POEMS syndrome differential diagnosis: Difference between revisions

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Revision as of 16:28, 18 February 2019

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Overview

The diagnosis of POEMS syndrome presents a diagnostic challenge for the physician. A thorough examination of organ systems should be attempted in order to reach a confirmed diagnosis. POEMS syndrome should be differentiated from other conditions presenting as a polyneuropathy (metabolic syndrome, vitamin B12 deficiency, Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy and multifocal motor polyneuropathy), organomegaly with lymphadenopathy (malaria, leshmaniasis or kala-azar, infective hepatitis, chronic myelogenous leukemia, lymphoma, primary amyloidosis, Gaucher's disease), endocrinopathy (hypogonadism, hypothyroidism, hypopituitarism), monoclonal plasma cell proliferation (multiple myeloma, monoclonal gammopathy of undetermined significance, plasmacytoma), mixed lytic/sclerotic bone lesions (osteomalacia, osteogenesis imperfecta) and skin changes.

Differentiating POEMS Syndrome From Other Diseases

The diagnosis of POEMS syndrome presents a diagnostic challenge for the physician. A thorough examination of organ systems should be attempted in order to reach a confirmed diagnosis. POEMS syndrome should be differentiated from other conditions presenting as a polyneuropathy, organomegaly, endocrinopathy, monoclonal plasma cell proliferation, mixed lytic/sclerotic bone lesions and skin changes. The differentials include the following:

Organ System Involvement		Differential Diagnosis	Causes	Clinical Features	Laboratory Findings	Gold Standard Test	Therapy
P = Polyneuropathy		POEMS syndrome (Demyelinating)^[1]	Monoclonal plasma cell proliferation Cytokine storm (IL-1, IL-6, IL-12, TNF alpha, VEGF)	Symmetrical, ascending chronic progressive polyneuropathy with both sensory (pin-prick and vibration) and motor disability (motor > sensory) Generalized/extermity pain Areflexia	Increased number of thrombocytes^[2]^[3]^[4] Increased number of erythrocytes^[2]^[3]^[4] Elevated cerebrospinal fluid (CSF) protein content^[3] Increased number of leukocytes^[4] High levels of IgG lambda or IgA lambda M-protein in the serum^[4] Increased number of plasma cells in the bone marrow^[4] Increased serum VEGF level^[5] Elevated levels of antitiroglobulin antibody and antithyroid peroxydase antibody^[6]	International Myeloma Working Group (IMWG) clinical and laboratory diagnostic criteria^[7]
		Metabolic Syndrome (Axonal pathology)^[8]	Diabetes mellitus	Symmetric sensorimotor distal polyneuropathy Asymmetric proximal neuropathy 3rd nerve palsy Carpel tunnel syndrome Autonomic neuropathy "Glove and stocking" type pain Muscle wasting Hammer toes Polyuria Polydipsia	Uncontrolled hyperglycemia Slowed nerve conduction Small fiber dysfunction Monofilament testing	Fasting blood sugar level greater than equal to 126 mg/dl on 2 separate occasions^[9]	Anti-diabetic therapy Gabapentin Carbamazepine Foot care
		Vitamin Deficiencies (Axonal Pathology)^[10]	Vitamin B12 deficiency (Decreased S-adenosyl methionine)^[11] Vitamin B1 deficiency	Primarily sensory deficits Vibration and proprioception affected Gait abnormalities Cognitive impairment Irritability Glossitis	Anemia (megaloblastic in case of B12 deficiency)^[12] Decreased serum Vitamin B12 levels (< 200 pg/ml) Elevated methylmalonic acid	Serum Vitamin B12 levels^[13] Methylmalonic acid levels Intrinsic factor antibodies^[14]	Vitamin B12 supplement (parenteral)^[15]
		Guillain-Barre Syndrome (Demyelinating)^[16]	Anti-ganglioside and anti-myelin antibodies^[17] Viral infections:^[18] Epstein Barr virus HIV Cytomegalovirus Varicella Zoster virus Bacterial infections:^[19] Campylobacter infection Mycoplasma pneumoniae	Rapid onset and quick progression Progression stops after 2-3 weeks Bilateral ascending paraesthesias and paralysis (generalized) Weakness Ataxia Areflexia No fever 4 sub-types: Acute inflammatory demyelinating polyneuropathy Acute motor axonal neuropathy Acute motor and sensory axonal neuropathy Miller Fisher syndrome	Delayed F waves^[20]	Clinical diagnostic criteria (progressive weakness of more than two limbs, areflexia, and progression for no more than four weeks)^[21]	Intravenous immunoglobulins^[22] Plasma exchange^[23] Respiratory support DVT/PE prevention
		Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) (Mixed axonal and demyelinatiing)^[24]^[25]	Abnormal immune response (both IgG based humoral and T-Cell mediated) response to unknown antigen (possible culprits include myelin proteins P0, P2 and PMP22)^[26]^[27]^[28]	Slow onset and gradual progression Relapsing and remitting course Symmetrical proximal and distal motor and sensory weakness (legs>arms) Foot drop Numbness, tingling and pain Areflexia	Elevated CSF protein (oligoclonal bands with normal WBCs)^[29] Slowed motor nerve conduction velocities^[30] Prolonged distal motor latencies (period between F wave and initial stimulation) Delayed F wave latencies (recorded from the feet, hence called "F" waves)^[31] MRI contrast enhancement and enlargement of T2 spinal segments^[32]	EFNS/PNS criteria^[33] Koski criteria^[34]	Corticosteroids Intravenous immunoglobulin (IVIG) Immunosupressants (Alemtuzemab Azathioprine Cyclophosphamide Cyclosporin Etanercept Interferon-alpha)
		Multifocal Motor Neuropathy^[35]	Abnormal immune response (Anti ganglioside GM-1 IgM antibodies)	Progressive, asymmetric, distal and upper limb predominant weakness No significant sensory abnormalities Areflexia	Elevated CSF protein	Clinical criteria (EFNS/PNS):^[36] Slowly progressive or step-wise progressive, focal, asymmetric limb weakness; i.e., motor involvement in the motor nerve distribution of at least two nerves for > 1 month. No objective sensory abnormalities except for minor vibration sense abnormalities in the lower limbs	Intravenous immunoglobulins Cyclophosphamide Rituximab
Organ System Involvement		Differential Diagnosis	Causes	Features	Laboratory Findings	Gold Standard Test	Therapy
O = Organomegaly (Hepatosplenomegaly and Lymphadenopathy)		Malaria^[37]^[38]^[39]	Plasmodium falciparum P. ovale P. malariae P. knowlesi	Tertian (vivax, ovale, falciparum), quartan (malariae), quotidian fever (knowlesi) Vector is female Anopheles mosquito Hepatosplenomegaly Lymphadenopathy Jaundice Icterus Tachycardia Tachypnea Productive cough Hematuria Altered mental status	Microcytic anemia Thick and thin blood films (Giemsa staining) Rapid diagnostic test (antigen detection Polymerase chain reaction (PCR) Enzyme linked immunosorbent assay (ELISA)	Thick and thin films	Non-falciparum species: Chloroquine (in susceptible) Artemisinin plus mefloquin or lumefantrine (in chloroquine resistant) Falciparum species: Chloroquine (in susceptible) Artemether plus lumefantrine (in chloroquin resistant) OR Artesunate plus mefloquin OR Artesunate plus sulfadoxine-pyrimethamine Atovaquone plus proguanil
		Kala-azar^[40]^[41]	Leshmania donovani L. infantum L. chagasi	Fever Vector is sandfly Hepatosplenomegaly Lymphadenopathy Hyperpigmentation	Anemia Direct agglutination test (DAT) rk39 dipstick ELISA	Splenic aspiration	Liposomal amphotericin B Sodium stibogluconate Pentamidine
		Infective Hepatitis^[42]^[43]	Hepatitis A virus (HAV) HBV HCV HDV (co-infection with HBV) HEV	Fever Transmitted via fecal-oral route (HAV, HBV, HDV, HEV), infected sera (HCV), sexual contact with infected individuals Hepatosplenomegaly (may become shrunken in cases of cirrhosis due to chronic infection) Lymphadenopathy Jaundice Palmar erythema Spider angiomata Gynecomastia Arthritis-dermatitis syndrome	Antigen and antibody detection Total and direct bilirubin (increased) Severe disease is often associated with persistent bilirubin levels >340 mmol/L ALT and AST (increased) Alkaline phosphatase (normal or mildly elevated) Prothrombin time (prolonged from synthetic defect, caused by hepatocellular necrosis) Total protein (decreased) Globulin (mildly elevated) Initial lymphopenia and neutropenia, followed by relative lymphocytosis Low hemoglobin	Antigen and antibody detection	Interferon (IFN) Nucleoside analogs Nucleotide analogs
		Chronic Myelogenous Leukemia (CML)^[44]^[45]^[46]^[47]^[48]^[49]^[50]^[51]^[52]^[51]	BCR/ABL gene fusion product due to translocation mutation t(9;22)(q34;q11)^[53]	Fever Weight loss Hepatosplenomegaly Lymphadenopathy Bruises Petechiae Ulcers Vesicles Malaise Early satiety	Anemia Leukocytosis (median of 100,000/µL) with a left shift Thrombocytosis Blasts usually <2% Absolute basophilia Absolute eosinophilia Monocytosis Thrombocytosis Thrombocytopenia suggests an alternative diagnosis or the presence of advanced stage Elevated uric acid Elevated histamine levels	Fluoroscent insitu hybridization (FISH)	Imatinib Dasatinib Nilotinib Bosutinib Ponatinib Cytarabine HDAC (high-dose cytarabine) Hydroxyurea Busulfan Busulfex Stem cell transplantation
		Lymphoma	Various causes based on type: Hodgkin's Non-Hodgkin's	Fever Weight loss Lymphadenopathy Hepatosplenomegaly Night sweats, constant fatigue Purplish scaly rash in cases of cutaneous lymphoma	Elevated ESR Increased CRP Increased LDH Anemia of chronic disease	Lymph node biopsy
		Primary (AL) Amyloidosis^[54]^[55]	Aggregation and deposition of immunoglobulin light chains that usually produced by plasma cell clones^[56]^[57]	Nephrotic syndrome (peripheral edema Restrictive cardiomyopathy (fatigue, dyspnea, syncope) Peripheral neuropathy (numbness, tingling) Hepatomegaly with elevated liver enzymes Macroglossia Purpura Bleeding diathesis	Typical green birefringence under polarized light after Congo red staining (appears in red under normal light)	Congo red staining	Melphalan-prednisone/dexamethasone^[58] Dexamethasone plus Cyclophosphamide-thalidomide ^[59] Stem cell transplantation^[60]
		Gaucher's Disease^[61]	GBA gene mutation Aberrant metabolism of glucocerebroside (lipid)	Hydrops fetalis Dry, scaly skin (ichthyosis) or other skin abnormalities Hepatosplenomegaly Distinctive facial features Neurological problems Gall stones Growth retardation	Hypocholesterolemia Splenic nodules Cytopenias (especially thrombocytopenia) Increased ferritin levels Increased tartarate resistant acid phosphatase (TRAP) levels	Enzyme assay for glucocerebrosidase DNA analysis for GBA mutation	Enzyme replacement Splenectomy Blood transfusion
Organ System Involvement		Differential Diagnosis	Causes	Features	Laboratory Findings	Gold Standard Test	Therapy
E = Endocrinopathy (Hypogonadism, Hypothyroidism, Hypopituitarism)	Hypogonadism^[62]^[63]	Primary Hypogonadism (Hypergonadotrophic)	Klinefelter's syndrome Myotonic dystrophy Sertoli-cell tumor Enzymatic defects Viral orchitis (mumps) Cryptorchidism Polyglandular autoimmune syndrome Testicular trauma and tumors Polycystic ovarian syndrome	Fatigue Decreased libido Delayed secondary sexual characteristics: Absent/scant pubic hair Impotence Erectile dysfunction Amenorrhea Delayed breast development Small testicular size Decreased muscle mass Osteoporosis Depression Infertility Irritability Mood swings Pot belly Weight gain	Decreased sex hormone levels: Decreased testosterone Decreased dihydrotestosterone Decreased estrogen Increased gonadrotrpins: Increased LH Increased FSH	Serum sex hormone levels	Hormone replacement therapy
	Hypogonadism^[62]^[63]	Secondary Hypogonadism (Hypogonadotrophic)	Panhypopituitarism Hyperprolactinemia Isolated gonadotropin deficiency Kallman's syndrome Congenital Prader-Willi syndrome Hemochromatosis Massive obesity Malnutrition		Decreased sex hormone levels: Decreased testosterone Decreased dihydrotestosterone Decreased estrogen Decreased gonadrotrpins: Decreased LH Decreased FSH	Serum sex hormone levels	Hormone replacement therapy
	Hypothyroidism^[64]^[65]	Primary Hypothyroidism	Congenital hypothyroidism Autoimmune (Hashimoto's) thyroiditis Resistance to TSH	Fatigue Cold intolerance Decreased sweating Hypothermia Coarse skin Weight gain Puffiness Hair loss Constipation Fever (thyroiditis) Hoarseness Goiter Fullness in the throat and neck Depression Emotional lability Attention deficit Macroglossia Obstructive sleep apnea Paresthesia Nerve entrapment syndromes (carpal tunnel syndrome) Blurred vision (central hypothyroidism) Ataxia Myxedema coma (with non-pitting edema) Cardiomegaly Pericardial effusion Ascites Hyperlipidemia Galactorrhea Infertility	Decreased T3 and T4 Increased TSH	Serum T3, T4, TSH levels	Hormone replacement therapy
		Secondary Hypothyroidism	Pituitary mass lesions, especially pituitary adenomas Brain cysts and abscesses Meningiomas Dysgerminomas Metastatic tumors Craniopharyngiomas Pituitary apoplexy Sheehan syndrome (postpartum pituitary necrosis) Idiopathic isolated TSH deficiency Lymphocytic or granulomatous hypophysitis		Decreased T3 and T4 Decreased TSH
		Tertiary Hypothyroidism	Hemochromatosis Histiocytosis Developmental abnormalities Internal carotid aneurysms Idiopathic isolated TRH deficiency		Decreased T3 and T4 Decreased TRH Decreased TSH
	Hypopituitarism^[66]^[67]	Congenital	Idiopathic Anatomic lesion in sella turcica (Rathke's cyst) CNS malformations: Septo-optic-dysplasia Kallmann syndrome Pituitary stalk interruption syndrome	Headache Nausea and vomiting Visual impairment Fatigue Cold intolerance Hypotension Dizziness Weight loss Features of hormonal deficiencies	Decreased FSH, LH Decreased TSH Decreased ACTH Decreased GH Decreased ADH Decreased oxytocin	Serum hormone levels produced by pituitary	Hormone replacement therapy
	Hypopituitarism^[66]^[67]	Acquired	Posterior pituitary tumor: astrocytoma, ganglioneuroma Metastatic: breast, lungs, colon, prostate Peripituitary lesions: Craniopharyngioma, meningioma, chordoma, optic nerve glioma Transsphenoidal or transcranial surgery Radiation Traumatic brain injury Sheehan's syndrome Pituitary apoplexy Meningitis Hypophysitis Lymphoma			Serum hormone levels produced by pituitary	Hormone replacement therapy
Organ System Involvement		Differential Diagnosis	Causes	Features	Laboratory Findings	Gold Standard Test	Therapy
M = M-protein ( Hematological Abnormality/Plasma Cell Dyscrasias)		Multiple myeloma^[68]^[69]^[70]	Chromosomal aberrations or other genetic insults Malignant transformation of plasma cells Clonal plasma cell proliferation	Diffuse bone pain and tenderness with osteolytic lesions Renal failure Hypercalcemia Anemia	Anemia Thrombocytopenia Leukopenia Decreased albumin (reversed albumin:globulin ratio) Increased serum creatinine, urea Hypercalcemia Elevated ESR Normal-low alkaline phosphatase RBC rouleaux formation Bence-Jones proteins in urine	Clonal plasma cells on bone marrow exam greater than equal to 10% AND Any one of the following: Evidence of end-organ damage Hypercalcemia (>11 mg/dl) Renal insufficiency Anemia (Hb < 10 mg/dl) Bone lesions Greater than 1 lesions on MRI	Induction chemotherapy with bortezomib, lenalidomide, and dexamethasone Bisphosphonates RANK ligand inhibitors (denosumab) Autologous stem cell transplantation
		Monoclonal gammopathy of undetermined significance (MGUS)^[71]	Chromosomal aberrations or other genetic insults Clonal plasma cell proliferation	Asymptomatic	Serum M protein of <3 g/L Fewer than 10% plasma cells in the bone marrow No evidence of bone or organ damage	Serum M protein (IgG or IgA) <3g/dl AND Clonal bone marrow plasma cells < 10% AND No end-organ damage	Observation
		Asymptomatic Plasma Cell Myeloma (Smoldering and Indolent plasma cell myeloma)	Chromosomal aberrations or other genetic insults Malignant transformation of plasma cells Clonal plasma cell proliferation	Asymptomatic	Serum M protein of greater than equal to 3 g/L Greater than 10% plasma cells in the bone marrow No evidence of bone or organ damage	Serum M protein (IgG or IgA greater than equal to 3 g/dl OR Urinary M protein greater than equal to 500 mg/24 h AND/OR Clonal bone marrow plasma cells 10-60% AND No end-organ damage	Observation
		Plasmacytoma	Chromosomal aberrations or other genetic insults Malignant transformation of plasma cells	Solitary bone plasmacytoma (bone) Extramedullary plasmacytoma (soft tissues) Clinical manifestations related to tumor mass and compression symptoms	On biopsy: Solitary infiltrate of clonal plasma cells in bone (SBP) or soft tissue (EMP). No evidence of infiltration by clonal plasma cells. Negative skeletal survey plus MRI/CT spine and pelvis except for the solitary lesion. Lack of hypercalcemia, renal insuffieciency, anemia, multiple bone lesions which would suggest MM	Diagnosis of exclusion	Radiotherapy
Bone Lesions		Osteoporosis	Imbalance between bone resorption and bone formation Preceded by osteopenia Decreased bone mineral density	Acute musculoskletal pain if fractures develop Severe decrease in BMD on dual-energy X-ray absorptiometry (DEXA) test T score less than -2.5 on DEXA scan	Normal serum calcium, phosphate, alkaline phosphatase and parathyroid hormone levels Decreased bone mass	T score less than -2.5 on DEXA scan	Calcium and vitamin D supplementation Bisphosphonates Weight-bearing exercise Teriparatide RANK ligand inhibitors (denosumab)
		Osteomalacia^[72]	Inadequate mineralization of bone Deficiency of vitamin D calcium, or phosphorus Renal tubular acidosis Malabsorption	Diffuse bone pain, fatigue, and fractures Low bone mineral density (BMD) Hypocalcemia	Decreased serum calcium Decreased serum phosphate Increased serum alkaline phosphatase Increased serum parathyroid hormone levels	Bone biopsy (increased osteoid and decreased calcification)	Vitamin D3 supplementation
		Osteogenesis imperfecta	Mutations in COL1A1 or COL1A2 Impaired type I collagen synthesis	Short stature, scoliosis, and propensity for fractures Blue discoloration of sclera	Normal serum calcium Normal serum phosphate Increased serum alkaline phosphatase	DNA analysis Collagen analysis	Bisphosphonates Physical therapy Surgical fixation of brittle bones Genetic counseling for offspring
Skin Changes		Scurvy	Vitamin C deficiency Malabsorption Hemodialysis	Gum disease such as gum bleeding Loose teeth Easy bruising Impaired immune response Impaired wound healing			Vitamin C supplementation Citrus fruits

Other Differentials

POEMS syndrome must also be differentiated from other similar conditions which lead to multiple endocrine disorders such as autoimmune polyendocrine syndrome, Hirata syndrome, Kearns–Sayre syndrome and Wolfram syndromes.^[73]^[74]^[75]^[76]^[77]

Disease	Addison's disease	Type 1 diabetes mellitus	Hypothyroidism	Other disorders present
POEMS syndrome	+	Less common	Less common	Hypoparathyroidism Candidiasis Hypogonadism
APS type 2	+	+	+	Hypogonadism Malabsorption
APS type 3	-	+	+	Malabsorption
Thymoma	+	-	+	Myasthenia gravis Cushing syndrome
Chromosomal abnormalities (Turner syndrome, Down's syndrome)	-	+	+	Cardiac dysfunction
Kearns–Sayre syndrome	-	+	-	Myopathy Hypoparathyroidism Hypogonadism
Wolfram syndrome	-	+	-	Diabetes insipidus Optic atrophy Deafness
POEMS syndrome	-	+	-	Polyneuropathy Hypogonadism Plasma cell dyscrasias

References

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↑ National Cancer Institute. Physician Data Query Database 2015.http://www.cancer.gov/types/leukemia/hp/cml-treatment-pdq#section/_19
↑ Jabbour E, Kantarjian H (May 2014). "Chronic myeloid leukemia: 2014 update on diagnosis, monitoring, and management". Am. J. Hematol. 89 (5): 547–56. doi:10.1002/ajh.23691. PMID 24729196.
↑ Thompson PA, Kantarjian HM, Cortes JE (October 2015). "Diagnosis and Treatment of Chronic Myeloid Leukemia in 2015". Mayo Clin. Proc. 90 (10): 1440–54. doi:10.1016/j.mayocp.2015.08.010. PMC 5656269. PMID 26434969.
↑ Faderl S, Talpaz M, Estrov Z, Kantarjian HM (August 1999). "Chronic myelogenous leukemia: biology and therapy". Ann. Intern. Med. 131 (3): 207–19. PMID 10428738.
↑ Canadian Cancer Society.2015.http://www.cancer.ca/en/cancer-information/cancer-type/leukemia-chronic-myelogenous-cml/treatment/chronic/?region=ab
↑ Tefferi A (2006). "Classification, diagnosis and management of myeloproliferative disorders in the JAK2V617F era". Hematology Am Soc Hematol Educ Program: 240–245. PMID 17124067.
↑ Canadian Cancer Society.2015.http://www.cancer.ca/en/cancer-information/cancer-type/leukemia-chronic-myelogenous-cml/signs-and-symptoms/?region=ab
↑ ^51.0 ^51.1 Thompson PA, Kantarjian HM, Cortes JE (October 2015). "Diagnosis and Treatment of Chronic Myeloid Leukemia in 2015". Mayo Clin. Proc. 90 (10): 1440–54. doi:10.1016/j.mayocp.2015.08.010. PMC 5656269. PMID 26434969.
↑ Wang YL, Bagg A, Pear W, Nowell PC, Hess JL (October 2001). "Chronic myelogenous leukemia: laboratory diagnosis and monitoring". Genes Chromosomes Cancer. 32 (2): 97–111. PMID 11550277.
↑ Zahra K, Ben Fredj W, Ben Youssef Y, Zaghouani H, Chebchoub I, Zaier M, Badreddine S, Braham N, Sennana H, Khelif A (2012). "Chronic myeloid leukemia as a secondary malignancy after lymphoma in a child. A case report and review of the literature". Onkologie. 35 (11): 690–3. doi:10.1159/000343952. PMID 23147546.
↑ Real de Asúa D, Costa R, Galván JM, Filigheddu MT, Trujillo D, Cadiñanos J (2014). "Systemic AA amyloidosis: epidemiology, diagnosis, and management". Clin Epidemiol. 6: 369–77. doi:10.2147/CLEP.S39981. PMC 4218891. PMID 25378951.
↑ Misumi Y, Ando Y (July 2014). "[Classification of amyloidosis]". Brain Nerve (in Japanese). 66 (7): 731–7. PMID 24998818.
↑ Bilginer Y, Akpolat T, Ozen S (August 2011). "Renal amyloidosis in children". Pediatr. Nephrol. 26 (8): 1215–27. doi:10.1007/s00467-011-1797-x. PMC 3119800. PMID 21360109.
↑ Khoor A, Colby TV (February 2017). "Amyloidosis of the Lung". Arch. Pathol. Lab. Med. 141 (2): 247–254. doi:10.5858/arpa.2016-0102-RA. PMID 28134587.
↑ Palladini G, Perfetti V, Obici L, Caccialanza R, Semino A, Adami F, Cavallero G, Rustichelli R, Virga G, Merlini G (April 2004). "Association of melphalan and high-dose dexamethasone is effective and well tolerated in patients with AL (primary) amyloidosis who are ineligible for stem cell transplantation". Blood. 103 (8): 2936–8. doi:10.1182/blood-2003-08-2788. PMID 15070667.
↑ Wechalekar AD, Goodman HJ, Lachmann HJ, Offer M, Hawkins PN, Gillmore JD (January 2007). "Safety and efficacy of risk-adapted cyclophosphamide, thalidomide, and dexamethasone in systemic AL amyloidosis". Blood. 109 (2): 457–64. doi:10.1182/blood-2006-07-035352. PMID 16990593.
↑ Skinner M, Sanchorawala V, Seldin DC, Dember LM, Falk RH, Berk JL, Anderson JJ, O'Hara C, Finn KT, Libbey CA, Wiesman J, Quillen K, Swan N, Wright DG (January 2004). "High-dose melphalan and autologous stem-cell transplantation in patients with AL amyloidosis: an 8-year study". Ann. Intern. Med. 140 (2): 85–93. PMID 14734330.
↑ Stirnemann J, Belmatoug N, Camou F, Serratrice C, Froissart R, Caillaud C, Levade T, Astudillo L, Serratrice J, Brassier A, Rose C, Billette de Villemeur T, Berger MG (February 2017). "A Review of Gaucher Disease Pathophysiology, Clinical Presentation and Treatments". Int J Mol Sci. 18 (2). doi:10.3390/ijms18020441. PMID 28218669.
↑ Carnegie C (2004). "Diagnosis of hypogonadism: clinical assessments and laboratory tests". Rev Urol. 6 Suppl 6: S3–8. PMC 1472884. PMID 16985909.
↑ Dandona P, Rosenberg MT (May 2010). "A practical guide to male hypogonadism in the primary care setting". Int. J. Clin. Pract. 64 (6): 682–96. doi:10.1111/j.1742-1241.2010.02355.x. PMID 20518947.
↑ Kostoglou-Athanassiou I, Ntalles K (April 2010). "Hypothyroidism - new aspects of an old disease". Hippokratia. 14 (2): 82–7. PMID 20596261.
↑ Koulouri O, Moran C, Halsall D, Chatterjee K, Gurnell M (December 2013). "Pitfalls in the measurement and interpretation of thyroid function tests". Best Pract. Res. Clin. Endocrinol. Metab. 27 (6): 745–62. doi:10.1016/j.beem.2013.10.003. PMID 24275187.
↑ Kim SY (December 2015). "Diagnosis and Treatment of Hypopituitarism". Endocrinol Metab (Seoul). 30 (4): 443–55. doi:10.3803/EnM.2015.30.4.443. PMID 26790380.
↑ Prabhakar VK, Shalet SM (April 2006). "Aetiology, diagnosis, and management of hypopituitarism in adult life". Postgrad Med J. 82 (966): 259–66. doi:10.1136/pgmj.2005.039768. PMID 16597813.
↑ "Multiple Myeloma | NEJM".
↑ Palumbo A, Chanan-Khan A, Weisel K, Nooka AK, Masszi T, Beksac M, Spicka I, Hungria V, Munder M, Mateos MV, Mark TM, Qi M, Schecter J, Amin H, Qin X, Deraedt W, Ahmadi T, Spencer A, Sonneveld P (August 2016). "Daratumumab, Bortezomib, and Dexamethasone for Multiple Myeloma". N. Engl. J. Med. 375 (8): 754–66. doi:10.1056/NEJMoa1606038. PMID 27557302.
↑ Rajkumar SV, Kumar S (January 2016). "Multiple Myeloma: Diagnosis and Treatment". Mayo Clin. Proc. 91 (1): 101–19. doi:10.1016/j.mayocp.2015.11.007. PMC 5223450. PMID 26763514.
↑ Kyle RA, Rajkumar SV (September 2006). "Monoclonal gammopathy of undetermined significance". Br. J. Haematol. 134 (6): 573–89. doi:10.1111/j.1365-2141.2006.06235.x. PMID 16938117.
↑ Allen SC, Raut S (November 2004). "Biochemical recovery time scales in elderly patients with osteomalacia". J R Soc Med. 97 (11): 527–30. doi:10.1258/jrsm.97.11.527. PMID 15520146.
↑ Sherer Y, Bardayan Y, Shoenfeld Y (1997). "Thymoma, thymic hyperplasia, thymectomy and autoimmune diseases (Review)". Int. J. Oncol. 10 (5): 939–43. PMID 21533467.
↑ Nozza, Andrea (2017). "POEMS SYNDROME: AN UPDATE". Mediterranean Journal of Hematology and Infectious Diseases. 9 (1): e2017051. doi:10.4084/mjhid.2017.051. ISSN 2035-3006.
↑ Maceluch JA, Niedziela M (2006). "The clinical diagnosis and molecular genetics of kearns-sayre syndrome: a complex mitochondrial encephalomyopathy". Pediatr Endocrinol Rev. 4 (2): 117–37. PMID 17342029.
↑ Rigoli L, Di Bella C (2012). "Wolfram syndrome 1 and Wolfram syndrome 2". Curr. Opin. Pediatr. 24 (4): 512–7. doi:10.1097/MOP.0b013e328354ccdf. PMID 22790102.
↑ Husebye, Eystein S.; Anderson, Mark S. (2010). "Autoimmune Polyendocrine Syndromes: Clues to Type 1 Diabetes Pathogenesis". Immunity. 32 (4): 479–487. doi:10.1016/j.immuni.2010.03.016. ISSN 1074-7613.

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@@ Line 96: / Line 96: @@
 | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |'''[[Guillain-Barré syndrome|Guillain-Barre Syndrome]] (Demyelinating)'''<ref name="pmid117249122">{{cite journal |vauthors=Winer JB |title=Guillain Barré syndrome |journal=MP, Mol. Pathol. |volume=54 |issue=6 |pages=381–5 |date=December 2001 |pmid=11724912 |pmc=1187127 |doi= |url=}}</ref>
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Anti-ganglioside and anti-myelin antibodies<ref name="pmid7486873">{{cite journal |vauthors=Rees JH, Gregson NA, Hughes RA |title=Anti-ganglioside GM1 antibodies in Guillain-Barré syndrome and their relationship to Campylobacter jejuni infection |journal=Ann. Neurol. |volume=38 |issue=5 |pages=809–16 |date=November 1995 |pmid=7486873 |doi=10.1002/ana.410380516 |url=}}</ref>
+* [[Anti-ganglioside antibodies|Anti-ganglioside]] and anti-[[myelin]] antibodies<ref name="pmid7486873">{{cite journal |vauthors=Rees JH, Gregson NA, Hughes RA |title=Anti-ganglioside GM1 antibodies in Guillain-Barré syndrome and their relationship to Campylobacter jejuni infection |journal=Ann. Neurol. |volume=38 |issue=5 |pages=809–16 |date=November 1995 |pmid=7486873 |doi=10.1002/ana.410380516 |url=}}</ref>
-* Viral infections:<ref name="pmid3404161">{{cite journal |vauthors=Winer JB, Hughes RA, Anderson MJ, Jones DM, Kangro H, Watkins RP |title=A prospective study of acute idiopathic neuropathy. II. Antecedent events |journal=J. Neurol. Neurosurg. Psychiatry |volume=51 |issue=5 |pages=613–8 |date=May 1988 |pmid=3404161 |pmc=1033063 |doi= |url=}}</ref>
+* [[Viral]] infections:<ref name="pmid3404161">{{cite journal |vauthors=Winer JB, Hughes RA, Anderson MJ, Jones DM, Kangro H, Watkins RP |title=A prospective study of acute idiopathic neuropathy. II. Antecedent events |journal=J. Neurol. Neurosurg. Psychiatry |volume=51 |issue=5 |pages=613–8 |date=May 1988 |pmid=3404161 |pmc=1033063 |doi= |url=}}</ref>
-** Epstein Barr virus
+** [[Epstein Barr virus]]
-** HIV
+** [[Human Immunodeficiency Virus (HIV)|HIV]]
-** Cytomegalovirus
+** [[Cytomegalovirus]]
-** Varicella Zoster virus
+** [[Varicella Zoster Virus|Varicella Zoster virus]]
-* Bacterial infections:<ref name="pmid16969154">{{cite journal |vauthors=Yuki N, Koga M |title=Bacterial infections in Guillain-Barré and Fisher syndromes |journal=Curr. Opin. Neurol. |volume=19 |issue=5 |pages=451–7 |date=October 2006 |pmid=16969154 |doi=10.1097/01.wco.0000245367.36576.e9 |url=}}</ref>
+* [[Bacterial]] infections:<ref name="pmid16969154">{{cite journal |vauthors=Yuki N, Koga M |title=Bacterial infections in Guillain-Barré and Fisher syndromes |journal=Curr. Opin. Neurol. |volume=19 |issue=5 |pages=451–7 |date=October 2006 |pmid=16969154 |doi=10.1097/01.wco.0000245367.36576.e9 |url=}}</ref>
-** Campylobacter infection
+** [[Campylobacter]] infection
-** Mycoplasma pneumoniae
+** [[Mycoplasma pneumoniae]]
 | style="padding: 5px 5px; background: #F5F5F5;" |
 * Rapid onset and quick progression
 * Progression stops after 2-3 weeks
-* Bilateral ascending paraesthesias and paralysis (generalized)
+* Bilateral ascending [[Paraesthesia|paraesthesias]] and [[paralysis]] (generalized)
-* Weakness
+* [[Muscle weakness|Weakness]]
-* Ataxia
+* [[Ataxia]]
-* Areflexia
+* [[Areflexia]]
 * No fever
 * 4 sub-types:
-**Acute inflammatory demyelinating polyneuropathy
+**[[Acute inflammatory demyelinating polyneuropathy]]
-**Acute motor axonal neuropathy
+**[[Acute motor axonal neuropathy]]
 **Acute motor and sensory axonal neuropathy
-**Miller Fisher syndrome
+**[[Miller Fisher syndrome]]
 | style="padding: 5px 5px; background: #F5F5F5;" |
 * Delayed F waves<ref name="pmid666277">{{cite journal |vauthors=Kimura J |title=Proximal versus distal slowing of motor nerve conduction velocity in the Guillain-Barré syndrome |journal=Ann. Neurol. |volume=3 |issue=4 |pages=344–50 |date=April 1978 |pmid=666277 |doi=10.1002/ana.410030412 |url=}}</ref>
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Clinical diagnostic criteria (progressive weakness of more than two limbs, areflexia, and progression for no more than four weeks)<ref name="pmid11724912">{{cite journal |vauthors=Winer JB |title=Guillain Barré syndrome |journal=MP, Mol. Pathol. |volume=54 |issue=6 |pages=381–5 |date=December 2001 |pmid=11724912 |pmc=1187127 |doi= |url=}}</ref>
+* Clinical diagnostic criteria (progressive weakness of more than two [[limbs]], [[areflexia]], and progression for no more than four weeks)<ref name="pmid11724912">{{cite journal |vauthors=Winer JB |title=Guillain Barré syndrome |journal=MP, Mol. Pathol. |volume=54 |issue=6 |pages=381–5 |date=December 2001 |pmid=11724912 |pmc=1187127 |doi= |url=}}</ref>
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Intravenous immunoglobulins<ref name="pmid9014908">{{cite journal |vauthors= |title=Randomised trial of plasma exchange, intravenous immunoglobulin, and combined treatments in Guillain-Barré syndrome. Plasma Exchange/Sandoglobulin Guillain-Barré Syndrome Trial Group |journal=Lancet |volume=349 |issue=9047 |pages=225–30 |date=January 1997 |pmid=9014908 |doi= |url=}}</ref>
+* [[Intravenous]] [[immunoglobulins]]<ref name="pmid9014908">{{cite journal |vauthors= |title=Randomised trial of plasma exchange, intravenous immunoglobulin, and combined treatments in Guillain-Barré syndrome. Plasma Exchange/Sandoglobulin Guillain-Barré Syndrome Trial Group |journal=Lancet |volume=349 |issue=9047 |pages=225–30 |date=January 1997 |pmid=9014908 |doi= |url=}}</ref>
-* Plasma exchange<ref name="pmid4022342">{{cite journal |vauthors= |title=Plasmapheresis and acute Guillain-Barré syndrome. The Guillain-Barré syndrome Study Group |journal=Neurology |volume=35 |issue=8 |pages=1096–104 |date=August 1985 |pmid=4022342 |doi= |url=}}</ref>
+* [[Plasma]] exchange<ref name="pmid4022342">{{cite journal |vauthors= |title=Plasmapheresis and acute Guillain-Barré syndrome. The Guillain-Barré syndrome Study Group |journal=Neurology |volume=35 |issue=8 |pages=1096–104 |date=August 1985 |pmid=4022342 |doi= |url=}}</ref>
-* Respiratory support
+* [[Mechanical ventilation|Respiratory support]]
-* DVT/PE prevention
+* [[DVT]]/[[PE]] [[prevention]]
 |-
 | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |'''[[Chronic inflammatory demyelinating polyneuropathy|Chronic Inflammatory Demyelinating Polyneuropathy]] (CIDP) (Mixed axonal and demyelinatiing)'''<ref name="urlChronic Inflammatory Demyelinating Polyradiculoneuropathy: Clinical Characteristics, Course, and Recommendations for Diagnostic Criteria | JAMA Neurology | JAMA Network">{{cite web |url=https://jamanetwork.com/journals/jamaneurology/article-abstract/589258 |title=Chronic Inflammatory Demyelinating Polyradiculoneuropathy: Clinical Characteristics, Course, and Recommendations for Diagnostic Criteria &#124; JAMA Neurology &#124; JAMA Network |format= |work= |accessdate=}}</ref><ref name="urlonlinelibrary.wiley.com2">{{cite web |url=https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1468-1331.2009.02930.x |title=onlinelibrary.wiley.com |format= |work= |accessdate=}}</ref>
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Abnormal immune (both IgG based humoral and T-Cell mediated) response to unknown antigen (possible culprits include myelin proteins P0, P2 and PMP22)<ref name="pmid2440998">{{cite journal |vauthors=Milner P, Lovelidge CA, Taylor WA, Hughes RA |title=P0 myelin protein produces experimental allergic neuritis in Lewis rats |journal=J. Neurol. Sci. |volume=79 |issue=3 |pages=275–85 |date=July 1987 |pmid=2440998 |doi= |url=}}</ref><ref name="pmid10713353">{{cite journal |vauthors=Gabriel CM, Gregson NA, Hughes RA |title=Anti-PMP22 antibodies in patients with inflammatory neuropathy |journal=J. Neuroimmunol. |volume=104 |issue=2 |pages=139–46 |date=May 2000 |pmid=10713353 |doi= |url=}}</ref><ref name="pmid10025777">{{cite journal |vauthors=Bouchard C, Lacroix C, Planté V, Adams D, Chedru F, Guglielmi JM, Said G |title=Clinicopathologic findings and prognosis of chronic inflammatory demyelinating polyneuropathy |journal=Neurology |volume=52 |issue=3 |pages=498–503 |date=February 1999 |pmid=10025777 |doi= |url=}}</ref>
+* Abnormal [[immune response]] (both [[Immunoglobulin G|IgG]] based [[Humoral immunity|humoral]] and [[Cell mediated immunity|T-Cell mediated]]) response to unknown [[antigen]] (possible culprits include [[myelin]] [[proteins]] P0, P2 and PMP22)<ref name="pmid2440998">{{cite journal |vauthors=Milner P, Lovelidge CA, Taylor WA, Hughes RA |title=P0 myelin protein produces experimental allergic neuritis in Lewis rats |journal=J. Neurol. Sci. |volume=79 |issue=3 |pages=275–85 |date=July 1987 |pmid=2440998 |doi= |url=}}</ref><ref name="pmid10713353">{{cite journal |vauthors=Gabriel CM, Gregson NA, Hughes RA |title=Anti-PMP22 antibodies in patients with inflammatory neuropathy |journal=J. Neuroimmunol. |volume=104 |issue=2 |pages=139–46 |date=May 2000 |pmid=10713353 |doi= |url=}}</ref><ref name="pmid10025777">{{cite journal |vauthors=Bouchard C, Lacroix C, Planté V, Adams D, Chedru F, Guglielmi JM, Said G |title=Clinicopathologic findings and prognosis of chronic inflammatory demyelinating polyneuropathy |journal=Neurology |volume=52 |issue=3 |pages=498–503 |date=February 1999 |pmid=10025777 |doi= |url=}}</ref>
 *
 | style="padding: 5px 5px; background: #F5F5F5;" |
 * Slow onset and gradual progression
-* Relapsing and remitting course
+* [[Relapse|Relapsing]] and remitting course
-* Symmetrical proximal and distal motor and sensory weakness (legs>arms)
+* Symmetrical [[Proximal muscle weakness|proximal]] and [[Distal muscle weakness|distal motor]] and [[Sensory system|sensory weakness]] (legs>arms)
-* Foot drop
+* [[Foot drop]]
-* Numbness, tingling and pain
+* [[Numbness]], [[tingling]] and [[pain]]
-* Areflexia
+* [[Areflexia]]
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Elevated CSF protein (oligoclonal bands with normal WBCs)<ref name="pmid11558784">{{cite journal |vauthors=Yan WX, Archelos JJ, Hartung HP, Pollard JD |title=P0 protein is a target antigen in chronic inflammatory demyelinating polyradiculoneuropathy |journal=Ann. Neurol. |volume=50 |issue=3 |pages=286–92 |date=September 2001 |pmid=11558784 |doi= |url=}}</ref>
+* Elevated [[CSF]] [[protein]] ([[oligoclonal bands]] with normal [[White blood cells|WBCs]])<ref name="pmid11558784">{{cite journal |vauthors=Yan WX, Archelos JJ, Hartung HP, Pollard JD |title=P0 protein is a target antigen in chronic inflammatory demyelinating polyradiculoneuropathy |journal=Ann. Neurol. |volume=50 |issue=3 |pages=286–92 |date=September 2001 |pmid=11558784 |doi= |url=}}</ref>
-* Slowed motor nerve conduction velocities<ref name="pmid2757528">{{cite journal |vauthors=Barohn RJ, Kissel JT, Warmolts JR, Mendell JR |title=Chronic inflammatory demyelinating polyradiculoneuropathy. Clinical characteristics, course, and recommendations for diagnostic criteria |journal=Arch. Neurol. |volume=46 |issue=8 |pages=878–84 |date=August 1989 |pmid=2757528 |doi= |url=}}</ref>
+* Slowed [[Nerve conduction study|motor nerve conduction velocities]]<ref name="pmid2757528">{{cite journal |vauthors=Barohn RJ, Kissel JT, Warmolts JR, Mendell JR |title=Chronic inflammatory demyelinating polyradiculoneuropathy. Clinical characteristics, course, and recommendations for diagnostic criteria |journal=Arch. Neurol. |volume=46 |issue=8 |pages=878–84 |date=August 1989 |pmid=2757528 |doi= |url=}}</ref>
-* Prolonged distal motor latencies (period between F wave and initial stimulation)
+* Prolonged distal [[Motor skill|motor]] latencies (period between F wave and initial stimulation)
-* Delayed F wave latencies (recorded from the feet, hence called "F" waves)<ref name="pmid27575282">{{cite journal |vauthors=Barohn RJ, Kissel JT, Warmolts JR, Mendell JR |title=Chronic inflammatory demyelinating polyradiculoneuropathy. Clinical characteristics, course, and recommendations for diagnostic criteria |journal=Arch. Neurol. |volume=46 |issue=8 |pages=878–84 |date=August 1989 |pmid=2757528 |doi= |url=}}</ref>
+* Delayed F wave latencies (recorded from the [[feet]], hence called "F" waves)<ref name="pmid27575282">{{cite journal |vauthors=Barohn RJ, Kissel JT, Warmolts JR, Mendell JR |title=Chronic inflammatory demyelinating polyradiculoneuropathy. Clinical characteristics, course, and recommendations for diagnostic criteria |journal=Arch. Neurol. |volume=46 |issue=8 |pages=878–84 |date=August 1989 |pmid=2757528 |doi= |url=}}</ref>
-* MRI contrast enhancement and enlargement of T2 spinal segments<ref name="pmid23564314">{{cite journal |vauthors=Dimachkie MM, Barohn RJ |title=Chronic inflammatory demyelinating polyneuropathy |journal=Curr Treat Options Neurol |volume=15 |issue=3 |pages=350–66 |date=June 2013 |pmid=23564314 |pmc=3987657 |doi=10.1007/s11940-013-0229-6 |url=}}</ref>
+* [[MRI]] contrast enhancement and enlargement of [[Vertebra|T2]] [[spinal segments]]<ref name="pmid23564314">{{cite journal |vauthors=Dimachkie MM, Barohn RJ |title=Chronic inflammatory demyelinating polyneuropathy |journal=Curr Treat Options Neurol |volume=15 |issue=3 |pages=350–66 |date=June 2013 |pmid=23564314 |pmc=3987657 |doi=10.1007/s11940-013-0229-6 |url=}}</ref>
 | style="padding: 5px 5px; background: #F5F5F5;" |
 * EFNS/PNS criteria<ref name="urlonlinelibrary.wiley.com">{{cite web |url=https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1468-1331.2009.02930.x |title=onlinelibrary.wiley.com |format= |work= |accessdate=}}</ref>
 * Koski criteria<ref name="pmid19091330">{{cite journal |vauthors=Koski CL, Baumgarten M, Magder LS, Barohn RJ, Goldstein J, Graves M, Gorson K, Hahn AF, Hughes RA, Katz J, Lewis RA, Parry GJ, van Doorn P, Cornblath DR |title=Derivation and validation of diagnostic criteria for chronic inflammatory demyelinating polyneuropathy |journal=J. Neurol. Sci. |volume=277 |issue=1-2 |pages=1–8 |date=February 2009 |pmid=19091330 |doi=10.1016/j.jns.2008.11.015 |url=}}</ref>
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Corticosteroids
+* [[Corticosteroids]]
-* Intravenous immunoglobulin (IVIG)
+* [[Intravenous immunoglobulin]] ([[IVIG]])
-* Imuunosupressants (Alemtuzemab Azathioprine Cyclophosphamide Cyclosporin Etanercept Interferon-alpha)
+* [[Immunosupressive drug|Immunosupressants]] ([[Alemtuzumab|Alemtuzemab]] [[Azathioprine]] [[Cyclophosphamide]] [[Cyclosporine|Cyclosporin]] [[Etanercept]] [[Interferon-alpha]])
 |-
 | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |'''[[Multifocal motor neuropathy|Multifocal Motor Neuropathy]]'''<ref name="RobbinsLawson2018">{{cite journal|last1=Robbins|first1=Nathaniel M|last2=Lawson|first2=Victoria|title=The Potential Misdiagnosis of Multifocal Motor Neuropathy as Amyotrophic Lateral Sclerosis—A Case Series|journal=US Neurology|volume=14|issue=2|year=2018|pages=102|issn=1758-4000|doi=10.17925/USN.2018.14.2.102}}</ref>
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Abnormal immune response (Anti ganglioside GM-1 IgM antibodies)
+* [[Immune response|Abnormal immune response]] ([[Anti-ganglioside antibodies|Anti ganglioside]] [[Anti-ganglioside antibodies|GM-1]] [[IgM]] [[antibodies]])
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Progressive, asymmetric, distal and upper limb predominant weakness
+* Progressive, asymmetric, distal and upper [[Limb (anatomy)|limb]] predominant weakness
-* No significant sensory abnormalities
+* No significant [[sensory]] abnormalities
-* Areflexia
+* [[Areflexia]]
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Elevated CSF protein
+* Elevated [[CSF]] [[protein]]
 *
 | style="padding: 5px 5px; background: #F5F5F5;" |
 * Clinical criteria (EFNS/PNS):<ref name="pmid21199100">{{cite journal |vauthors= |title=European Federation of Neurological Societies/Peripheral Nerve Society guideline on management of multifocal motor neuropathy. Report of a joint task force of the European Federation of Neurological Societies and the Peripheral Nerve Society--first revision |journal=J. Peripher. Nerv. Syst. |volume=15 |issue=4 |pages=295–301 |date=December 2010 |pmid=21199100 |doi=10.1111/j.1529-8027.2010.00290.x |url=}}</ref>
-** Slowly progressive or stepwise progressive, focal, asymmetric  limb weakness; i.e., motor involvement in the motor nerve  distribution of at least two nerves for  > 1 month.
+** Slowly progressive or step-wise progressive, focal, asymmetric  [[limb]] weakness; i.e., [[Motor skill|motor]] involvement in the [[motor nerve]]  distribution of at least two nerves for  > 1 month.
-** No objective sensory  abnormalities except  for minor vibration  sense abnormalities in  the lower limbs
+** No objective [[Sensory system|sensory]]  abnormalities except  for minor vibration  sense abnormalities in  the [[lower limbs]]
 *
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Intravenous immunoglobilins
+* [[Intravenous immunoglobulin|Intravenous immunoglobulins]]
-* Cyclophosphamide
+* [[Cyclophosphamide]]
-* Rituximab
+* [[Rituximab]]
 |-
 | colspan="2" style="background: #4479BA; width: 200px;" | {{fontcolor|#FFF|'''Organ System Involvement'''}}
@@ Line 187: / Line 187: @@
 | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |'''[[Malaria]]'''<ref name="pmid22708041">{{cite journal |vauthors=Bartoloni A, Zammarchi L |title=Clinical aspects of uncomplicated and severe malaria |journal=Mediterr J Hematol Infect Dis |volume=4 |issue=1 |pages=e2012026 |date=2012 |pmid=22708041 |doi=10.4084/MJHID.2012.026 |url=}}</ref><ref name="pmid19488414">{{cite journal |vauthors=Tangpukdee N, Duangdee C, Wilairatana P, Krudsood S |title=Malaria diagnosis: a brief review |journal=Korean J. Parasitol. |volume=47 |issue=2 |pages=93–102 |date=June 2009 |pmid=19488414 |doi=10.3347/kjp.2009.47.2.93 |url=}}</ref><ref name="pmid8703186">{{cite journal |vauthors=White NJ |title=The treatment of malaria |journal=N. Engl. J. Med. |volume=335 |issue=11 |pages=800–6 |date=September 1996 |pmid=8703186 |doi=10.1056/NEJM199609123351107 |url=}}</ref>
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Plasmodium falciparum
+* [[Plasmodium falciparum]]
-* P. ovale
+* [[Plasmodium ovale|P. ovale]]
-* P. malariae
+* [[P. malariae]]
-* P. knowlesi
+* [[Plasmodium knowlesi|P. knowlesi]]
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Tertian (vivax, ovale, falciparum), quartan (malariae), quotidian fever (knowlesi)
+* Tertian ([[Plasmodium vivax|vivax]], [[Plasmodium ovale|ovale]], [[Plasmodium falciparum|falciparum]]), quartan (malariae), quotidian fever ([[Plasmodium knowlesi|knowlesi]])
-* Vector is female Anopheles mosquito
+* [[Vector]] is female [[Anopheles]] mosquito
-* Hepatosplenomegaly
+* [[Hepatosplenomegaly]]
-* Lymphadenopathy
+* [[Lymphadenopathy]]
-* Jaundice
+* [[Jaundice]]
-* Icterus
+* [[Icterus (medicine)|Icterus]]
-* Tachycardia
+* [[Tachycardia]]
-* Tachypnea
+* [[Tachypnea]]
-* Productive cough
+* [[Productive cough]]
-* Hemeturia
+* [[Hematuria]]
-* Altered mental status
+* [[Altered mental status]]
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Microcytic anemia
+* [[Microcytic anemia]]
-* Thick and thin blood films (Giemsa staining)
+* [[Malaria differential diagnosis|Thick and thin blood films]] ([[Giemsa stain|Giemsa staining]])
-* Rapid diagnostic test (antigen detection
+* Rapid diagnostic test ([[antigen]] detection
-* Polymerase chain reaction (PCR)
+* [[Polymerase chain reaction]] ([[Polymerase chain reaction|PCR]])
-* Enzyme linked immunosorbent assay (ELISA)
+* [[Enzyme linked immunosorbent assay (ELISA)|Enzyme linked immunosorbent assay]] ([[Enzyme linked immunosorbent assay (ELISA)|ELISA]])
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Thick and thin films
+* [[Malaria differential diagnosis|Thick and thin films]]
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Non-falciparum species:
+* Non-[[Plasmodium falciparum|falciparum]] species:
-** Choloroquine (in susceptible)
+** [[Chloroquine]] (in susceptible)
-** Artemisinin plus mefloquin or lumefantrine (in chloroquine resistant)
+** [[Artemisinin]] plus [[Mefloquine|mefloquin]] or [[lumefantrine]] (in [[chloroquine]] resistant)
-* Falciparum species:
+* [[Plasmodium falciparum|Falciparum]] species:
-** Chloroquine (in susceptible)
+** [[Chloroquine]] (in susceptible)
-** Artemether plus lumefantrine (in chloroquin resistant) OR
+** [[Artemether]] plus [[lumefantrine]] (in [[Chloroquine|chloroquin]] resistant) OR
-** Artesunate plus mefloquin OR
+** [[Artesunate]] plus [[Mefloquine|mefloquin]] OR
-** Artesunate plus sulfadoxine-pyrimethamine
+** [[Artesunate]] plus [[Sulfadoxine|sulfadoxine-pyrimethamine]]
-** Atovaquone plus proguanil
+** [[Atovaquone-Proguanil|Atovaquone plus proguanil]]
 |-
 | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |'''[[Kala-azar]]'''<ref name="pmid10798038">{{cite journal |vauthors=Aggarwal P, Handa R, Singh S, Wali JP |title=Kala-azar--new developments in diagnosis and treatment |journal=Indian J Pediatr |volume=66 |issue=1 |pages=63–71 |date=1999 |pmid=10798038 |doi= |url=}}</ref><ref name="pmid28649370">{{cite journal |vauthors=Torres-Guerrero E, Quintanilla-Cedillo MR, Ruiz-Esmenjaud J, Arenas R |title=Leishmaniasis: a review |journal=F1000Res |volume=6 |issue= |pages=750 |date=2017 |pmid=28649370 |doi=10.12688/f1000research.11120.1 |url=}}</ref>
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Leshmania donovani
+* [[Leishmaniasis|Leshmania donovani]]
 * L. infantum
 * L. chagasi
@@ Line 231: / Line 231: @@
 *
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Fever
+* [[Fever]]
-* Vector is sandfly
+* Vector is [[sandfly]]
-* Hepatosplenomegaly
+* [[Hepatosplenomegaly]]
-* Lymphadenopathy
+* [[Lymphadenopathy]]
-* Hyperpigmentation
+* [[Hyperpigmentation]]
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Anemia
+* [[Anemia]]
-* Direct Agglutination Test (DAT)
+* [[Direct agglutination test]] (DAT)
 * rk39 dipstick
-* ELISA
+* [[Enzyme linked immunosorbent assay (ELISA)|ELISA]]
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Splenic aspiration
+* [[Splenic]] aspiration
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Liposomal amphotericin B
+* [[Liposomal amphotericin B]]
-* Sodium stibogluconate
+* [[Sodium stibogluconate]]
-* Pentamidine
+* [[Pentamidine]]
 |-
 | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |'''[[Hepatitis|Infective Hepatitis]]'''<ref name="pmid19399811">{{cite journal |vauthors=Liang TJ |title=Hepatitis B: the virus and disease |journal=Hepatology |volume=49 |issue=5 Suppl |pages=S13–21 |date=May 2009 |pmid=19399811 |pmc=2809016 |doi=10.1002/hep.22881 |url=}}</ref><ref name="pmid26052383">{{cite journal |vauthors=Li HC, Lo SY |title=Hepatitis C virus: Virology, diagnosis and treatment |journal=World J Hepatol |volume=7 |issue=10 |pages=1377–89 |date=June 2015 |pmid=26052383 |pmc=4450201 |doi=10.4254/wjh.v7.i10.1377 |url=}}</ref>
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Hepatitis A virus (HAV)
+* [[Hepatitis A virus|Hepatitis A virus (HAV)]]
-* HBV
+* [[HBV]]
-* HCV
+* [[Hepatitis C|HCV]]
-* HDV (co-infection with HBV)
+* [[Hepatitis D|HDV]] (co-infection with [[HBV]])
-* HEV
+* [[Hepatitis E|HEV]]
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Fever
+* [[Fever]]
-* Transmitted via fecal-oral route (HAV, HBV, HDV, HEV), infected sera (HCV), sexual contact with infected individuals
+* Transmitted via [[fecal-oral route]] ([[Hepatitis A|HAV]], [[Hepatitis B virus|HBV]], [[HDV]], [[HEV]]), infected sera ([[HCV]]), [[sexual contact]] with infected individuals
-* Hepatosplenomegaly (may become shrunken in cases of cirrhosis due to chronic infection)
+* [[Hepatosplenomegaly]] (may become shrunken in cases of [[cirrhosis]] due to chronic infection)
-* Lymphadenopathy
+* [[Lymphadenopathy]]
 * [[Jaundice]]
 * [[Palmar erythema]]
 * [[Spider angiomata]]
 * [[Gynecomastia]]
-* Arthritis-dermatitis syndrome
+* [[Arthritis-dermatitis syndrome]]
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Antigen and antibody detection
+* [[Antigen]] and [[antibody]] detection
 * Total and direct [[bilirubin]] (increased)
-* Severe disease is often associated with persistent [[bilirubin]] levels >340 mol/L
+* Severe disease is often associated with persistent [[bilirubin]] levels >340 mmol/L
 * [[ALT]] and [[AST]] (increased)
 * [[Alkaline phosphatase]] (normal or mildly elevated)
@@ Line 277: / Line 277: @@
 * [[Anemia|Low hemoglobin]]
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Antigen and antibody detection
+* [[Antigen]] and [[antibody]] detection
 | style="padding: 5px 5px; background: #F5F5F5;" |
 * [[Interferon]] ([[IFN]])
@@ Line 287: / Line 287: @@
 | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |'''[[Chronic myelogenous leukemia|Chronic Myelogenous Leukemia]] (CML)'''<ref name="cancergov">National Cancer Institute. Physician Data Query Database 2015.http://www.cancer.gov/types/leukemia/hp/cml-treatment-pdq#section/_19</ref><ref name="pmid24729196">{{cite journal |vauthors=Jabbour E, Kantarjian H |title=Chronic myeloid leukemia: 2014 update on diagnosis, monitoring, and management |journal=Am. J. Hematol. |volume=89 |issue=5 |pages=547–56 |date=May 2014 |pmid=24729196 |doi=10.1002/ajh.23691 |url=}}</ref><ref name="pmid26434969">{{cite journal |vauthors=Thompson PA, Kantarjian HM, Cortes JE |title=Diagnosis and Treatment of Chronic Myeloid Leukemia in 2015 |journal=Mayo Clin. Proc. |volume=90 |issue=10 |pages=1440–54 |date=October 2015 |pmid=26434969 |pmc=5656269 |doi=10.1016/j.mayocp.2015.08.010 |url=}}</ref><ref name="pmid10428738">{{cite journal |vauthors=Faderl S, Talpaz M, Estrov Z, Kantarjian HM |title=Chronic myelogenous leukemia: biology and therapy |journal=Ann. Intern. Med. |volume=131 |issue=3 |pages=207–19 |date=August 1999 |pmid=10428738 |doi= |url=}}</ref><ref name="cancer.ca">Canadian Cancer Society.2015.http://www.cancer.ca/en/cancer-information/cancer-type/leukemia-chronic-myelogenous-cml/treatment/chronic/?region=ab</ref><ref name="Tefferi">{{cite journal|title=Classification, diagnosis and management of myeloproliferative disorders in the JAK2V617F era|author=Tefferi A|journal=Hematology Am Soc Hematol Educ Program|date=2006|pages=240-245|pmid=17124067}}</ref><ref name="cancer.ca2">Canadian Cancer Society.2015.http://www.cancer.ca/en/cancer-information/cancer-type/leukemia-chronic-myelogenous-cml/signs-and-symptoms/?region=ab</ref><ref name="pmid264349692">{{cite journal |vauthors=Thompson PA, Kantarjian HM, Cortes JE |title=Diagnosis and Treatment of Chronic Myeloid Leukemia in 2015 |journal=Mayo Clin. Proc. |volume=90 |issue=10 |pages=1440–54 |date=October 2015 |pmid=26434969 |pmc=5656269 |doi=10.1016/j.mayocp.2015.08.010 |url=}}</ref><ref name="pmid11550277">{{cite journal |vauthors=Wang YL, Bagg A, Pear W, Nowell PC, Hess JL |title=Chronic myelogenous leukemia: laboratory diagnosis and monitoring |journal=Genes Chromosomes Cancer |volume=32 |issue=2 |pages=97–111 |date=October 2001 |pmid=11550277 |doi= |url=}}</ref><ref name="pmid264349692">{{cite journal |vauthors=Thompson PA, Kantarjian HM, Cortes JE |title=Diagnosis and Treatment of Chronic Myeloid Leukemia in 2015 |journal=Mayo Clin. Proc. |volume=90 |issue=10 |pages=1440–54 |date=October 2015 |pmid=26434969 |pmc=5656269 |doi=10.1016/j.mayocp.2015.08.010 |url=}}</ref>
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* BCR/ABL gene fusion product due to translocation mutation t(9;22)(q34;q11)<ref name="pmid23147546">{{cite journal |vauthors=Zahra K, Ben Fredj W, Ben Youssef Y, Zaghouani H, Chebchoub I, Zaier M, Badreddine S, Braham N, Sennana H, Khelif A |title=Chronic myeloid leukemia as a secondary malignancy after lymphoma in a child. A case report and review of the literature |journal=Onkologie |volume=35 |issue=11 |pages=690–3 |date=2012 |pmid=23147546 |doi=10.1159/000343952 |url=}}</ref>
+* [[Philadelphia chromosome|BCR/ABL gene]] fusion product due to [[Chromosomal translocation|translocation]] [[mutation]] [[Philadelphia chromosome|t(9;22)]](q34;q11)<ref name="pmid23147546">{{cite journal |vauthors=Zahra K, Ben Fredj W, Ben Youssef Y, Zaghouani H, Chebchoub I, Zaier M, Badreddine S, Braham N, Sennana H, Khelif A |title=Chronic myeloid leukemia as a secondary malignancy after lymphoma in a child. A case report and review of the literature |journal=Onkologie |volume=35 |issue=11 |pages=690–3 |date=2012 |pmid=23147546 |doi=10.1159/000343952 |url=}}</ref>
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Fever
+* [[Fever]]
-* Weight loss
+* [[Weight loss]]
-* Hepatosplenomegaly
+* [[Hepatosplenomegaly]]
-* Lymphadenopathy
+* [[Lymphadenopathy]]
 * [[Bruises]]
@@ Line 298: / Line 298: @@
 * [[Ulcers]]
 * [[Vesicles]]
-* Malaise
+* [[Malaise]]
-* Early satiety
+* [[Early satiety]]
 | style="padding: 5px 5px; background: #F5F5F5;" |
 * [[Anemia]]
@@ Line 314: / Line 314: @@
 * Elevated [[histamine]] levels
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* Flouroscent insitu hybridization (FISH)
+* [[Fluorescence in situ hybridization|Fluoroscent insitu hybridization (FISH)]]
 | style="padding: 5px 5px; background: #F5F5F5;" |
 * [[Imatinib]]
@@ Line 323: / Line 323: @@
 * [[Cytarabine]]
-* [[Cytarabine|HDAC]] (high-dose cytarabine)
+* [[Cytarabine|HDAC]] (high-dose [[cytarabine]])
 * [[Hydroxyurea]]
 * [[Busulfan]]
 * [[Busulfex]]
-* Stem cell transplantation
+* [[Stem cell transplantation]]
 |-