Psoriatic arthritis: Difference between revisions
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* Pharmacologic therapy for [[psoriatic arthritis]] include, [[Non-steroidal anti-inflammatory drug|non-steroidal anti-inflammatory drugs]] ([[Non-steroidal anti-inflammatory drug|NSAID]]<nowiki/>s), conventional synthetic [[Disease-modifying antirheumatic drug|DMARDs]] (eg, [[methotrexate]], [[sulfasalazine]], [[Cyclosporine|cyclosporin A]], [[leflunomide]]), biologic[[Disease-modifying antirheumatic drug|DMARD]]<nowiki/>s<nowiki/> including, [[TNF inhibitor|TNF inhibitors]] (eg, [[etanercept]], [[infliximab]], [[adalimumab]], [[golimumab]]), [[Phosphodiesterase inhibitors|phosphodiesterase (PDE) inhibitors]] (eg, [[apremilast]]), interleukin(IL) inhibitors (eg, [[secukinumab]], [[ixekizumab]], [[abatacept]]) and [[Joint|intraarticular]] [[Glucocorticoids|glucocorticoid]] injections. | * Pharmacologic therapy for [[psoriatic arthritis]] include, [[Non-steroidal anti-inflammatory drug|non-steroidal anti-inflammatory drugs]] ([[Non-steroidal anti-inflammatory drug|NSAID]]<nowiki/>s), conventional synthetic [[Disease-modifying antirheumatic drug|DMARDs]] (eg, [[methotrexate]], [[sulfasalazine]], [[Cyclosporine|cyclosporin A]], [[leflunomide]]), biologic[[Disease-modifying antirheumatic drug|DMARD]]<nowiki/>s<nowiki/> including, [[TNF inhibitor|TNF inhibitors]] (eg, [[etanercept]], [[infliximab]], [[adalimumab]], [[golimumab]]), [[Phosphodiesterase inhibitors|phosphodiesterase (PDE) inhibitors]] (eg, [[apremilast]]), interleukin(IL) inhibitors (eg, [[secukinumab]], [[ixekizumab]], [[abatacept]]) and [[Joint|intraarticular]] [[Glucocorticoids|glucocorticoid]] injections. | ||
* '''Peripheral [[arthritis]]''': | * '''Peripheral [[arthritis]]''': | ||
** '''Mild disease''': [[Non-steroidal anti-inflammatory drug|Nonsteroidal antiinflammatory drugs]] ([[Non-steroidal anti-inflammatory drug|NSAID]]<nowiki/>s) are the most | ** '''Mild disease''': [[Non-steroidal anti-inflammatory drug|Nonsteroidal antiinflammatory drugs]] ([[Non-steroidal anti-inflammatory drug|NSAID]]<nowiki/>s) are the most commonly used drugs for the management of mild active [[psoriatic arthritis]].<ref name="pmid15708943">{{cite journal |vauthors=Nash P, Clegg DO |title=Psoriatic arthritis therapy: NSAIDs and traditional DMARDs |journal=Ann. Rheum. Dis. |volume=64 Suppl 2 |issue= |pages=ii74–7 |date=March 2005 |pmid=15708943 |pmc=1766880 |doi=10.1136/ard.2004.030783 |url=}}</ref><ref name="pmid11296544">{{cite journal |vauthors=Sarzi-Puttini P, Santandrea S, Boccassini L, Panni B, Caruso I |title=The role of NSAIDs in psoriatic arthritis: evidence from a controlled study with nimesulide |journal=Clin. Exp. Rheumatol. |volume=19 |issue=1 Suppl 22 |pages=S17–20 |date=2001 |pmid=11296544 |doi= |url=}}</ref> | ||
*** '''Preferred regimen (1)''': [[Naproxen sodium|Naproxen]]: 375-500 mg/twice a day | *** '''Preferred regimen (1)''': [[Naproxen sodium|Naproxen]]: 375-500 mg/twice a day | ||
*** '''Preferred regimen (2):''' [[Celecoxib]]: 200 mg/twice a day | *** '''Preferred regimen (2):''' [[Celecoxib]]: 200 mg/twice a day | ||
*** '''Preferred regimen (3)''': [[Nimesulide]]: 200 and 400 mg/day | *** '''Preferred regimen (3)''': [[Nimesulide]]: 200 and 400 mg/day | ||
*** '''Preferred regimen (4)''': [[Ibuprofen]]: Max dose of up to 2400 mg/day | *** '''Preferred regimen (4)''': [[Ibuprofen]]: Max dose of up to 2400 mg/day | ||
**** [[Adverse effect (medicine)|Adverse effects]] of [[Non-steroidal anti-inflammatory drug| | **** [[Adverse effect (medicine)|Adverse effects]] of [[Non-steroidal anti-inflammatory drug|non-steroidal anti-inflammatory drugs]] include increased cardiovascular risk, [[gastritis]], [[Peptic ulcer|ulcers]] and [[Renal insufficiency|low renal clearance]]. | ||
** '''Moderate to severe disease''': Conventional synthetic [[Disease-modifying antirheumatic drug|disease-modifying antirheumatic drugs]] ([[Disease-modifying antirheumatic drug|DMARD]]<nowiki/>s) may be considered in [[Patient|patients]] with moderate to severe active peripheral [[arthritis]]. These are also considered in [[Patient|patients]] who are resistant or not responding to [[Non-steroidal anti-inflammatory drug|NSAIDs]], and local [[corticosteroid]] injections. | ** '''Moderate to severe disease''': Conventional synthetic [[Disease-modifying antirheumatic drug|disease-modifying antirheumatic drugs]] ([[Disease-modifying antirheumatic drug|DMARD]]<nowiki/>s) may be considered in [[Patient|patients]] with moderate to severe active peripheral [[arthritis]]. These are also considered in [[Patient|patients]] who are resistant or not responding to [[Non-steroidal anti-inflammatory drug|NSAIDs]], and local [[corticosteroid]] injections. | ||
*** Preferred regimen (1): [[Methotrexate]]<ref name="pmid24219040">{{cite journal |vauthors=Mease P |title=Methotrexate in psoriatic arthritis |journal=Bull Hosp Jt Dis (2013) |volume=71 Suppl 1 |issue= |pages=S41–5 |date=2013 |pmid=24219040 |doi= |url=}}</ref><ref name="pmid7868484">{{cite journal |vauthors=Singh YN, Verma KK, Kumar A, Malaviya AN |title=Methotrexate in psoriatic arthritis |journal=J Assoc Physicians India |volume=42 |issue=11 |pages=860–2 |date=November 1994 |pmid=7868484 |doi= |url=}}</ref>: 15 to 25 mg/week | *** Preferred regimen (1): [[Methotrexate]]<ref name="pmid24219040">{{cite journal |vauthors=Mease P |title=Methotrexate in psoriatic arthritis |journal=Bull Hosp Jt Dis (2013) |volume=71 Suppl 1 |issue= |pages=S41–5 |date=2013 |pmid=24219040 |doi= |url=}}</ref><ref name="pmid7868484">{{cite journal |vauthors=Singh YN, Verma KK, Kumar A, Malaviya AN |title=Methotrexate in psoriatic arthritis |journal=J Assoc Physicians India |volume=42 |issue=11 |pages=860–2 |date=November 1994 |pmid=7868484 |doi= |url=}}</ref>: 15 to 25 mg/week | ||
Revision as of 15:22, 18 April 2018
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Chandrakala Yannam, MD [2]
Overview
Historical Perspective
- [Disease name] was first discovered by [scientist name], a [nationality + occupation], in [year] during/following [event].
- In [year], [gene] mutations were first identified in the pathogenesis of [disease name].
- In [year], the first [discovery] was developed by [scientist] to treat/diagnose [disease name].
Classification
- [Disease name] may be classified according to [classification method] into [number] subtypes/groups:
- [group1]
- [group2]
- [group3]
- Other variants of [disease name] include [disease subtype 1], [disease subtype 2], and [disease subtype 3].
Pathophysiology
- The pathogenesis of [disease name] is characterized by [feature1], [feature2], and [feature3].
- The [gene name] gene/Mutation in [gene name] has been associated with the development of [disease name], involving the [molecular pathway] pathway.
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Clinical Features
Differentiating [disease name] from other Diseases
- [Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as:
- [Differential dx1]
- [Differential dx2]
- [Differential dx3]
Epidemiology and Demographics
- The prevalence of [disease name] is approximately [number or range] per 100,000 individuals worldwide.
- In [year], the incidence of [disease name] was estimated to be [number or range] cases per 100,000 individuals in [location].
Age
- Patients of all age groups may develop [disease name].
- [Disease name] is more commonly observed among patients aged [age range] years old.
- [Disease name] is more commonly observed among [elderly patients/young patients/children].
Gender
- In general, there is no gender predilection to psoriatic arthritis.
Race
- There is no racial predilection for [disease name].
- [Disease name] usually affects individuals of the [race 1] race.
- [Race 2] individuals are less likely to develop [disease name].
Risk Factors
- Common risk factors in the development of [disease name] are [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].
Natural History, Complications and Prognosis
- The majority of patients with [disease name] remain asymptomatic for [duration/years].
- Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
- If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
- Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
- Prognosis is generally [excellent/good/poor], and the [1/5/10year mortality/survival rate] of patients with [disease name] is approximately [#%].
Diagnosis
Diagnostic Criteria
- The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met:
- [criterion 1]
- [criterion 2]
- [criterion 3]
- [criterion 4]
Symptoms
- [Disease name] is usually asymptomatic.
- Symptoms of [disease name] may include the following:
- [symptom 1]
- [symptom 2]
- [symptom 3]
- [symptom 4]
- [symptom 5]
- [symptom 6]
Physical Examination
- Patients with [disease name] usually appear [general appearance].
- Physical examination may be remarkable for:
- [finding 1]
- [finding 2]
- [finding 3]
- [finding 4]
- [finding 5]
- [finding 6]
Laboratory Findings
- There are no specific laboratory findings associated with psoriatic arthritis and most the tests are non-specific.
- However, there are certain laboratory tests that can check for markers of inflammation and to exclude other diseases. These include:[1]
- CBC with differential count
- Elevated ESR
- Elevated CRP (C- reactive protein)
- Autoantibodies: The following autoantibodies may be found in patients with psoriatic arthritis.[2]
- Rheumatoid factor
- ANA (Antinuclear antibodies)
- Anti-citrullinated peptide antibodies (ACPA)
- Genetic markers:[3][4]
- Synovial fluid analysis: Elevated WBC count suggestive of inflammation.
Imaging Findings
- X-ray of digits:[5][6][7]
- Bone destructive changes including formation of subchondral cyst and erosions
- Fluffy periostitis
- Ankylosis
- Phalangeal tuft acroosteolysis
- New bone formation: Perisoteal and endosteal bone formation may result in increased bone density of an entire phalanx resulting in so called ivory phalanx.
- Pencil-in-cup deformity (osteolytic lesions) usually involving DIP joints but also affects PIP joints
- Osteolysis and ankylosis both coexists in the same joints of hands and foot
- Enthesitis
- Dactylitis (sausage digit)
- Gross finger deformity
- Arthritis mutilans: It may lead to "telescoping of fingers" caused by marked bony resorption and the subsequent collapse of soft tissue
- Asymmetrical sacroiliitis
- Spondylitis: Asymmetric paravertebral ossifications and relative sparing of the facet joints
- MRI:
Other Diagnostic Studies
- Bone mineral density (BMD) testing: Bone density may be decreased in psoriatic arthritis resulting in osteoporosis and increased risk for fractures. [8]
Treatment
Medical Therapy
- Medical therapy for psoriatic arthritis is according to the guidelines proposed by
- European League Against Rheumatism (EULAR): Guidelines were first proposed in 2012 and they were updated in 2015.[9][10]
- Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA)[11]
- American College of Rheumatology (ACR)
- National Psoriasis Foundation (NPF)
- American Academy of Dermatology (AAD) Psoriasis Guidelines of Care[12]
- British Society of Rheumatology (BSR)[13]
- Pharmacologic therapy for psoriatic arthritis include, non-steroidal anti-inflammatory drugs (NSAIDs), conventional synthetic DMARDs (eg, methotrexate, sulfasalazine, cyclosporin A, leflunomide), biologicDMARDs including, TNF inhibitors (eg, etanercept, infliximab, adalimumab, golimumab), phosphodiesterase (PDE) inhibitors (eg, apremilast), interleukin(IL) inhibitors (eg, secukinumab, ixekizumab, abatacept) and intraarticular glucocorticoid injections.
- Peripheral arthritis:
- Mild disease: Nonsteroidal antiinflammatory drugs (NSAIDs) are the most commonly used drugs for the management of mild active psoriatic arthritis.[14][15]
- Preferred regimen (1): Naproxen: 375-500 mg/twice a day
- Preferred regimen (2): Celecoxib: 200 mg/twice a day
- Preferred regimen (3): Nimesulide: 200 and 400 mg/day
- Preferred regimen (4): Ibuprofen: Max dose of up to 2400 mg/day
- Adverse effects of non-steroidal anti-inflammatory drugs include increased cardiovascular risk, gastritis, ulcers and low renal clearance.
- Moderate to severe disease: Conventional synthetic disease-modifying antirheumatic drugs (DMARDs) may be considered in patients with moderate to severe active peripheral arthritis. These are also considered in patients who are resistant or not responding to NSAIDs, and local corticosteroid injections.
- Preferred regimen (1): Methotrexate[16][17]: 15 to 25 mg/week
- Adverse effects of methotrexate: Liver toxicity, immunosuppression, interstitial pneumonitis, increased infection risk.
- Folic acid supplementation should be given to all patients taking methotrexate.
- Preferred regimen (2): Leflunomide: 20 mg/day
- Adverse effects of Leflunomide: Liver toxicity, diarrhea, rash, alopecia, pneumonitis.
- Preferred regimen (3): Sulfasalazine[17]: 2-3 gms/day
- Adverse effects of sulfasalazine: Nausea, diarrhea, abdominal pain, rash, and neutropenia.
- Preferred regimen (4): Cyclosporine A: 3.5 mg/kg per day[18]
- Preferred regimen (1): Methotrexate[16][17]: 15 to 25 mg/week
- Mild disease: Nonsteroidal antiinflammatory drugs (NSAIDs) are the most commonly used drugs for the management of mild active psoriatic arthritis.[14][15]
- Non pharmacologic therapy:
- Exercise
- Weight reduction
- Physical therapy
- Occupational therapy
- Educating the patient about disease course, joint protection and comorbid conditions.
- Orthotics
Surgery
- Surgery is the mainstay of therapy for [disease name].
- [Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
- [Surgical procedure] can only be performed for patients with [disease stage] [disease name].
Prevention
- There are no primary preventive measures available for [disease name].
- Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
- Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].
References
- ↑ Punzi L, Podswiadek M, Oliviero F, Lonigro A, Modesti V, Ramonda R, Todesco S (2007). "Laboratory findings in psoriatic arthritis". Reumatismo. 59 Suppl 1: 52–5. PMID 17828345.
- ↑ Johnson SR, Schentag CT, Gladman DD (May 2005). "Autoantibodies in biological agent naive patients with psoriatic arthritis". Ann. Rheum. Dis. 64 (5): 770–2. doi:10.1136/ard.2004.031286. PMC 1755477. PMID 15834057.
- ↑ Chandran V, Bull SB, Pellett FJ, Ayearst R, Rahman P, Gladman DD (October 2013). "Human leukocyte antigen alleles and susceptibility to psoriatic arthritis". Hum. Immunol. 74 (10): 1333–8. doi:10.1016/j.humimm.2013.07.014. PMID 23916976.
- ↑ Eder L, Chandran V, Pellet F, Shanmugarajah S, Rosen CF, Bull SB, Gladman DD (January 2012). "Human leucocyte antigen risk alleles for psoriatic arthritis among patients with psoriasis". Ann. Rheum. Dis. 71 (1): 50–5. doi:10.1136/ard.2011.155044. PMID 21900282.
- ↑ McGonagle D, Hermann KG, Tan AL (January 2015). "Differentiation between osteoarthritis and psoriatic arthritis: implications for pathogenesis and treatment in the biologic therapy era". Rheumatology (Oxford). 54 (1): 29–38. doi:10.1093/rheumatology/keu328. PMC 4269795. PMID 25231177.
- ↑ Siannis F, Farewell VT, Cook RJ, Schentag CT, Gladman DD (April 2006). "Clinical and radiological damage in psoriatic arthritis". Ann. Rheum. Dis. 65 (4): 478–81. doi:10.1136/ard.2005.039826. PMC 1798082. PMID 16126794.
- ↑ Haddad A, Chandran V (2013). "Arthritis mutilans". Curr Rheumatol Rep. 15 (4): 321. doi:10.1007/s11926-013-0321-7. PMID 23430715.
- ↑ Frediani B, Allegri A, Falsetti P, Storri L, Bisogno S, Baldi F, Filipponi P, Marcolongo R (January 2001). "Bone mineral density in patients with psoriatic arthritis". J. Rheumatol. 28 (1): 138–43. PMID 11196516.
- ↑ Gossec L, Smolen JS, Ramiro S, de Wit M, Cutolo M, Dougados M, Emery P, Landewé R, Oliver S, Aletaha D, Betteridge N, Braun J, Burmester G, Cañete JD, Damjanov N, FitzGerald O, Haglund E, Helliwell P, Kvien TK, Lories R, Luger T, Maccarone M, Marzo-Ortega H, McGonagle D, McInnes IB, Olivieri I, Pavelka K, Schett G, Sieper J, van den Bosch F, Veale DJ, Wollenhaupt J, Zink A, van der Heijde D (March 2016). "European League Against Rheumatism (EULAR) recommendations for the management of psoriatic arthritis with pharmacological therapies: 2015 update". Ann. Rheum. Dis. 75 (3): 499–510. doi:10.1136/annrheumdis-2015-208337. PMID 26644232.
- ↑ Gossec L, Smolen JS, Gaujoux-Viala C, Ash Z, Marzo-Ortega H, van der Heijde D, FitzGerald O, Aletaha D, Balint P, Boumpas D, Braun J, Breedveld FC, Burmester G, Cañete JD, de Wit M, Dagfinrud H, de Vlam K, Dougados M, Helliwell P, Kavanaugh A, Kvien TK, Landewé R, Luger T, Maccarone M, McGonagle D, McHugh N, McInnes IB, Ritchlin C, Sieper J, Tak PP, Valesini G, Vencovsky J, Winthrop KL, Zink A, Emery P (January 2012). "European League Against Rheumatism recommendations for the management of psoriatic arthritis with pharmacological therapies". Ann. Rheum. Dis. 71 (1): 4–12. doi:10.1136/annrheumdis-2011-200350. PMID 21953336.
- ↑ Ritchlin CT, Kavanaugh A, Gladman DD, Mease PJ, Helliwell P, Boehncke WH, de Vlam K, Fiorentino D, Fitzgerald O, Gottlieb AB, McHugh NJ, Nash P, Qureshi AA, Soriano ER, Taylor WJ (September 2009). "Treatment recommendations for psoriatic arthritis". Ann. Rheum. Dis. 68 (9): 1387–94. doi:10.1136/ard.2008.094946. PMC 2719080. PMID 18952643.
- ↑ Menter A, Korman NJ, Elmets CA, Feldman SR, Gelfand JM, Gordon KB, Gottlieb A, Koo JY, Lebwohl M, Leonardi CL, Lim HW, Van Voorhees AS, Beutner KR, Ryan C, Bhushan R (July 2011). "Guidelines of care for the management of psoriasis and psoriatic arthritis: section 6. Guidelines of care for the treatment of psoriasis and psoriatic arthritis: case-based presentations and evidence-based conclusions". J. Am. Acad. Dermatol. 65 (1): 137–74. doi:10.1016/j.jaad.2010.11.055. PMID 21306785.
- ↑ Coates LC, Tillett W, Chandler D, Helliwell PS, Korendowych E, Kyle S, McInnes IB, Oliver S, Ormerod A, Smith C, Symmons D, Waldron N, McHugh NJ (October 2013). "The 2012 BSR and BHPR guideline for the treatment of psoriatic arthritis with biologics". Rheumatology (Oxford). 52 (10): 1754–7. doi:10.1093/rheumatology/ket187. PMID 23887065.
- ↑ Nash P, Clegg DO (March 2005). "Psoriatic arthritis therapy: NSAIDs and traditional DMARDs". Ann. Rheum. Dis. 64 Suppl 2: ii74–7. doi:10.1136/ard.2004.030783. PMC 1766880. PMID 15708943.
- ↑ Sarzi-Puttini P, Santandrea S, Boccassini L, Panni B, Caruso I (2001). "The role of NSAIDs in psoriatic arthritis: evidence from a controlled study with nimesulide". Clin. Exp. Rheumatol. 19 (1 Suppl 22): S17–20. PMID 11296544.
- ↑ Mease P (2013). "Methotrexate in psoriatic arthritis". Bull Hosp Jt Dis (2013). 71 Suppl 1: S41–5. PMID 24219040.
- ↑ 17.0 17.1 Singh YN, Verma KK, Kumar A, Malaviya AN (November 1994). "Methotrexate in psoriatic arthritis". J Assoc Physicians India. 42 (11): 860–2. PMID 7868484.
- ↑ Steinsson K, Jónsdóttir I, Valdimarsson H (August 1990). "Cyclosporin A in psoriatic arthritis: an open study". Ann. Rheum. Dis. 49 (8): 603–6. PMC 1004173. PMID 2396865.