parameter for the diagnosis of liver disease. \| journal=Hepat Med \| year= 2010 \| volume= 2 \| issue= \| pages= 49-67 \| pmid=24367208 \| doi=10.2147/hmer.s7394 \| pmc=3846375 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24367208 }} </ref>		Two-dimensional shear wave elastography [SWE]) can estimate liver stiffness measurements: "LS of 8 and 12.5 kPa represent generally accepted cut-off values for F3 and F4 fibrosis. LS highly correlates with portal pressure, and esophageal varices are likely at values >20 kPa."<ref name="pmid24367208">{{cite journal\| author=Mueller S, Sandrin L\| title=Liver stiffness: a novel parameter for the diagnosis of liver disease. \| journal=Hepat Med \| year= 2010 \| volume= 2 \| issue= \| pages= 49-67 \| pmid=24367208 \| doi=10.2147/hmer.s7394 \| pmc=3846375 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24367208 }} </ref>
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	==Hepatic steatosis==		==Hepatic steatosis==
	Hepattic steatosis can be measured with the Controlled attenuation parameter (CAP).<ref name="pmid33460567">{{cite journal\| author=Petroff D, Blank V, Newsome PN, Voican CS, Thiele M \| display-authors=etal\| title=Assessment of hepatic steatosis by controlled attenuation parameter using the M and XL probes: an individual patient data meta-analysis. \| journal=Lancet Gastroenterol Hepatol \| year= 2021 \| volume= 6 \| issue= 3 \| pages= 185-198 \| pmid=33460567 \| doi=10.1016/S2468-1253(20)30357-5 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33460567 }} </ref><ref name="pmid30689971">{{cite journal\| author=Eddowes PJ, Sasso M, Allison M, Tsochatzis E, Anstee QM, Sheridan D \| display-authors=etal\| title=Accuracy of FibroScan Controlled Attenuation Parameter and Liver Stiffness Measurement in Assessing Steatosis and Fibrosis in Patients With Nonalcoholic Fatty Liver Disease. \| journal=Gastroenterology \| year= 2019 \| volume= 156 \| issue= 6 \| pages= 1717-1730 \| pmid=30689971 \| doi=10.1053/j.gastro.2019.01.042 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30689971 }} </ref>		Hepattic steatosis can be measured with the Controlled attenuation parameter (CAP).<ref name="pmid33460567">{{cite journal\| author=Petroff D, Blank V, Newsome PN, Voican CS, Thiele M \| display-authors=etal\| title=Assessment of hepatic steatosis by controlled attenuation parameter using the M and XL probes: an individual patient data meta-analysis. \| journal=Lancet Gastroenterol Hepatol \| year= 2021 \| volume= 6 \| issue= 3 \| pages= 185-198 \| pmid=33460567 \| doi=10.1016/S2468-1253(20)30357-5 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33460567 }} </ref><ref name="pmid30689971">{{cite journal\| author=Eddowes PJ, Sasso M, Allison M, Tsochatzis E, Anstee QM, Sheridan D \| display-authors=etal\| title=Accuracy of FibroScan Controlled Attenuation Parameter and Liver Stiffness Measurement in Assessing Steatosis and Fibrosis in Patients With Nonalcoholic Fatty Liver Disease. \| journal=Gastroenterology \| year= 2019 \| volume= 156 \| issue= 6 \| pages= 1717-1730 \| pmid=30689971 \| doi=10.1053/j.gastro.2019.01.042 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30689971 }} </ref><ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>

			The controlled attenuation parameter measures attenuation of ultrasound waves through the liver and is usually performed with vibration-controlled transient elastography. A controlled attenuation parameter value of 248 dB/m or greater is considered diagnostic for hepatic steatosis, and higher values indicate more severe steatosis.

			Compared with conventional ultrasonography, controlled attenuation parameter has similar sensitivity and slightly higher specificity, approximately 90%, for detecting hepatic steatosis.

	==Other imaging==		==Other imaging==

Non-alcoholic fatty liver disease MRI

2026-05-20T01:44:11Z

JAMA article updates

← Older revision		Revision as of 01:44, 20 May 2026
Line 1:		Line 1:
	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
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	==MRI==		==MRI==
	*[[Abdominal]] [[MRI]] may be helpful in the diagnosis of NAFLD.<ref name="urlNonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician">{{cite web \|url=http://www.aafp.org/afp/2013/0701/p35.html#afp20130701p35-b13 \|title=Nonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician \|format= \|work= \|accessdate=}}</ref><ref name="urlNonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician2">{{cite web \|url=http://www.aafp.org/afp/2013/0701/p35.html \|title=Nonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician \|format= \|work= \|accessdate=}}</ref>		*[[Abdominal]] [[MRI]] may be helpful in the diagnosis of NAFLD.<ref name="urlNonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician">{{cite web \|url=http://www.aafp.org/afp/2013/0701/p35.html#afp20130701p35-b13 \|title=Nonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician \|format= \|work= \|accessdate=}}</ref><ref name="urlNonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician2">{{cite web \|url=http://www.aafp.org/afp/2013/0701/p35.html \|title=Nonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician \|format= \|work= \|accessdate=}}</ref><ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
	*Findings on [[MRI]] suggestive NAFLD include:		*Findings on [[MRI]] suggestive NAFLD include:
	**[[Quantification]] of [[hepatic steatosis]].<ref name="pmid24040614">{{cite journal \|vauthors=Ligabue G, Besutti G, Scaglioni R, Stentarelli C, Guaraldi G \|title=MR quantitative biomarkers of non-alcoholic fatty liver disease: technical evolutions and future trends \|journal=Quant Imaging Med Surg \|volume=3 \|issue=4 \|pages=192–5 \|year=2013 \|pmid=24040614 \|pmc=3759141 \|doi=10.3978/j.issn.2223-4292.2013.08.01 \|url=}}</ref><ref name="pmid24966609">{{cite journal \|vauthors=Lee SS, Park SH \|title=Radiologic evaluation of nonalcoholic fatty liver disease \|journal=World J. Gastroenterol. \|volume=20 \|issue=23 \|pages=7392–402 \|year=2014 \|pmid=24966609 \|pmc=4064084 \|doi=10.3748/wjg.v20.i23.7392 \|url=}}</ref>		**[[Quantification]] of [[hepatic steatosis]].<ref name="pmid24040614">{{cite journal \|vauthors=Ligabue G, Besutti G, Scaglioni R, Stentarelli C, Guaraldi G \|title=MR quantitative biomarkers of non-alcoholic fatty liver disease: technical evolutions and future trends \|journal=Quant Imaging Med Surg \|volume=3 \|issue=4 \|pages=192–5 \|year=2013 \|pmid=24040614 \|pmc=3759141 \|doi=10.3978/j.issn.2223-4292.2013.08.01 \|url=}}</ref><ref name="pmid24966609">{{cite journal \|vauthors=Lee SS, Park SH \|title=Radiologic evaluation of nonalcoholic fatty liver disease \|journal=World J. Gastroenterol. \|volume=20 \|issue=23 \|pages=7392–402 \|year=2014 \|pmid=24966609 \|pmc=4064084 \|doi=10.3748/wjg.v20.i23.7392 \|url=}}</ref>
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	*MRI also helps longitudinal follow-up of patients with non-alcoholic fatty liver disease to check response to therapy		*MRI also helps longitudinal follow-up of patients with non-alcoholic fatty liver disease to check response to therapy
	*Another kind of MRI is magnetic resonance spectroscopy (MRS) which reflects fat in the whole liver like [[Triglyceride\|triglycerides]] in a specific volume; and [[proton]] density fat fraction (PDFF).<ref name="pmid288000872">{{cite journal \|vauthors=Di Martino M, Koryukova K, Bezzi M, Catalano C \|title=Imaging Features of Non-Alcoholic Fatty Liver Disease in Children and Adolescents \|journal=Children (Basel) \|volume=4 \|issue=8 \|pages= \|year=2017 \|pmid=28800087 \|pmc=5575595 \|doi=10.3390/children4080073 \|url=}}</ref>		*Another kind of MRI is magnetic resonance spectroscopy (MRS) which reflects fat in the whole liver like [[Triglyceride\|triglycerides]] in a specific volume; and [[proton]] density fat fraction (PDFF).<ref name="pmid288000872">{{cite journal \|vauthors=Di Martino M, Koryukova K, Bezzi M, Catalano C \|title=Imaging Features of Non-Alcoholic Fatty Liver Disease in Children and Adolescents \|journal=Children (Basel) \|volume=4 \|issue=8 \|pages= \|year=2017 \|pmid=28800087 \|pmc=5575595 \|doi=10.3390/children4080073 \|url=}}</ref>
			*Magnetic resonance imaging-proton density fat fraction has a sensitivity of 77% to 92% and specificity of 87% to 94% for detecting any degree of hepatic steatosis. Magnetic resonance spectroscopy has sensitivity and specificity of approximately 95% to 98%, but these methods are primarily used in clinical trials and specialized centers.<ref name="pmid412125502">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>

	==References==		==References==

Non-alcoholic fatty liver disease ultrasound

2026-05-20T01:42:12Z

JAMA article updates

← Older revision		Revision as of 01:42, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{MKK}}		{{CMG}}; {{AE}} {{MKK}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==

	[[Ultrasound]] ~~may be~~ helpful in the diagnosis of non-alcoholic fatty liver disease. ~~Increased~~ echogenicity ~~and~~ coarsened echotexture of the liver is the ~~most prominent~~ and ~~diagnostic finding on an ultrasound~~ in ~~patients diagnosed non-alcoholic fatty liver disease~~.		[[Ultrasound]] is helpful in the diagnosis of non-alcoholic fatty liver disease and is the first-line imaging test for diagnosis of hepatic steatosis. Sonographic findings include increased hepatic echogenicity compared with the renal cortex, decreased visibility of intrahepatic vessels, coarsened echotexture of the liver and impaired visualization of the diaphragm and deeper liver tissue. Ultrasonography has a sensitivity of 80% to 89% and specificity of 87% to 90% for detecting moderate to severe steatosis, but sensitivity is less than 50% for mild steatosis when hepatic fat content is less than 20%.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>

	==Ultrasound==		==Ultrasound==

Non-alcoholic fatty liver disease laboratory findings

2026-05-20T01:37:59Z

JAMA article updates

← Older revision		Revision as of 01:37, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{MKK}}		{{CMG}}; {{AE}} {{MKK}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
	There are no specific diagnostic laboratory findings associated with non alcoholic fatty liver disease. Laboratory findings include abnormal liver function tests but are unspecific. Other laboratory tests are generally performed to rule out other diagnosis.		There are no specific diagnostic laboratory findings associated with non alcoholic fatty liver disease. Laboratory findings include abnormal liver function tests but are unspecific. Other laboratory tests are generally performed to rule out other diagnosis.
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	**Typical finding include a 2-4 fold elevation of the [[ALT]]		**Typical finding include a 2-4 fold elevation of the [[ALT]]
	**An [[ALT]]/[[AST]] ratio of greater than 1.		**An [[ALT]]/[[AST]] ratio of greater than 1.
			**Normal aminotransferase levels do not exclude MASLD, advanced fibrosis, or cirrhosis. Up to two-thirds of patients with MASLD, including patients with advanced fibrosis or cirrhosis, may have normal serum aminotransferase levels, and serum ALT levels do not correlate well with histological severity.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>

	* Evaluation for alternative causes of liver disease should be performed.		* Evaluation for alternative causes of liver disease should be performed.
	** These include [[HCV\|HCV serology]], serologies for [[autoimmune hepatitis]], and copper studies including serum [[ceruloplasmin]] and 24-hour urinary copper if [[Wilson's disease\|Wilson disease]] is suspected.		** These include [[HCV\|HCV serology]], serologies for [[autoimmune hepatitis]], and copper studies including serum [[ceruloplasmin]] and 24-hour urinary copper if [[Wilson's disease\|Wilson disease]] is suspected.

	* [[Fasting plasma glucose]] testing following an overnight fast is important to look for [[hyperglycemia]], which is an indicator of [[insulin resistance]].		* Laboratory evaluation should include assessment of metabolic risk factors. [[Fasting plasma glucose]] testing following an overnight fast is important to look for [[hyperglycemia]], which is an indicator of [[insulin resistance]].
	** Fasting [[insulin]] levels can confirm [[hyperinsulinemia]] and [[insulin resistance]]		** Fasting [[insulin]] levels can confirm [[hyperinsulinemia]] and [[insulin resistance]]
	* [[Lipid]] levels ( serum [[cholesterol]] and fasting [[triglycerides]] ) should be evaluated		* [[Lipid]] levels ( serum [[cholesterol]] and fasting [[triglycerides]] ) should be evaluated
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	* Iron studies (in particular elevated [[ferritin]] and transferring saturation) are often abnormal in NAFLD		* Iron studies (in particular elevated [[ferritin]] and transferring saturation) are often abnormal in NAFLD
	* Some patients with NAFLD may have low titers of [[Autoimmune disease\|autoimmune]] [[antibodies]].		* Some patients with NAFLD may have low titers of [[Autoimmune disease\|autoimmune]] [[antibodies]].
			* Noninvasive fibrosis assessment commonly includes the Fibrosis-4 index and the enhanced liver fibrosis test.
			** The Fibrosis-4 index includes age, serum alanine aminotransferase level, serum aspartate aminotransferase level, and platelet count. It estimates the risk of advanced liver fibrosis as low when the score is less than 1.30, indeterminate when the score is 1.30 to 2.67, and high when the score is greater than 2.67. A Fibrosis-4 index less than 1.3 has a negative predictive value of 85% to 90% for detecting advanced liver fibrosis.

	* [[Biomarkers]]		* [[Biomarkers]]
	** CK18 represents a promising [[biomarker]] for evaluation of the presence of NASH.		** CK18 represents a promising [[biomarker]] for evaluation of the presence of NASH.
	** A defining characteristic of NASH is [[cellular]] death, and [[serum]] CK18 levels had been shown to correlate with [[steatohepatitis]].		** A defining characteristic of NASH is [[cellular]] death, and [[serum]] CK18 levels had been shown to correlate with [[steatohepatitis]].

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	** F3. Bridging fibrosis. Numerous septa		** F3. Bridging fibrosis. Numerous septa
	** F4. Cirrhosis		** F4. Cirrhosis
			* The enhanced liver fibrosis test uses tissue inhibitor of metalloproteinase 1, type III procollagen amino terminal peptide, and hyaluronic acid to generate a fibrosis severity score. The enhanced liver fibrosis test has a sensitivity of approximately 98% for detecting advanced liver fibrosis.
			* The Agile 3+ score combines liver stiffness measured by vibration-controlled transient elastography with aspartate aminotransferase to alanine aminotransferase ratio, platelet count, diabetes status, sex, and age. It may identify advanced fibrosis more accurately than the Fibrosis-4 index or liver stiffness measurement alone.
	* Nonivasive serological liver fibrosis score such as AST to platelet ratio (APRI), and proprietary tests such as: FibroTest, FibroSure, Hepascore, and FibroSpect. An example is based on the "serum hyaluronic acid, procollagen type III N-terminal peptide, and tissue inhibitor of metalloproteinase 1"<ref name="pmid33185364">{{cite journal\| author=Newsome PN, Buchholtz K, Cusi K, Linder M, Okanoue T, Ratziu V \| display-authors=etal\| title=A Placebo-Controlled Trial of Subcutaneous Semaglutide in Nonalcoholic Steatohepatitis. \| journal=N Engl J Med \| year= 2021 \| volume= 384 \| issue= 12 \| pages= 1113-1124 \| pmid=33185364 \| doi=10.1056/NEJMoa2028395 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33185364 }} </ref>.		* Nonivasive serological liver fibrosis score such as AST to platelet ratio (APRI), and proprietary tests such as: FibroTest, FibroSure, Hepascore, and FibroSpect. An example is based on the "serum hyaluronic acid, procollagen type III N-terminal peptide, and tissue inhibitor of metalloproteinase 1"<ref name="pmid33185364">{{cite journal\| author=Newsome PN, Buchholtz K, Cusi K, Linder M, Okanoue T, Ratziu V \| display-authors=etal\| title=A Placebo-Controlled Trial of Subcutaneous Semaglutide in Nonalcoholic Steatohepatitis. \| journal=N Engl J Med \| year= 2021 \| volume= 384 \| issue= 12 \| pages= 1113-1124 \| pmid=33185364 \| doi=10.1056/NEJMoa2028395 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33185364 }} </ref>.
	** A score > "9.8 indicates a moderate risk of advanced fibrosis"<ref name="pmid33185364">/		** A score > "9.8 indicates a moderate risk of advanced fibrosis"<nowiki><ref name="pmid33185364">/</nowiki>
	** A score > "11.3 denotes a high risk of advanced fibrosis"<ref name="pmid33185364"/>		** A score > "11.3 denotes a high risk of advanced fibrosis"<ref name="pmid33185364" />
	* Noninvasive imaging scores such as the Fibroscan.		* Noninvasive imaging scores such as the Fibroscan.

Non-alcoholic fatty liver disease physical examination

2026-05-20T01:31:29Z

JAMA article updates

← Older revision		Revision as of 01:31, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}}[[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
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	==Physical Examination==		==Physical Examination==
	Patients with NAFLD usually appear [[asymptomatic]]. Physical examination of patients with NAFLD is usually unremarkable.<ref name="urlNonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician">{{cite web \|url=https://www.aafp.org/afp/2013/0701/p35.html \|title=Nonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician \|format= \|work= \|accessdate=}}</ref>		Patients with NAFLD usually appear [[asymptomatic]]. Physical examination of patients with NAFLD is usually unremarkable.<ref name="urlNonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician">{{cite web \|url=https://www.aafp.org/afp/2013/0701/p35.html \|title=Nonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician \|format= \|work= \|accessdate=}}</ref>

			Approximately 50% to 60% of patients with MASLD have mild to moderate hepatomegaly, while less than 5% have splenomegaly. More than 80% of patients are overweight or obese, 60% to 70% have atherogenic dyslipidemia, approximately 60% have prediabetes or type 2 diabetes, and up to 50% have hypertension.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>

	==References==		==References==

Non-alcoholic fatty liver disease history and symptoms

2026-05-20T01:29:18Z

JAMA article updates

← Older revision		Revision as of 01:29, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{MKK}}		{{CMG}}; {{AE}} {{MKK}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
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	==History==		==History==
	There is no significant history associated in patients with the non-alcoholic fatty liver disease. However, history of alcohol consumption and family history of non-alcoholic fatty liver disease must be obtained.		There is no significant history associated in patients with the non-alcoholic fatty liver disease. MASLD is often detected incidentally when hepatic steatosis is identified on abdominal ultrasonography performed for another indication or when mild to moderate elevations in serum aminotransferase levels are found. However, history of alcohol consumption and family history of non-alcoholic fatty liver disease must be obtained.

	==Symptoms==		==Symptoms==
	Usually, nonalcoholic fatty liver disease presents with no or few symptoms and sighs but when it does it shows the following<ref>{{Cite web\|url=https://www.mayoclinic.org/diseases-conditions/nonalcoholic-fatty-liver-disease/symptoms-causes/syc-20354567\|title=Nafld\|last=\|first=\|date=\|website=\|publisher=\|access-date=}}</ref><ref name="pmid28507929">{{cite journal \|vauthors=Vizuete J, Camero A, Malakouti M, Garapati K, Gutierrez J \|title=Perspectives on Nonalcoholic Fatty Liver Disease: An Overview of Present and Future Therapies \|journal=J Clin Transl Hepatol \|volume=5 \|issue=1 \|pages=67–75 \|year=2017 \|pmid=28507929 \|pmc=5411359 \|doi=10.14218/JCTH.2016.00061 \|url=}}</ref><ref name="urlNonalcoholic Fatty Liver Disease">{{cite web \|url=http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/hepatology/nonalcoholic-fatty-liver-disease/ \|title=Nonalcoholic Fatty Liver Disease \|format= \|work= \|accessdate=}}</ref>		Usually, nonalcoholic fatty liver disease presents with no or few symptoms and sighs but when it does it shows the following<ref>{{Cite web\|url=https://www.mayoclinic.org/diseases-conditions/nonalcoholic-fatty-liver-disease/symptoms-causes/syc-20354567\|title=Nafld\|last=\|first=\|date=\|website=\|publisher=\|access-date=}}</ref><ref name="pmid28507929">{{cite journal \|vauthors=Vizuete J, Camero A, Malakouti M, Garapati K, Gutierrez J \|title=Perspectives on Nonalcoholic Fatty Liver Disease: An Overview of Present and Future Therapies \|journal=J Clin Transl Hepatol \|volume=5 \|issue=1 \|pages=67–75 \|year=2017 \|pmid=28507929 \|pmc=5411359 \|doi=10.14218/JCTH.2016.00061 \|url=}}</ref><ref name="urlNonalcoholic Fatty Liver Disease">{{cite web \|url=http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/hepatology/nonalcoholic-fatty-liver-disease/ \|title=Nonalcoholic Fatty Liver Disease \|format= \|work= \|accessdate=}}</ref><ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
	*[[Hepatomegaly]]		*[[Hepatomegaly]]
			*Malaise
	*[[Fatigue]]		*[[Fatigue]]
	*[[Ascites]]		*[[Ascites]]

User:Parth Vikram Singh

2026-05-20T01:11:43Z

← Older revision		Revision as of 01:11, 20 May 2026
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	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease causes.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease causes\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_causes]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease causes.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease causes\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_causes]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease differential diagnosis.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease differential diagnosis\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_differential_diagnosis]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease differential diagnosis.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease differential diagnosis\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_differential_diagnosis]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ~~overview~~.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ~~overview~~\|https://www.wikidoc.org/index.php/Non-~~alcoholic_fatty_liver_disease_overview~~]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease epidemiology and demographics.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease epidemiology and demographics\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_epidemiology_and_demographics]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ~~overview~~.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ~~overview~~\|https://www.wikidoc.org/index.php/Non-~~alcoholic_fatty_liver_disease_overview~~]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease risk factors.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease risk factors\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_risk_factors]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ~~overview~~.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ~~overview~~\|https://www.wikidoc.org/index.php/Non-~~alcoholic_fatty_liver_disease_overview~~]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease disease screening.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease screening\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_screening]]
	# Gibson CM, ~~Gunnam V~~, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ~~overview~~.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ~~overview~~\|https://www.wikidoc.org/index.php/Non-~~alcoholic_fatty_liver_disease_overview~~]]		# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease natural history, complications and prognosis.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease natural history, complications and prognosis\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_natural_history,_complications_and_prognosis]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]

Non-alcoholic fatty liver disease natural history, complications and prognosis

2026-05-20T01:10:03Z

JAMA article updates

← Older revision		Revision as of 01:10, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{MKK}}		{{CMG}}; {{AE}} {{MKK}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
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	**1) Patients with [[Non-alcoholic fatty liver disease\|NAFLD]] has overall high [[morbidity]] and [[mortality]] rate and the common cause of death in NAFLD patients is cardiovascular disease.		**1) Patients with [[Non-alcoholic fatty liver disease\|NAFLD]] has overall high [[morbidity]] and [[mortality]] rate and the common cause of death in NAFLD patients is cardiovascular disease.
	**2) Patients with [[NASH]] has more liver-related mortality rate		**2) Patients with [[NASH]] has more liver-related mortality rate
			* Approximately 15% to 40% of patients with isolated hepatic steatosis progress to MASH. Fibrosis progression is usually slow, with progression of approximately 1 fibrosis stage over 14 years among patients with isolated steatosis and approximately 1 fibrosis stage over 7 years among patients with MASH. More advanced fibrosis is the strongest risk factor for progression to cirrhosis, hepatic decompensation, and liver-related mortality.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
			* In a systematic review and meta-analysis of patients with histologically confirmed MASLD, 2% to 3% of patients with isolated steatosis developed advanced fibrosis over 15 to 20 years, while approximately 25% to 30% of patients with MASH developed advanced fibrosis within 8 to 10 years. Among patients with biopsy-confirmed MASH and F3 fibrosis, 22% progressed to cirrhosis over 2 years.
			* Cirrhosis is associated with hepatic decompensation events, including ascites, hepatic encephalopathy, and variceal bleeding, which occur at rates of about 10% annually. Up to nearly 2.5% of patients with cirrhosis develop incident hepatocellular carcinoma annually.
	* If left untreated, patients with NAFLD may progress to develop hepato-cellular carcinoma ([[HCC]]). But it is directly propotional to the degree of [[fibrosis]] and advanced [[cirrhosis]]		* If left untreated, patients with NAFLD may progress to develop hepato-cellular carcinoma ([[HCC]]). But it is directly propotional to the degree of [[fibrosis]] and advanced [[cirrhosis]]
	* Children who are positive with NAFLD are also prone to short lifespan when compared to general population.<ref name="pmid27213358">{{cite journal\| author=Calzadilla Bertot L, Adams LA\| title=The Natural Course of Non-Alcoholic Fatty Liver Disease. \| journal=Int J Mol Sci \| year= 2016 \| volume= 17 \| issue= 5 \| pages= \| pmid=27213358 \| doi=10.3390/ijms17050774 \| pmc=4881593 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27213358 }} </ref>		* Children who are positive with NAFLD are also prone to short lifespan when compared to general population.<ref name="pmid27213358">{{cite journal\| author=Calzadilla Bertot L, Adams LA\| title=The Natural Course of Non-Alcoholic Fatty Liver Disease. \| journal=Int J Mol Sci \| year= 2016 \| volume= 17 \| issue= 5 \| pages= \| pmid=27213358 \| doi=10.3390/ijms17050774 \| pmc=4881593 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27213358 }} </ref>
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	**[[Cirrhosis]]. Amon patients with both [[hepatic steatosis]] and elevated [[liver function tests]], the incidence rate of cirrhosis is 3.37 (95% CI: 2.34-4.86) per 1000 1000 person-years.		**[[Cirrhosis]]. Amon patients with both [[hepatic steatosis]] and elevated [[liver function tests]], the incidence rate of cirrhosis is 3.37 (95% CI: 2.34-4.86) per 1000 1000 person-years.
	**[[Internal bleeding]]		**[[Internal bleeding]]
	**~~Encepholopathy~~		**Hepatic decompensation events include ascites, hepatic encephalopathy, and variceal bleeding.

			* Other complications of MASLD include hepatocellular carcinoma, cardiovascular disease, chronic kidney disease, heart failure, atrial fibrillation, incident type 2 diabetes, and certain extrahepatic cancers.

	[[Non-alcoholic fatty liver disease]], especially if with cirrhosis, may be associated with [[thrombocytopenia]]<ref name="pmid34312112">{{cite journal\| author=Rivera-Álvarez M, Córdova-Ramírez AC, Elías-De-La-Cruz GD, Murrieta-Álvarez I, León-Peña AA, Cantero-Fortiz Y \| display-authors=etal\| title=Non-alcoholic fatty liver disease and thrombocytopenia IV: its association with granulocytopenia. \| journal=Hematol Transfus Cell Ther \| year= 2021 \| volume= \| issue= \| pages= \| pmid=34312112 \| doi=10.1016/j.htct.2021.06.004 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=34312112 }} </ref><ref name="pmid31575467">{{cite journal\| author=Panke CL, Tovo CV, Villela-Nogueira CA, Cravo CM, Ferreira FC, Rezende GFM \| display-authors=etal\| title=Evaluation of thrombocytopenia in patients with non-alcoholic fatty liver disease without cirrhosis. \| journal=Ann Hepatol \| year= 2020 \| volume= 19 \| issue= 1 \| pages= 88-91 \| pmid=31575467 \| doi=10.1016/j.aohep.2019.05.011 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31575467 }} </ref>.		[[Non-alcoholic fatty liver disease]], especially if with cirrhosis, may be associated with [[thrombocytopenia]]<ref name="pmid34312112">{{cite journal\| author=Rivera-Álvarez M, Córdova-Ramírez AC, Elías-De-La-Cruz GD, Murrieta-Álvarez I, León-Peña AA, Cantero-Fortiz Y \| display-authors=etal\| title=Non-alcoholic fatty liver disease and thrombocytopenia IV: its association with granulocytopenia. \| journal=Hematol Transfus Cell Ther \| year= 2021 \| volume= \| issue= \| pages= \| pmid=34312112 \| doi=10.1016/j.htct.2021.06.004 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=34312112 }} </ref><ref name="pmid31575467">{{cite journal\| author=Panke CL, Tovo CV, Villela-Nogueira CA, Cravo CM, Ferreira FC, Rezende GFM \| display-authors=etal\| title=Evaluation of thrombocytopenia in patients with non-alcoholic fatty liver disease without cirrhosis. \| journal=Ann Hepatol \| year= 2020 \| volume= 19 \| issue= 1 \| pages= 88-91 \| pmid=31575467 \| doi=10.1016/j.aohep.2019.05.011 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31575467 }} </ref>.

	===Prognosis===		===Prognosis===
			* Cardiovascular disease is the leading cause of death in patients with noncirrhotic MASLD, followed by extrahepatic cancer and liver-related complications. In patients with MASLD-related cirrhosis, liver-related and cardiovascular disease-related deaths are the predominant causes of mortality.<ref name="pmid412125502">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
	* In a cohort study of patient who had biopsy-proven NAFLD, 6% developed death, hepatocellular carcinoma, or death with 5 years<ref name="pmid37290471">{{cite journal\| author=Mózes FE, Lee JA, Vali Y, Alzoubi O, Staufer K, Trauner M \| display-authors=etal\| title=Performance of non-invasive tests and histology for the prediction of clinical outcomes in patients with non-alcoholic fatty liver disease: an individual participant data meta-analysis. \| journal=Lancet Gastroenterol Hepatol \| year= 2023 \| volume= \| issue= \| pages= \| pmid=37290471 \| doi=10.1016/S2468-1253(23)00141-3 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=37290471 }} </ref>.		* In a cohort study of patient who had biopsy-proven NAFLD, 6% developed death, hepatocellular carcinoma, or death with 5 years<ref name="pmid37290471">{{cite journal\| author=Mózes FE, Lee JA, Vali Y, Alzoubi O, Staufer K, Trauner M \| display-authors=etal\| title=Performance of non-invasive tests and histology for the prediction of clinical outcomes in patients with non-alcoholic fatty liver disease: an individual participant data meta-analysis. \| journal=Lancet Gastroenterol Hepatol \| year= 2023 \| volume= \| issue= \| pages= \| pmid=37290471 \| doi=10.1016/S2468-1253(23)00141-3 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=37290471 }} </ref>.

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	** 25% (4 of 16) (Supplementary table 1)		** 25% (4 of 16) (Supplementary table 1)
	* Histology is the most reliable means to grade the severity of the disease and thus estimate prognosis.		* Histology is the most reliable means to grade the severity of the disease and thus estimate prognosis.
			** Fibrosis stage is the strongest prognostic factor for liver-related morbidity and mortality. Compared with patients with no fibrosis, patients with cirrhosis have substantially higher risks of liver-related events, liver-related mortality, liver transplantation, and all-cause mortality.
	** The presence of [[fibrosis]] and [[cirrhosis]] is associated with a particularly poor prognosis among patients with NAFLD. <ref name="pmid22102440">{{cite journal\| author=Jepsen P, Grønbæk H\| title=Prognosis and staging of non-alcoholic fatty liver disease. \| journal=BMJ \| year= 2011 \| volume= 343 \| issue= \| pages= d7302 \| pmid=22102440 \| doi=10.1136/bmj.d7302 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22102440 }} </ref>		** The presence of [[fibrosis]] and [[cirrhosis]] is associated with a particularly poor prognosis among patients with NAFLD. <ref name="pmid22102440">{{cite journal\| author=Jepsen P, Grønbæk H\| title=Prognosis and staging of non-alcoholic fatty liver disease. \| journal=BMJ \| year= 2011 \| volume= 343 \| issue= \| pages= d7302 \| pmid=22102440 \| doi=10.1136/bmj.d7302 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22102440 }} </ref>
	** Depending on the extent of the [[fibrosis]] and [[cirrhosis]] at the time of diagnosis, the prognosis may vary.<ref name="SumanKhullar2016">{{cite journal\|last1=Suman\|first1=A.\|last2=Khullar\|first2=V.\|last3=Limaye\|first3=A.\|title=Complications of Non-Alcoholic Fatty Liver Disease\|journal=Journal of Hepatology\|volume=64\|issue=2\|year=2016\|pages=S473\|issn=01688278\|doi=10.1016/S0168-8278(16)00798-4}}</ref>		** Depending on the extent of the [[fibrosis]] and [[cirrhosis]] at the time of diagnosis, the prognosis may vary.<ref name="SumanKhullar2016">{{cite journal\|last1=Suman\|first1=A.\|last2=Khullar\|first2=V.\|last3=Limaye\|first3=A.\|title=Complications of Non-Alcoholic Fatty Liver Disease\|journal=Journal of Hepatology\|volume=64\|issue=2\|year=2016\|pages=S473\|issn=01688278\|doi=10.1016/S0168-8278(16)00798-4}}</ref>

Non-alcoholic fatty liver disease screening

2026-05-20T01:01:48Z

JAMA article updates

← Older revision		Revision as of 01:01, 20 May 2026
Line 1:		Line 1:
	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}}[[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
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	* However, American Gastroenterological Association Technical Review recommends screening for non-alcoholic fatty liver disease in population at high risk such as [[obesity]], [[insulin resistance]], and [[metabolic syndrome]].		* However, American Gastroenterological Association Technical Review recommends screening for non-alcoholic fatty liver disease in population at high risk such as [[obesity]], [[insulin resistance]], and [[metabolic syndrome]].
	* Screening is however complicated by the lack of accurate, noninvasive diagnostic tools for NAFLD and the lack of clear treatment that can be proposed to the patient.		* Screening is however complicated by the lack of accurate, noninvasive diagnostic tools for NAFLD and the lack of clear treatment that can be proposed to the patient.
			* Current guidelines summarized in the JAMA review<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref> recommend a 2-tier testing approach to screen for advanced liver fibrosis in high-risk populations, including individuals with prediabetes or type 2 diabetes, obesity, 2 or more cardiometabolic risk factors, imaging-detected hepatic steatosis, or persistently elevated serum aminotransferase levels.
	~~However~~, the AGA ~~recommend~~ screening<ref name="pmid37542503">{{cite journal\| author=Wattacheril JJ, Abdelmalek MF, Lim JK, Sanyal AJ\| title=AGA Clinical Practice Update on the Role of Noninvasive Biomarkers in the Evaluation and Management of Nonalcoholic Fatty Liver Disease: Expert Review. \| journal=Gastroenterology \| year= 2023 \| volume= \| issue= \| pages= \| pmid=37542503 \| doi=10.1053/j.gastro.2023.06.013 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=37542503 }} </ref>.		** The first step is calculation of the Fibrosis-4 index, usually performed in primary care. Patients with a Fibrosis-4 index greater than 1.3 should undergo vibration-controlled transient elastography or another noninvasive test, such as the enhanced liver fibrosis test. Patients with liver stiffness greater than 8.0 kPa or an enhanced liver fibrosis test score greater than 9.8 should be referred to a hepatologist.
			** Patients with a FIB-4 score less than 1.3 should undergo lifestyle modification, avoidance of alcohol intake, and treatment of type 2 diabetes, obesity, dyslipidemia, and hypertension. Repeat FIB-4 testing may be performed every 1 to 3 years. Patients with indeterminate or high-risk findings should undergo additional noninvasive fibrosis assessment and may require hepatology referral.
			{\| class="wikitable"
			\|'''FIB-4 score'''
			\|'''Interpretation'''
			\|-
			\|<1.30
			\|Low risk of advanced fibrosis
			\|-
			\|1.30-2.67
			\|Indeterminate risk of advanced fibrosis
			\|-
			\|>2.67
			\|High risk of advanced fibrosis
			\|}
			The AGA also recommends screening<ref name="pmid37542503">{{cite journal\| author=Wattacheril JJ, Abdelmalek MF, Lim JK, Sanyal AJ\| title=AGA Clinical Practice Update on the Role of Noninvasive Biomarkers in the Evaluation and Management of Nonalcoholic Fatty Liver Disease: Expert Review. \| journal=Gastroenterology \| year= 2023 \| volume= \| issue= \| pages= \| pmid=37542503 \| doi=10.1053/j.gastro.2023.06.013 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=37542503 }} </ref>.

	Workflows to promote screening may increase treatment<ref name="pmid37549979">{{cite journal\| author=Zhang X, Yip TC, Wong GL, Leow WX, Liang LY, Lim LL \| display-authors=etal\| title=Clinical care pathway to detect advanced liver disease in patients with type 2 diabetes through automated fibrosis score calculation and electronic reminder messages: a randomised controlled trial. \| journal=Gut \| year= 2023 \| volume= \| issue= \| pages= \| pmid=37549979 \| doi=10.1136/gutjnl-2023-330269 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=37549979 }} </ref>.		Workflows to promote screening may increase treatment<ref name="pmid37549979">{{cite journal\| author=Zhang X, Yip TC, Wong GL, Leow WX, Liang LY, Lim LL \| display-authors=etal\| title=Clinical care pathway to detect advanced liver disease in patients with type 2 diabetes through automated fibrosis score calculation and electronic reminder messages: a randomised controlled trial. \| journal=Gut \| year= 2023 \| volume= \| issue= \| pages= \| pmid=37549979 \| doi=10.1136/gutjnl-2023-330269 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=37549979 }} </ref>.

Non-alcoholic fatty liver disease risk factors

2026-05-20T00:56:27Z

JAMA article updates

← Older revision		Revision as of 00:56, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
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	==Risk Factors==		==Risk Factors==
	Risk factors in the development of non-alcoholic fatty liver disease include:<ref name="pmid25892859">{{cite journal\| author=Streba LA, Vere CC, Rogoveanu I, Streba CT\| title=Nonalcoholic fatty liver disease, metabolic risk factors, and hepatocellular carcinoma: an open question. \| journal=World J Gastroenterol \| year= 2015 \| volume= 21 \| issue= 14 \| pages= 4103-10 \| pmid=25892859 \| doi=10.3748/wjg.v21.i14.4103 \| pmc=4394070 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25892859 }} </ref><ref name="pmid22319959">{{cite journal\| author=He S, Bao W, Shao M, Wang W, Wang C, Sun J et al.\| title=Risk factors for non-alcoholic fatty liver disease in a Chinese population. \| journal=Acta Gastroenterol Belg \| year= 2011 \| volume= 74 \| issue= 4 \| pages= 503-8 \| pmid=22319959 \| doi= \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22319959 }} </ref><ref name="pmid258928592">{{cite journal \|vauthors=Streba LA, Vere CC, Rogoveanu I, Streba CT \|title=Nonalcoholic fatty liver disease, metabolic risk factors, and hepatocellular carcinoma: an open question \|journal=World J. Gastroenterol. \|volume=21 \|issue=14 \|pages=4103–10 \|year=2015 \|pmid=25892859 \|pmc=4394070 \|doi=10.3748/wjg.v21.i14.4103 \|url=}}</ref>		Risk factors in the development of non-alcoholic fatty liver disease include:<ref name="pmid25892859">{{cite journal\| author=Streba LA, Vere CC, Rogoveanu I, Streba CT\| title=Nonalcoholic fatty liver disease, metabolic risk factors, and hepatocellular carcinoma: an open question. \| journal=World J Gastroenterol \| year= 2015 \| volume= 21 \| issue= 14 \| pages= 4103-10 \| pmid=25892859 \| doi=10.3748/wjg.v21.i14.4103 \| pmc=4394070 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25892859 }} </ref><ref name="pmid22319959">{{cite journal\| author=He S, Bao W, Shao M, Wang W, Wang C, Sun J et al.\| title=Risk factors for non-alcoholic fatty liver disease in a Chinese population. \| journal=Acta Gastroenterol Belg \| year= 2011 \| volume= 74 \| issue= 4 \| pages= 503-8 \| pmid=22319959 \| doi= \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22319959 }} </ref><ref name="pmid258928592">{{cite journal \|vauthors=Streba LA, Vere CC, Rogoveanu I, Streba CT \|title=Nonalcoholic fatty liver disease, metabolic risk factors, and hepatocellular carcinoma: an open question \|journal=World J. Gastroenterol. \|volume=21 \|issue=14 \|pages=4103–10 \|year=2015 \|pmid=25892859 \|pmc=4394070 \|doi=10.3748/wjg.v21.i14.4103 \|url=}}</ref><ref name="pmid412125502">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
	*[[Viral hepatitis]]		*[[Viral hepatitis]]
	*Rapid [[weight loss]]		*Rapid [[weight loss]]
	*[[Malnutrition]]		*[[Malnutrition]]
	*[[Hypertriglyceridemia]]		*[[Hypertriglyceridemia]]
			*Low HDL cholesterol
	*[[Sleep apnea]]		*[[Sleep apnea]]
	*[[Hypothyroidism]]		*[[Hypothyroidism]]
	*[[Obesity]]		*Abdominal overweight or [[Obesity]]
	*[[Hypopituitarism]]		*[[Hypopituitarism]]
	*[[Diabetes mellitus type 2]]		*Prediabetes or [[Diabetes mellitus type 2]]
			*Insulin resistance
			*Hypertension
	*[[Polycystic ovary syndrome\|PCOS]] ([[polycystic ovarian syndrome]])		*[[Polycystic ovary syndrome\|PCOS]] ([[polycystic ovarian syndrome]])
			*Older age
			*Male sex
			*Postmenopausal status
			*PNPLA3 and TM6SF2 genetic variants
			*Sedentary lifestyle
			*Smoking
			*High intake of fructose, especially from sugar-sweetened beverages
			*High-calorie diets rich in saturated fats, sugars, and processed foods
			*Alcohol intake above MASLD thresholds
	*Medications like [[tamoxifen]], [[corticosteriods]], [[methotrexate]]		*Medications like [[tamoxifen]], [[corticosteriods]], [[methotrexate]]


			Cardiometabolic risk factors used in the classification of MASLD include body mass index of 25 or greater, or 23 or greater in Asian individuals; waist circumference of 80 cm or greater in women and 94 cm or greater in men; fasting glucose level of 5.6 mmol/L or greater, 2-hour postload glucose level of 7.8 mmol/L or greater, hemoglobin A1c level of 5.7% or greater, established type 2 diabetes, or use of glucose-lowering medication; blood pressure of 130/85 mm Hg or greater or use of antihypertensive medication; plasma triglyceride level of 1.70 mmol/L or greater or use of triglyceride-lowering medication; and low HDL cholesterol.

	==References==		==References==
	{{reflist\|2}}		{{reflist\|2}}

User:Parth Vikram Singh

2026-05-20T00:49:46Z

← Older revision		Revision as of 00:49, 20 May 2026
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	# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease pathophysiology.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease pathophysiology\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_pathophysiology]]		# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease pathophysiology.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease pathophysiology\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_pathophysiology]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease causes.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease causes\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_causes]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease causes.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease causes\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_causes]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ~~overview~~.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ~~overview~~\|https://www.wikidoc.org/index.php/Non-~~alcoholic_fatty_liver_disease_overview~~]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease differential diagnosis.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease differential diagnosis\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_differential_diagnosis]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]

Non-alcoholic fatty liver disease epidemiology and demographics

2026-05-20T00:49:32Z

JAMA article updates

← Older revision		Revision as of 00:49, 20 May 2026
Line 1:		Line 1:
	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
Line 17:		Line 17:

	===Prevalance===		===Prevalance===
			* MASLD is the most common chronic liver disease worldwide. Approximately 30% to 40% of adults worldwide have MASLD. The prevalence is substantially higher among individuals with type 2 diabetes and obesity, affecting approximately 60% to 70% of individuals with type 2 diabetes and approximately 70% to 80% of individuals with obesity.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
			* In a systematic review of 92 population-based studies from 1990 to 2019, the highest prevalence of ultrasound-detected MASLD was observed in Latin America and the lowest in Western Europe. By 2040, the global prevalence of MASLD among adults is projected to exceed 55%. In 2021, the global age-standardized prevalence of MASLD was 15,018 per 100,000 population, and the annual incidence was 608 per 100,000 population. The prevalence was higher in men than women and peaked at 45 to 49 years of age in men and 50 to 54 years of age in women.
			* Among individuals with type 2 diabetes, the global pooled prevalence of MASLD based on ultrasonography was 65.3%. Among individuals with type 2 diabetes who had liver biopsy data, the global histological prevalence of MASH was 66.4%, stage F2 fibrosis was present in 40.8%, and advanced fibrosis, defined as stage F3 or F4, was present in 15.5%.
	* The prevalence of non-alcoholic liver disease in the United States is estimated to be 10,000 to 24,000 cases per 100,000 individuals annually.		* The prevalence of non-alcoholic liver disease in the United States is estimated to be 10,000 to 24,000 cases per 100,000 individuals annually.

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	=== Gender ===		=== Gender ===
	* Men are more commonly affected by non-alcoholic liver disease than women.		* Men are more commonly affected by non-alcoholic liver disease than women. In global 2021 estimates, prevalence peaked at 45 to 49 years of age in men and at 50 to 54 years of age in women.
	* Among women it is more common in post-menopausal women than pre-menopausal.		* Among women it is more common in post-menopausal women than pre-menopausal.

Non-alcoholic fatty liver disease differential diagnosis

2026-05-20T00:37:05Z

JAMA article updates

← Older revision		Revision as of 00:37, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
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	==Differential Diagnosis==		==Differential Diagnosis==
	NAFLD must be differentiated from other diseases that cause [[jaundice]] and [[abdominal pain]].<ref name="pmid259378622">{{cite journal \|vauthors=Abd El-Kader SM, El-Den Ashmawy EM \|title=Non-alcoholic fatty liver disease: The diagnosis and management \|journal=World J Hepatol \|volume=7 \|issue=6 \|pages=846–58 \|year=2015 \|pmid=25937862 \|pmc=4411527 \|doi=10.4254/wjh.v7.i6.846 \|url=}}</ref>		NAFLD must be differentiated from other diseases that cause [[jaundice]] and [[abdominal pain]] like including alcohol-associated liver disease, metabolic dysfunction and alcohol-related liver disease, drug-induced liver injury, hepatitis C virus infection, iron overload, celiac disease, HIV infection, malnutrition, Wilson disease, lysosomal acid lipase deficiency, hypobetalipoproteinemia, and inborn errors of metabolism.<ref name="pmid259378622">{{cite journal \|vauthors=Abd El-Kader SM, El-Den Ashmawy EM \|title=Non-alcoholic fatty liver disease: The diagnosis and management \|journal=World J Hepatol \|volume=7 \|issue=6 \|pages=846–58 \|year=2015 \|pmid=25937862 \|pmc=4411527 \|doi=10.4254/wjh.v7.i6.846 \|url=}}</ref><ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>

	{\| align="center"		{\| align="center"

User:Parth Vikram Singh

2026-05-20T00:34:54Z

← Older revision		Revision as of 00:34, 20 May 2026
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	# Gibson CM, Singh P, Singh PV. Contribution to: '''Sepsis future or investigational therapies'''. In WikiDoc. 11 August 2025. [[Sepsis future or investigational therapies\|https://www.wikidoc.org/index.php?title=Sepsis_future_or_investigational_therapies]]		# Gibson CM, Singh P, Singh PV. Contribution to: '''Sepsis future or investigational therapies'''. In WikiDoc. 11 August 2025. [[Sepsis future or investigational therapies\|https://www.wikidoc.org/index.php?title=Sepsis_future_or_investigational_therapies]]
	# Gibson CM, Singh PV. Contribution to: '''Drug coated balloon'''. In WikiDoc. 11 April 2025. [[Drug coated balloon\|https://www.wikidoc.org/index.php?title=Drug_coated_balloon]]		# Gibson CM, Singh PV. Contribution to: '''Drug coated balloon'''. In WikiDoc. 11 April 2025. [[Drug coated balloon\|https://www.wikidoc.org/index.php?title=Drug_coated_balloon]]
	# Gibson CM, Singh PV. Contribution to:. '''Cardiac Optical Coherence Tomography.''' In WikiDoc. 7 May 2025. [[Cardiac Optical Coherence Tomography (OCT)\|https://www.wikidoc.org/index.php?title=Cardiac_Optical_Coherence_Tomography_(OCT)]]		# Gibson CM, Singh PV. Contribution to: '''Cardiac Optical Coherence Tomography.''' In WikiDoc. 7 May 2025. [[Cardiac Optical Coherence Tomography (OCT)\|https://www.wikidoc.org/index.php?title=Cardiac_Optical_Coherence_Tomography_(OCT)]]
	# Gibson CM, Singh PV. Contribution to:. '''Extracorporeal Membrane Oxygenation.''' In WikiDoc. 16 June 2025. [[Extracorporeal Membrane Oxygenation\|https://www.wikidoc.org/index.php?title='''Extracorporeal_Membrane_Oxygenation''']]		# Gibson CM, Singh PV. Contribution to: '''Extracorporeal Membrane Oxygenation.''' In WikiDoc. 16 June 2025. [[Extracorporeal Membrane Oxygenation\|https://www.wikidoc.org/index.php?title='''Extracorporeal_Membrane_Oxygenation''']]
	# Gibson CM, Zorkun C, Guddeti R, Singh PV. Contribution to:. '''Obesity.''' In WikiDoc. 30 December 2025. [[Obesity\|https://www.wikidoc.org/index.php/Obesity]]		# Gibson CM, Zorkun C, Guddeti R, Singh PV. Contribution to: '''Obesity.''' In WikiDoc. 30 December 2025. [[Obesity\|https://www.wikidoc.org/index.php/Obesity]]
	# Gibson CM, Singh PV. Contribution to:. '''Anti-obesity drug.''' In WikiDoc. 30 December 2025. [[Anti-obesity drug\|http://www.wikidoc.org/index.php/Anti-obesity_drug]]		# Gibson CM, Singh PV. Contribution to: '''Anti-obesity drug.''' In WikiDoc. 30 December 2025. [[Anti-obesity drug\|http://www.wikidoc.org/index.php/Anti-obesity_drug]]
	# Badgett RG, Singh PV. Contribution to:. '''Chronic pain medical therapy.''' In WikiDoc. 20 January 2026. [[Chronic pain medical therapy\|https://www.wikidoc.org/index.php/Chronic_pain_medical_therapy]]		# Badgett RG, Singh PV. Contribution to: '''Chronic pain medical therapy.''' In WikiDoc. 20 January 2026. [[Chronic pain medical therapy\|https://www.wikidoc.org/index.php/Chronic_pain_medical_therapy]]
	# Feinberg SD, Tariq MU, Singh PV. Contribution to:. '''Chronic pain.''' In WikiDoc. 20 January 2026. [[Chronic pain\|https://www.wikidoc.org/index.php/Chronic_pain]]		# Feinberg SD, Tariq MU, Singh PV. Contribution to: '''Chronic pain.''' In WikiDoc. 20 January 2026. [[Chronic pain\|https://www.wikidoc.org/index.php/Chronic_pain]]
	# Gibson CM, Marketkar S, Singh PV. Contribution to:. '''Neuralgia.''' In WikiDoc. 30 June 2025. [[Neuralgia\|https://www.wikidoc.org/index.php'''/Neuralgia''']]		# Gibson CM, Marketkar S, Singh PV. Contribution to: '''Neuralgia.''' In WikiDoc. 30 June 2025. [[Neuralgia\|https://www.wikidoc.org/index.php'''/Neuralgia''']]
	# Gibson CM, Singh PV. Contribution to:. '''Neuralgia medical therapy.''' In WikiDoc. 30 June 2025. [[Neuralgia medical therapy\|https://www.wikidoc.org/index.php/Neuralgia_medical_therapy]]		# Gibson CM, Singh PV. Contribution to: '''Neuralgia medical therapy.''' In WikiDoc. 30 June 2025. [[Neuralgia medical therapy\|https://www.wikidoc.org/index.php/Neuralgia_medical_therapy]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
			# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease pathophysiology.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease pathophysiology\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_pathophysiology]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease causes.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease causes\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_causes]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]

	==[[Imam Ali Shah Professional Experience\|Professional Experience]]==		==[[Imam Ali Shah Professional Experience\|Professional Experience]]==

Non-alcoholic fatty liver disease causes

2026-05-20T00:33:03Z

JAMA article updates

← Older revision		Revision as of 00:33, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
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	*Less common causes of non-alcoholic fatty liver disease include [[hypertension]] and [[dyslipidemia]].		*Less common causes of non-alcoholic fatty liver disease include [[hypertension]] and [[dyslipidemia]].
			*The risk of developing MASLD and progressing to MASH increases with the number of metabolic syndrome features, including abdominal obesity, hypertension, hypertriglyceridemia, low HDL cholesterol, and elevated blood glucose.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref> Cardiometabolic risk factors used in the classification of MASLD include body mass index of 25 or greater, or 23 or greater in Asian individuals; waist circumference of 80 cm or greater in women and 94 cm or greater in men; fasting glucose level of 5.6 mmol/L or greater, 2-hour postload glucose level of 7.8 mmol/L or greater, hemoglobin A1c level of 5.7% or greater, established type 2 diabetes, or use of glucose-lowering medication; blood pressure of 130/85 mm Hg or greater or use of antihypertensive medication; plasma triglyceride level of 1.70 mmol/L or greater or use of triglyceride-lowering medication; and low HDL cholesterol.
			*Other contributors include older age, male sex, postmenopausal status, PNPLA3 and TM6SF2 genetic variants, sedentary lifestyle, smoking, high fructose intake, alcohol consumption above MASLD thresholds, and high-calorie diets rich in saturated fats, sugars, and processed foods.
			*Other known causes of hepatic steatosis that should be excluded include use of corticosteroids, methotrexate, or tamoxifen; hepatitis C virus infection; iron overload; celiac disease; HIV infection; malnutrition; Wilson disease; lysosomal acid lipase deficiency; hypobetalipoproteinemia; and inborn errors of metabolism.

	===Secondary NAFLD===		===Secondary NAFLD===

Non-alcoholic fatty liver disease pathophysiology

2026-05-20T00:27:40Z

JAMA article updates

← Older revision		Revision as of 00:27, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{MKK}}		{{CMG}}; {{AE}} {{MKK}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
	The exact pathogenesis of NAFLD is not fully understood but is believed due to the interaction of multiple factors such as obesity, Insulin resistance, and metabolic syndrome. Pathogenesis of non-alcoholic liver disease ~~can be best~~ explained by 2 hit hypothesis. The first hit is [[steatosis]]. The second hit is controversial and is likely cause changes that leads from [[hepatic steatosis]] to [[hepatic]] [[inflammation]] and [[fibrosis]] by way of [[lipid peroxidation]].		The pathogenesis of MASLD is multifactorial. The exact pathogenesis of NAFLD is not fully understood but is believed due to the interaction of multiple factors such as obesity, Insulin resistance, and metabolic syndrome. Hepatic steatosis develops due to increased hepatic uptake of free fatty acids, increased de novo hepatic lipogenesis, decreased hepatic fatty acid oxidation, and reduced hepatic export of triglycerides into very low-density lipoproteins. Systemic insulin resistance promotes adipose tissue lipolysis and hepatic de novo lipogenesis, thereby increasing hepatic lipid accumulation. Progression from isolated steatosis to MASH is associated with lipotoxicity, in which accumulation of triglycerides, free cholesterol, saturated fatty acids, and ceramides contributes to hepatic inflammation, cellular dysfunction, and cell death. Metabolic factors, diet, genetic susceptibility, adipose tissue inflammation, and the gut microbiome may also contribute to disease progression. Dietary factors, including high intake of glucose, fructose, saturated fats, and processed foods, may promote low-grade inflammation in the liver and extrahepatic organs. Excess adipose tissue contributes to systemic inflammation through increased release of proinflammatory cytokines and recruitment and activation of immune cells, particularly macrophages.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>

			Pathogenesis of non-alcoholic liver disease was previously explained by 2 hit hypothesis. The first hit is [[steatosis]]. The second hit is controversial and is likely cause changes that leads from [[hepatic steatosis]] to [[hepatic]] [[inflammation]] and [[fibrosis]] by way of [[lipid peroxidation]]. The older two-hit hypothesis should be regarded as historical background. Current evidence supports a broader multifactorial model in which insulin resistance, lipotoxicity, diet, adipose tissue inflammation, genetics, and gut microbiome-related pathways act together to promote progression from steatosis to MASH and fibrosis.

	==Pathophysiology==		==Pathophysiology==
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	== Associated Conditions ==		== Associated Conditions ==
	* Most patients have associated features of the [[metabolic syndrome]] including [[obesity]], [[diabetes mellitus type 2]], [[hyperlipidemia]] ([[hypertriglyceridemia]]), and [[hypertension]]		* Most patients have associated features of the [[metabolic syndrome]] including [[obesity]], [[diabetes mellitus type 2]], [[hyperlipidemia]] ([[hypertriglyceridemia]]), and [[hypertension]]
			* MASLD is a multisystem metabolic disease associated with cardiovascular disease, chronic kidney disease, heart failure, atrial fibrillation, incident type 2 diabetes, and certain extrahepatic cancers, particularly gastrointestinal, breast, and gynecologic cancers.
	* Patients may suffer from complications of obesity such as [[obstructive sleep apnea]] , orthopedic complications, and [[polycystic ovary syndrome]].		* Patients may suffer from complications of obesity such as [[obstructive sleep apnea]] , orthopedic complications, and [[polycystic ovary syndrome]].

Non-alcoholic fatty liver disease classification

2026-05-20T00:22:39Z

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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}}{{PVS}}

	==Overview==		==Overview==
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	** Conditions such as [[abetalipoproteinemia]] or [[Wilson's disease\|Wilson’s disease]]		** Conditions such as [[abetalipoproteinemia]] or [[Wilson's disease\|Wilson’s disease]]
	\|}		\|}


			Steatotic liver disease may be subclassified according to the presence of cardiometabolic risk factors, alcohol intake, and other causes of hepatic steatosis.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
			{\| class="wikitable"
			!Category
			!Definition
			\|-
			\|MASLD
			\|Hepatic steatosis with at least 1 cardiometabolic risk factor, alcohol intake less than 140 g/week in women and less than 210 g/week in men, and no other known cause of hepatic steatosis
			\|-
			\|Metabolic dysfunction and alcohol-related liver disease (MetALD)
			\|Hepatic steatosis with metabolic dysfunction and alcohol intake of 140-350 g/week in women or 210-420 g/week in men
			\|-
			\|Alcohol-associated liver disease
			\|Alcohol intake greater than 350 g/week in women or greater than 420 g/week in men
			\|-
			\|Cryptogenic steatotic liver disease
			\|Hepatic steatosis without cardiometabolic risk factors and without an identifiable cause
			\|-
			\|Specific-etiology steatotic liver disease
			\|Hepatic steatosis due to another identifiable cause, such as drug-induced liver injury, iron overload, genotype 3 hepatitis C, Wilson disease, lysosomal acid lipase deficiency, hypobetalipoproteinemia, inborn errors of metabolism, celiac disease, malnutrition, or HIV infection
			\|}
			One standard drink is approximately equivalent to 10 g of alcohol, corresponding approximately to 12 oz of beer, 5 oz of wine, or 1.5 oz of 80-proof distilled spirits.

	==Histopathological classification==		==Histopathological classification==
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	\|}		\|}
	===Staging===		===Staging===
	Based on ~~the degree of [[~~fibrosis~~]] on [[biopsy]] non~~-~~alochoic fatty liver disease can be classified into 4 stages.~~
	{~~\| border="1" cellpadding="5" cellspacing="0" align="center"~~ \|class="wikitable"		Based on liver biopsy histology, liver fibrosis in MASLD is scored using a '''5-stage scale:'''
	~~! colspan="2" style="background:#efefef;"~~ \|~~Staging~~		{\| class="wikitable"
			\|'''Stage'''
			\|'''Histologic description'''
			\|-
			\|F0
			\|Absence of fibrosis
	\|-		\|-
	\|~~Stage 1~~		\|F1
	\|		\|Perisinusoidal or portal fibrosis
	~~Zone 3 [[fibrosis]]<br>~~
	Perisinusoidal ~~[[fibrosis]]<br>~~
	~~Portal/ periportal [[~~fibrosis]]
	\|-		\|-
	\|~~Stage 2~~		\|F2
	\|Perisinusoidal and portal/periportal fibrosis		\|Perisinusoidal and portal or periportal fibrosis
	\|-		\|-
	\|~~Stage 3~~		\|F3
	\|~~Bridging [[~~fibrosis]]		\|Septal and bridging fibrosis
	\|-		\|-
	\|~~Stage 4~~		\|F4
	\|[[Cirrhosis]]		\|Cirrhosis
	\|}		\|}

Non-alcoholic fatty liver disease overview

2026-05-20T00:01:49Z

← Older revision		Revision as of 00:01, 20 May 2026
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	==Overview==		==Overview==
	A non-alcoholic fatty liver disease, also called metabolic dysfunction-associated steatotic liver disease (MASLD) in the new [https://www.aasld.org/new-nafld-nomenclature AASLD nomenclature], is a form of [[Hepatitis\|chronic hepatitis]] that shares the histologic features of alcohol-induced [[hepatitis]] but is found in patients without prior history of alcohol abuse. MASLD is the most common chronic liver disease worldwide.Based on the severity of the disease non-alcoholic fatty liver disease encompasses a range of disorders including mild [[steatosis]], [[steatohepatitis]], advanced [[fibrosis]], [[cirrhosis]], [[fulminant]] hepatic failure, and less commonly hepatocellular carcinoma. Risk factors for non alcoholic liver disease include [[obesity]], [[diabetes mellitus type 2]], [[hyperlipidemia]], and sudden dramatic weight loss. The diagnosis of NAFLD should be considered in any patient presenting with elevated [[Transaminase\|transaminases]] without any underlying condition or pathological process. NAFLD is diagnosed when hepatic steatosis is detected, usually by abdominal ultrasonography, in association with at least one cardiometabolic risk factor and in the absence of significant alcohol intake or another known cause of hepatic steatosis. NAFLD must be distinguished from steatosis and steatohepatitis due to secondary causes. These include various forms of [[malnutrition]], drugs (eg, [[warfarin]], [[methotrexate]], [[amiodarone]], [[glucocorticoids]], synthetic [[Estrogen\|estrogens]], [[tamoxifen]], and various [[antibiotic]] and [[Antiviral\|antivira]]<nowiki/>l agents), metabolic and genetic disorders (eg [[lipodystrophy]], [[dysbetalipoproteinemia]], and acute [[fatty liver]] of [[pregnancy]]), use of total [[Parenteral nutrition\|parenteral]] nutrition, and [[gastric bypass]] and other weight loss surgeries. NAFLD is mostly seen in obese individuals but may be encountered in thin or normal weight patients. MASLD affects approximately 30% to 40% of adults worldwide, including approximately 60% to 70% of individuals with type 2 diabetes and approximately 70% to 80% of individuals with obesity. [[Insulin resistance]] is a core feature of NAFLD, diabetes, obesity, and dyslipidemia. NAFLD can therefore be considered part of the insulin resistance (or metabolic) syndrome. Insulin resistance leads to accumulation of fat within hepatocytesvialipogenesis (and inhibition of lipolysis) and [[Hyperinsulinism\|hyperinsulinemia]]. The pathogenesis of NAFLD and its progression to NASH appears to result from a two-step process, whereby an initial insult in the form of insulin resistance due to genetic and acquired factors leads to hyperinsulinemia and accumulation of fat within hepatocytes (steatosis). The steatotic liver is then vulnerable to further insult; hepatocellular injury and fibrosis may develop in the presence of [[oxidative stress]] and the [[proinflammatory]] activity of cytokines and similar agents. This leads to exacerbation of insulin resistance; further [[oxidative stress]]; and acceleration of inflammatory, [[degenerative]], and fibrotic processes. The natural history of NAFLD is dependent on the stage of the disease. The prognosis of simple steatosis seems to be relatively benign, with a 1% to 2% risk of developing [[cirrhosis]] over 15 to 20 years. Patients with NASH and fibrosis can progress to [[cirrhosis]], which can lead to end-stage liver disease; hepatic [[decompensation]]; or [[hepatocellular carcinoma]], a rare, end-stage outcome. Cardiovascular disease is the leading cause of death among patients with noncirrhotic MASLD, followed by certain extrahepatic cancers and liver-related complications. In patients with MASLD-related cirrhosis, liver-related and cardiovascular disease-related deaths are the predominant causes of mortality. Imaging techniques can be helpful by showing steatosis, but liver biopsy is the only way to assess the severity of inflammation and fibrosis. The mainstay of treatment for NAFLD is lifestyle modifications and treatment of underlying risk factors such as obesity, diabetes mellitus type 2, and hyperlipidemia. First-line treatment includes behavioral modification with a weight-reducing diet, increased physical activity, alcohol avoidance, and management of type 2 diabetes, obesity, hypertension, and hyperlipidemia. Resmetirom and semaglutide are conditionally approved by the US Food and Drug Administration for adults with noncirrhotic MASH and moderate to advanced fibrosis.[[File:FIGURE NAFLD.png\|center\|thumb\|~~601x601px~~\|Figure 1. Overview of prevalence, diagnosis, complications, and fibrosis risk stratification in MASLD.]]		A non-alcoholic fatty liver disease, also called metabolic dysfunction-associated steatotic liver disease (MASLD) in the new [https://www.aasld.org/new-nafld-nomenclature AASLD nomenclature], is a form of [[Hepatitis\|chronic hepatitis]] that shares the histologic features of alcohol-induced [[hepatitis]] but is found in patients without prior history of alcohol abuse. MASLD is the most common chronic liver disease worldwide.Based on the severity of the disease non-alcoholic fatty liver disease encompasses a range of disorders including mild [[steatosis]], [[steatohepatitis]], advanced [[fibrosis]], [[cirrhosis]], [[fulminant]] hepatic failure, and less commonly hepatocellular carcinoma. Risk factors for non alcoholic liver disease include [[obesity]], [[diabetes mellitus type 2]], [[hyperlipidemia]], and sudden dramatic weight loss. The diagnosis of NAFLD should be considered in any patient presenting with elevated [[Transaminase\|transaminases]] without any underlying condition or pathological process. NAFLD is diagnosed when hepatic steatosis is detected, usually by abdominal ultrasonography, in association with at least one cardiometabolic risk factor and in the absence of significant alcohol intake or another known cause of hepatic steatosis. NAFLD must be distinguished from steatosis and steatohepatitis due to secondary causes. These include various forms of [[malnutrition]], drugs (eg, [[warfarin]], [[methotrexate]], [[amiodarone]], [[glucocorticoids]], synthetic [[Estrogen\|estrogens]], [[tamoxifen]], and various [[antibiotic]] and [[Antiviral\|antivira]]<nowiki/>l agents), metabolic and genetic disorders (eg [[lipodystrophy]], [[dysbetalipoproteinemia]], and acute [[fatty liver]] of [[pregnancy]]), use of total [[Parenteral nutrition\|parenteral]] nutrition, and [[gastric bypass]] and other weight loss surgeries. NAFLD is mostly seen in obese individuals but may be encountered in thin or normal weight patients. MASLD affects approximately 30% to 40% of adults worldwide, including approximately 60% to 70% of individuals with type 2 diabetes and approximately 70% to 80% of individuals with obesity. [[Insulin resistance]] is a core feature of NAFLD, diabetes, obesity, and dyslipidemia. NAFLD can therefore be considered part of the insulin resistance (or metabolic) syndrome. Insulin resistance leads to accumulation of fat within hepatocytesvialipogenesis (and inhibition of lipolysis) and [[Hyperinsulinism\|hyperinsulinemia]]. The pathogenesis of NAFLD and its progression to NASH appears to result from a two-step process, whereby an initial insult in the form of insulin resistance due to genetic and acquired factors leads to hyperinsulinemia and accumulation of fat within hepatocytes (steatosis). The steatotic liver is then vulnerable to further insult; hepatocellular injury and fibrosis may develop in the presence of [[oxidative stress]] and the [[proinflammatory]] activity of cytokines and similar agents. This leads to exacerbation of insulin resistance; further [[oxidative stress]]; and acceleration of inflammatory, [[degenerative]], and fibrotic processes. The natural history of NAFLD is dependent on the stage of the disease. The prognosis of simple steatosis seems to be relatively benign, with a 1% to 2% risk of developing [[cirrhosis]] over 15 to 20 years. Patients with NASH and fibrosis can progress to [[cirrhosis]], which can lead to end-stage liver disease; hepatic [[decompensation]]; or [[hepatocellular carcinoma]], a rare, end-stage outcome. Cardiovascular disease is the leading cause of death among patients with noncirrhotic MASLD, followed by certain extrahepatic cancers and liver-related complications. In patients with MASLD-related cirrhosis, liver-related and cardiovascular disease-related deaths are the predominant causes of mortality. Imaging techniques can be helpful by showing steatosis, but liver biopsy is the only way to assess the severity of inflammation and fibrosis. The mainstay of treatment for NAFLD is lifestyle modifications and treatment of underlying risk factors such as obesity, diabetes mellitus type 2, and hyperlipidemia. First-line treatment includes behavioral modification with a weight-reducing diet, increased physical activity, alcohol avoidance, and management of type 2 diabetes, obesity, hypertension, and hyperlipidemia. Resmetirom and semaglutide are conditionally approved by the US Food and Drug Administration for adults with noncirrhotic MASH and moderate to advanced fibrosis.[[File:FIGURE NAFLD.png\|center\|thumb\|613x613px\|Figure 1. Overview of prevalence, diagnosis, complications, and fibrosis risk stratification in MASLD.]]

	==Historical Perspective==		==Historical Perspective==

← Older revision		Revision as of 14:25, 20 May 2026
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	*The dose of [[aspirin]] is usually between 160-300mg daily.<ref name="pmid9174558">{{cite journal \|vauthors= \|title=The International Stroke Trial (IST): a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19435 patients with acute ischaemic stroke. International Stroke Trial Collaborative Group \|journal=Lancet \|volume=349 \|issue=9065 \|pages=1569–81 \|date=May 1997 \|pmid=9174558 \|doi= \|url=}}</ref>		*The dose of [[aspirin]] is usually between 160-300mg daily.<ref name="pmid9174558">{{cite journal \|vauthors= \|title=The International Stroke Trial (IST): a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19435 patients with acute ischaemic stroke. International Stroke Trial Collaborative Group \|journal=Lancet \|volume=349 \|issue=9065 \|pages=1569–81 \|date=May 1997 \|pmid=9174558 \|doi= \|url=}}</ref>
	*[[Aspirin\|IV aspirin]] administration within 90 minutes after the start of [[Alteplase\|IV alteplase]] is associated with symptomatic intracranial hemorrhage, for which co administration is discouraged but benefits should be assessed in each individual case.<ref name="PowersRabinstein2019" /><ref name="ZinkstokRoos2012">{{cite journal\|last1=Zinkstok\|first1=Sanne M\|last2=Roos\|first2=Yvo B\|title=Early administration of aspirin in patients treated with alteplase for acute ischaemic stroke: a randomised controlled trial\|journal=The Lancet\|volume=380\|issue=9843\|year=2012\|pages=731–737\|issn=01406736\|doi=10.1016/S0140-6736(12)60949-0}}</ref>		*[[Aspirin\|IV aspirin]] administration within 90 minutes after the start of [[Alteplase\|IV alteplase]] is associated with symptomatic intracranial hemorrhage, for which co administration is discouraged but benefits should be assessed in each individual case.<ref name="PowersRabinstein2019" /><ref name="ZinkstokRoos2012">{{cite journal\|last1=Zinkstok\|first1=Sanne M\|last2=Roos\|first2=Yvo B\|title=Early administration of aspirin in patients treated with alteplase for acute ischaemic stroke: a randomised controlled trial\|journal=The Lancet\|volume=380\|issue=9843\|year=2012\|pages=731–737\|issn=01406736\|doi=10.1016/S0140-6736(12)60949-0}}</ref>
	*[[Dual antiplatelet therapy]] with [[aspirin~~]] and [[~~clopidogrel~~]] (75 mg/d, with a loading dose of 600mg) may~~ be started within 24 hours ~~after [[symptom]] onset~~ and continued ~~for~~ 21 days in patients with ~~no cardioembolic [[~~ischemic stroke]].<ref name="~~JohnstonEaston2018~~">{{cite journal\|~~last1~~=Johnston\|~~first1~~=~~S. Claiborne~~\|~~last2~~=~~Easton~~\|~~first2~~=~~J. Donald~~\|~~last3~~=~~Farrant~~\|~~first3~~=~~Mary~~\|~~last4~~=~~Barsan~~\|~~first4~~=~~William~~\|~~last5~~=~~Conwit~~\|~~first5~~=~~Robin~~ A.\|~~last6~~=~~Elm~~\|~~first6~~=~~Jordan J.~~\|~~last7~~=~~Kim~~\|~~first7~~=~~Anthony S.~~\|~~last8~~=~~Lindblad~~\|~~first8~~=~~Anne S~~.\|~~last9~~=~~Palesch~~\|~~first9~~=~~Yuko Y.~~\|title=~~Clopidogrel and Aspirin in~~ Acute Ischemic Stroke ~~and High-Risk TIA~~\|journal=~~New England Journal of Medicine~~\|volume=~~379~~\|issue=3\|~~year~~=~~2018~~\|~~pages~~=~~215–225~~\|~~issn~~=~~0028-4793~~\|doi=10.~~1056~~/~~NEJMoa1800410~~}}</ref>		*[[Dual antiplatelet therapy]] (DAPT) with aspirin plus clopidogrel should be started early (ideally within 24 hours) and continued short term (commonly ~21 days) in patients with minor noncardioembolic ischemic stroke or high-risk TIA who did not receive IV thrombolysis, followed by single antiplatelet therapy.<ref name="pmid41582814">{{cite journal \|vauthors=Prabhakaran S, Gonzalez NR, Zachrison KS, Adeoye O, Alexandrov AW, Ansari SA, Chapman S, Czap AL, Dumitrascu OM, Ishida K, Jadhav AP, Johnson B, Johnston KC, Khatri P, Kimberly WT, Lee VH, Leslie-Mazwi TM, Mac Grory B, Madsen TE, Menon B, Mistry EA, Park S, Parker S, Pérez de la Ossa N, Reeves M, Saiz T, Scott PA, Schwartzberg D, Sheth SA, Sporns PB, Times S, Tjoumakaris S, Wolfe SQ, Yaghi S \|title=2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association \|journal=Stroke \|volume= \|issue= \|pages= \|date=January 2026 \|pmid=41582814 \|doi=10.1161/STR.0000000000000513 \|url=}}</ref><ref name="pmid33724327">{{cite journal \|vauthors=Mendelson SJ, Prabhakaran S \|title=Diagnosis and Management of Transient Ischemic Attack and Acute Ischemic Stroke: A Review \|journal=JAMA \|volume=325 \|issue=11 \|pages=1088–1098 \|date=March 2021 \|pmid=33724327 \|doi=10.1001/jama.2020.26867 \|url=}}</ref>.
			*In patients with recent stroke/TIA attributable to severe symptomatic intracranial stenosis (Intracranial athrosclerotic diseas i.e ICAD), DAPT for up to 90 days is reasonable<ref name="pmid41582814">{{cite journal \|vauthors=Prabhakaran S, Gonzalez NR, Zachrison KS, Adeoye O, Alexandrov AW, Ansari SA, Chapman S, Czap AL, Dumitrascu OM, Ishida K, Jadhav AP, Johnson B, Johnston KC, Khatri P, Kimberly WT, Lee VH, Leslie-Mazwi TM, Mac Grory B, Madsen TE, Menon B, Mistry EA, Park S, Parker S, Pérez de la Ossa N, Reeves M, Saiz T, Scott PA, Schwartzberg D, Sheth SA, Sporns PB, Times S, Tjoumakaris S, Wolfe SQ, Yaghi S \|title=2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association \|journal=Stroke \|volume= \|issue= \|pages= \|date=January 2026 \|pmid=41582814 \|doi=10.1161/STR.0000000000000513 \|url=}}</ref>.
	*[[Aspirin]] should not substitute [[Alteplase\|IV alteplase]] or mechanical thrombectomy in patients eligible for these therapies.<ref name="PowersRabinstein2019" />		*[[Aspirin]] should not substitute [[Alteplase\|IV alteplase]] or mechanical thrombectomy in patients eligible for these therapies.<ref name="PowersRabinstein2019" />

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	\|-		\|-
	\| style="padding: 5px 5px; background: #F5F5F5;" \|'''Reperfusion therapy'''		\| style="padding: 5px 5px; background: #F5F5F5;" \|'''Reperfusion therapy'''
	\| style="padding: 5px 5px; background: #F5F5F5;" \|~~[[Tissue plasminogen activator\|'''Tissue plasminogen activator''']] '''~~(~~t-PA~~)~~'''~~		\| style="padding: 5px 5px; background: #F5F5F5;" \|IV thrombolysis (alteplase or tenecteplase); Endovascular thrombectomy (EVT)
	\| style="padding: 5px 5px; background: #F5F5F5;" \|		\| style="padding: 5px 5px; background: #F5F5F5;" \|
	* Recommended within 3-4.5 hours of onset of ischemic stroke in eligible patients by guidelines<ref name="pmid23370205">{{cite journal\| author=Jauch EC, Saver JL, Adams HP, Bruno A, Connors JJ, Demaerschalk BM et al.\| title=Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. \| journal=Stroke \| year= 2013 \| volume= 44 \| issue= 3 \| pages= 870-947 \| pmid=23370205 \| doi=10.1161/STR.0b013e318284056a \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23370205 }} </ref><ref name="pmid 22315273">{{cite journal\| author=Lansberg MG, O'Donnell MJ, Khatri P, Lang ES, Nguyen-Huynh MN, Schwartz NE et al.\| title=Antithrombotic and thrombolytic therapy for ischemic stroke: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. \| journal=Chest \| year= 2012 \| volume= 141 \| issue= 2 Suppl \| pages= e601S-36S \| pmid= 22315273 \| doi=10.1378/chest.11-2302 \| pmc=3278065 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22315273 }} </ref><ref>{{cite web\|url=http://www.aaem.org/em-resources/position-statements/clinical-practice/thrombolytic-therapy \|title=Position Statement on the Use of Intravenous Thrombolytic Therapy in the Treatment of Stroke \|publisher=American Academy of Emergency Medicine \|accessdate=2008-01-25}}</ref> and [[systematic review]]s<ref name="pmid25871671">{{cite journal\| author=Prabhakaran S, Ruff I, Bernstein RA\| title=Acute stroke intervention: a systematic review. \| journal=JAMA \| year= 2015 \| volume= 313 \| issue= 14 \| pages= 1451-62 \| pmid=25871671 \| doi=10.1001/jama.2015.3058 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25871671 }} </ref><ref name="pmid25072528">{{cite journal\| author=Wardlaw JM, Murray V, Berge E, del Zoppo GJ\| title=Thrombolysis for acute ischaemic stroke. \| journal=Cochrane Database Syst Rev \| year= 2014 \| volume= 7 \| issue= \| pages= CD000213 \| pmid=25072528 \| doi=10.1002/14651858.CD000213.pub3 \| pmc=4153726 \| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25072528 }} </ref><ref name="pmid25106063">{{cite journal\| author=Emberson J, Lees KR, Lyden P, Blackwell L, Albers G, Bluhmki E et al.\| title=Effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials. \| journal=Lancet \| year= 2014 \| volume= \| issue= \| pages= \| pmid=25106063 \| doi=10.1016/S0140-6736(14)60584-5 \| pmc= \| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25106063 }} </ref>		* Recommended within 3-4.5 hours of onset of ischemic stroke in eligible patients by guidelines<ref name="pmid23370205">{{cite journal\| author=Jauch EC, Saver JL, Adams HP, Bruno A, Connors JJ, Demaerschalk BM et al.\| title=Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. \| journal=Stroke \| year= 2013 \| volume= 44 \| issue= 3 \| pages= 870-947 \| pmid=23370205 \| doi=10.1161/STR.0b013e318284056a \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23370205 }} </ref><ref name="pmid 22315273">{{cite journal\| author=Lansberg MG, O'Donnell MJ, Khatri P, Lang ES, Nguyen-Huynh MN, Schwartz NE et al.\| title=Antithrombotic and thrombolytic therapy for ischemic stroke: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. \| journal=Chest \| year= 2012 \| volume= 141 \| issue= 2 Suppl \| pages= e601S-36S \| pmid= 22315273 \| doi=10.1378/chest.11-2302 \| pmc=3278065 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22315273 }} </ref><ref>{{cite web\|url=http://www.aaem.org/em-resources/position-statements/clinical-practice/thrombolytic-therapy \|title=Position Statement on the Use of Intravenous Thrombolytic Therapy in the Treatment of Stroke \|publisher=American Academy of Emergency Medicine \|accessdate=2008-01-25}}</ref> and [[systematic review]]s<ref name="pmid25871671">{{cite journal\| author=Prabhakaran S, Ruff I, Bernstein RA\| title=Acute stroke intervention: a systematic review. \| journal=JAMA \| year= 2015 \| volume= 313 \| issue= 14 \| pages= 1451-62 \| pmid=25871671 \| doi=10.1001/jama.2015.3058 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25871671 }} </ref><ref name="pmid25072528">{{cite journal\| author=Wardlaw JM, Murray V, Berge E, del Zoppo GJ\| title=Thrombolysis for acute ischaemic stroke. \| journal=Cochrane Database Syst Rev \| year= 2014 \| volume= 7 \| issue= \| pages= CD000213 \| pmid=25072528 \| doi=10.1002/14651858.CD000213.pub3 \| pmc=4153726 \| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25072528 }} </ref><ref name="pmid25106063">{{cite journal\| author=Emberson J, Lees KR, Lyden P, Blackwell L, Albers G, Bluhmki E et al.\| title=Effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials. \| journal=Lancet \| year= 2014 \| volume= \| issue= \| pages= \| pmid=25106063 \| doi=10.1016/S0140-6736(14)60584-5 \| pmc= \| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25106063 }} </ref>
			* IV alteplase in eligible patients within ≤4.5 h; tenecteplase 0.25 mg/kg IV bolus may be used as an alternative per protocol <ref name="pmid38884324">{{cite journal \|vauthors=Xiong Y, Campbell BC, Schwamm LH, Meng X, Jin A, Parsons MW, Fisher M, Jiang Y, Che F, Wang L, Zhou L, Dai H, Liu X, Pan Y, Duan C, Xu Y, Xu A, Zong L, Tan Z, Ye W, Wang H, Wang Z, Hao M, Cao Z, Wang L, Wu S, Li H, Li Z, Zhao X, Wang Y \|title=Tenecteplase for Ischemic Stroke at 4.5 to 24 Hours without Thrombectomy \|journal=N Engl J Med \|volume=391 \|issue=3 \|pages=203–212 \|date=July 2024 \|pmid=38884324 \|doi=10.1056/NEJMoa2402980 \|url=}}</ref>; evaluate urgently for EVT in eligible large-vessel occlusion (LVO).
	\| style="padding: 5px 5px; background: #F5F5F5;" \|		\| style="padding: 5px 5px; background: #F5F5F5;" \|
	* None		* None
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	*Oral administration of [[aspirin]] (initial dose is 325 mg) is recommended within 24 to 48 hours after stroke onset in most patients<ref name="pmid23370205">{{cite journal\| author=Jauch EC, Saver JL, Adams HP, Bruno A, Connors JJ, Demaerschalk BM et al.\| title=Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. \| journal=Stroke \| year= 2013 \| volume= 44 \| issue= 3 \| pages= 870-947 \| pmid=23370205 \| doi=10.1161/STR.0b013e318284056a \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23370205 }} </ref>		*Oral administration of [[aspirin]] (initial dose is 325 mg) is recommended within 24 to 48 hours after stroke onset in most patients<ref name="pmid23370205">{{cite journal\| author=Jauch EC, Saver JL, Adams HP, Bruno A, Connors JJ, Demaerschalk BM et al.\| title=Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. \| journal=Stroke \| year= 2013 \| volume= 44 \| issue= 3 \| pages= 870-947 \| pmid=23370205 \| doi=10.1161/STR.0b013e318284056a \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23370205 }} </ref>
	*Aspirin is contraindicated in patients with ischemic stroke within 24 hours of t-PA administration<ref name="pmid23370205">{{cite journal\| author=Jauch EC, Saver JL, Adams HP, Bruno A, Connors JJ, Demaerschalk BM et al.\| title=Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. \| journal=Stroke \| year= 2013 \| volume= 44 \| issue= 3 \| pages= 870-947 \| pmid=23370205 \| doi=10.1161/STR.0b013e318284056a \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23370205 }} </ref>		*Aspirin is contraindicated in patients with ischemic stroke within 24 hours of t-PA administration<ref name="pmid23370205">{{cite journal\| author=Jauch EC, Saver JL, Adams HP, Bruno A, Connors JJ, Demaerschalk BM et al.\| title=Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. \| journal=Stroke \| year= 2013 \| volume= 44 \| issue= 3 \| pages= 870-947 \| pmid=23370205 \| doi=10.1161/STR.0b013e318284056a \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23370205 }} </ref>
	*DAPT ~~therapy~~ (aspirin ~~and~~ clopidogrel) ~~is recommended~~ for 90 days in patients with symptomatic intracranial ~~large artery disease~~		*DAPT (aspirin + clopidogrel) for up to 90 days is reasonable only for selected patients with recent stroke/TIA attributable to severe symptomatic intracranial stenosis; routine minor stroke/high-risk TIA DAPT is generally shorter (~21 days) followed by SAPT <ref name="pmid41582814">{{cite journal \|vauthors=Prabhakaran S, Gonzalez NR, Zachrison KS, Adeoye O, Alexandrov AW, Ansari SA, Chapman S, Czap AL, Dumitrascu OM, Ishida K, Jadhav AP, Johnson B, Johnston KC, Khatri P, Kimberly WT, Lee VH, Leslie-Mazwi TM, Mac Grory B, Madsen TE, Menon B, Mistry EA, Park S, Parker S, Pérez de la Ossa N, Reeves M, Saiz T, Scott PA, Schwartzberg D, Sheth SA, Sporns PB, Times S, Tjoumakaris S, Wolfe SQ, Yaghi S \|title=2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association \|journal=Stroke \|volume= \|issue= \|pages= \|date=January 2026 \|pmid=41582814 \|doi=10.1161/STR.0000000000000513 \|url=}}</ref> <ref name="pmid33724327">{{cite journal \|vauthors=Mendelson SJ, Prabhakaran S \|title=Diagnosis and Management of Transient Ischemic Attack and Acute Ischemic Stroke: A Review \|journal=JAMA \|volume=325 \|issue=11 \|pages=1088–1098 \|date=March 2021 \|pmid=33724327 \|doi=10.1001/jama.2020.26867 \|url=}}</ref>.
	\| style="padding: 5px 5px; background: #F5F5F5;" \|		\| style="padding: 5px 5px; background: #F5F5F5;" \|
	* Long term therapy with [[clopidogrel]] or aspirin extended release [[dipyridamole]] may be used for secondary prevention of non cardioembolic stroke		* Long term therapy with [[clopidogrel]] or aspirin extended release [[dipyridamole]] may be used for secondary prevention of non cardioembolic stroke

← Older revision		Revision as of 02:29, 20 May 2026
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	# Gibson CM, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease other imaging findings.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease other imaging findings\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_other_imaging_findings]]		# Gibson CM, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease other imaging findings.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease other imaging findings\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_other_imaging_findings]]
	# Gibson CM, Ganti A V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease other diagnostic studies.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease other diagnostic studies\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_other_diagnostic_studies]]		# Gibson CM, Ganti A V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease other diagnostic studies.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease other diagnostic studies\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_other_diagnostic_studies]]
	# Gibson CM, ~~Gunnam V~~, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ~~overview~~.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ~~overview~~\|https://www.wikidoc.org/index.php/Non-~~alcoholic_fatty_liver_disease_overview~~]]		# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease medical therapy.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease medical therapy\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_medical_therapy]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ~~overview~~.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ~~overview~~\|https://www.wikidoc.org/index.php/Non-~~alcoholic_fatty_liver_disease_overview~~]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease surgery.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease surgery\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_surgery]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ~~overview~~.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ~~overview~~\|https://www.wikidoc.org/index.php/Non-~~alcoholic_fatty_liver_disease_overview~~]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease primary prevention.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease primary prevention\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_primary_prevention]]
	#		#Gibson CM, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease future or investigational therapies.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease future or investigational therapies\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_future_or_investigational_therapies]]

	==[[Imam Ali Shah Professional Experience\|Professional Experience]]==		==[[Imam Ali Shah Professional Experience\|Professional Experience]]==

← Older revision		Revision as of 01:53, 20 May 2026
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	# Gibson CM, Marketkar S, Singh PV. Contribution to: '''Neuralgia.''' In WikiDoc. 30 June 2025. [[Neuralgia\|https://www.wikidoc.org/index.php'''/Neuralgia''']]		# Gibson CM, Marketkar S, Singh PV. Contribution to: '''Neuralgia.''' In WikiDoc. 30 June 2025. [[Neuralgia\|https://www.wikidoc.org/index.php'''/Neuralgia''']]
	# Gibson CM, Singh PV. Contribution to: '''Neuralgia medical therapy.''' In WikiDoc. 30 June 2025. [[Neuralgia medical therapy\|https://www.wikidoc.org/index.php/Neuralgia_medical_therapy]]		# Gibson CM, Singh PV. Contribution to: '''Neuralgia medical therapy.''' In WikiDoc. 30 June 2025. [[Neuralgia medical therapy\|https://www.wikidoc.org/index.php/Neuralgia_medical_therapy]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
	# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease pathophysiology.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease pathophysiology\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_pathophysiology]]		# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease pathophysiology.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease pathophysiology\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_pathophysiology]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease causes.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease causes\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_causes]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease causes.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease causes\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_causes]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease differential diagnosis.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease differential diagnosis\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_differential_diagnosis]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease differential diagnosis.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease differential diagnosis\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_differential_diagnosis]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease epidemiology and demographics.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease epidemiology and demographics\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_epidemiology_and_demographics]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease epidemiology and demographics.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease epidemiology and demographics\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_epidemiology_and_demographics]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease risk factors.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease risk factors\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_risk_factors]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease risk factors.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease risk factors\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_risk_factors]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease disease screening.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease screening\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_screening]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease disease screening.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease screening\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_screening]]
	# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease natural history, complications and prognosis.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease natural history, complications and prognosis\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_natural_history,_complications_and_prognosis]]		# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease natural history, complications and prognosis.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease natural history, complications and prognosis\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_natural_history,_complications_and_prognosis]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]		# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease history and symptoms.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease history and symptoms\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_history_and_symptoms]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease physical examination.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease physical examination\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_physical_examination]]
			# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease laboratory findings.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease laboratory findings\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_laboratory_findings]]
			# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ultrasound.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ultrasound\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_ultrasound]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease MRI.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease MRI\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_MRI]]
			# Gibson CM, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease other imaging findings.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease other imaging findings\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_other_imaging_findings]]
			# Gibson CM, Ganti A V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease other diagnostic studies.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease other diagnostic studies\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_other_diagnostic_studies]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
			# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
			#

	==[[Imam Ali Shah Professional Experience\|Professional Experience]]==		==[[Imam Ali Shah Professional Experience\|Professional Experience]]==

← Older revision		Revision as of 01:11, 20 May 2026
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	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease causes.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease causes\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_causes]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease causes.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease causes\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_causes]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease differential diagnosis.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease differential diagnosis\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_differential_diagnosis]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease differential diagnosis.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease differential diagnosis\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_differential_diagnosis]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ~~overview~~.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ~~overview~~\|https://www.wikidoc.org/index.php/Non-~~alcoholic_fatty_liver_disease_overview~~]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease epidemiology and demographics.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease epidemiology and demographics\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_epidemiology_and_demographics]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ~~overview~~.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ~~overview~~\|https://www.wikidoc.org/index.php/Non-~~alcoholic_fatty_liver_disease_overview~~]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease risk factors.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease risk factors\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_risk_factors]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ~~overview~~.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ~~overview~~\|https://www.wikidoc.org/index.php/Non-~~alcoholic_fatty_liver_disease_overview~~]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease disease screening.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease screening\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_screening]]
	# Gibson CM, ~~Gunnam V~~, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ~~overview~~.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ~~overview~~\|https://www.wikidoc.org/index.php/Non-~~alcoholic_fatty_liver_disease_overview~~]]		# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease natural history, complications and prognosis.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease natural history, complications and prognosis\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_natural_history,_complications_and_prognosis]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]

← Older revision		Revision as of 00:49, 20 May 2026
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	# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease pathophysiology.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease pathophysiology\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_pathophysiology]]		# Gibson CM, Kaur M, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease pathophysiology.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease pathophysiology\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_pathophysiology]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease causes.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease causes\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_causes]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease causes.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease causes\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_causes]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease ~~overview~~.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease ~~overview~~\|https://www.wikidoc.org/index.php/Non-~~alcoholic_fatty_liver_disease_overview~~]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease differential diagnosis.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease differential diagnosis\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_differential_diagnosis]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]
	# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]		# Gibson CM, Gunnam V, Singh PV. Contribution to: '''Non-alcoholic fatty liver disease overview.''' In WikiDoc. 19 May 2025. [[Non-alcoholic fatty liver disease overview\|https://www.wikidoc.org/index.php/Non-alcoholic_fatty_liver_disease_overview]]