Primary amyloidosis differential diagnosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

Differentiating Primary amyloidosis from Other Diseases

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	Clinical Features	Laboratory Findings	Gold Standard Test	Therapy
Polyneuropathy	POEMS syndrome (Demyelinating)	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 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 Elevated levels of antitiroglobulin antibody and antithyroid peroxydase antibody	International Myeloma Working Group (IMWG) clinical and laboratory diagnostic criteria
	Metabolic Syndrome (Axonal pathology)	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	Anti-diabetic therapy Gabapentin Carbamazepine Foot care
	Vitamin Deficiencies (Axonal Pathology)	Vitamin B12 deficiency (Decreased S-adenosyl methionine) Vitamin B1 deficiency	Primarily sensory deficits Vibration and proprioception affected Gait abnormalities Cognitive impairment Irritability Glossitis	Anemia (megaloblastic in case of B12 deficiency) Decreased serum Vitamin B12 levels (< 200 pg/ml) Elevated methylmalonic acid	Serum Vitamin B12 levels Methylmalonic acid levels Intrinsic factor antibodies	Vitamin B12 supplement (parenteral)
	Guillain-Barre Syndrome (Demyelinating)	Anti-ganglioside and anti-myelin antibodies Viral infections: Epstein Barr virus HIV Cytomegalovirus Varicella Zoster virus Bacterial infections: 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	Clinical diagnostic criteria (progressive weakness of more than two limbs, areflexia, and progression for no more than four weeks)	Intravenous immunoglobulins Plasma exchange Respiratory support DVT/PE prevention
	Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) (Mixed axonal and demyelinatiing)	Abnormal immune response (both IgG based humoral and T-Cell mediated) response to unknown antigen (possible culprits include myelin proteins P0, P2 and PMP22)	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) Slowed motor nerve conduction velocities Prolonged distal motor latencies (period between F wave and initial stimulation) Delayed F wave latencies (recorded from the feet, hence called "F" waves) MRI contrast enhancement and enlargement of T2 spinal segments	EFNS/PNS criteria Koski criteria	Corticosteroids Intravenous immunoglobulin (IVIG) Immunosupressants (Alemtuzemab Azathioprine Cyclophosphamide Cyclosporin Etanercept Interferon-alpha)
	Multifocal Motor Neuropathy	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): 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
Organomegaly (Hepatosplenomegaly and Lymphadenopathy)	Malaria	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	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	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)^[37]	BCR/ABL gene fusion product due to translocation mutation t(9;22)(q34;q11)	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	Aggregation and deposition of immunoglobulin light chains that are usually produced by plasma cell clones	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 Dexamethasone plus Cyclophosphamide-thalidomide Stem cell transplantation
	Gaucher's Disease	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
Cardiac Failure




		I

Organ System Involvement	Differential Diagnosis	Causes	Features	Laboratory Findings	Gold Standard Test	Therapy
Plasma Cell Dyscrasias	Multiple myeloma	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)	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
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

↑ Gherardi RK, Bélec L, Soubrier M, Malapert D, Zuber M, Viard JP, Intrator L, Degos JD, Authier FJ (February 1996). "Overproduction of proinflammatory cytokines imbalanced by their antagonists in POEMS syndrome". Blood. 87 (4): 1458–65. PMID 8608236.
↑ ^2.0 ^2.1 ^2.2 Nozza A (2017). "POEMS SYNDROME: an Update". Mediterr J Hematol Infect Dis. 9 (1): e2017051. doi:10.4084/MJHID.2017.051. PMC 5584767. PMID 28894560.
↑ ^3.0 ^3.1 ^3.2 ^3.3 ^3.4 Bardwick PA, Zvaifler NJ, Gill GN, Newman D, Greenway GD, Resnick DL (July 1980). "Plasma cell dyscrasia with polyneuropathy, organomegaly, endocrinopathy, M protein, and skin changes: the POEMS syndrome. Report on two cases and a review of the literature". Medicine (Baltimore). 59 (4): 311–22. PMID 6248720.
↑ ^4.0 ^4.1 ^4.2 ^4.3 ^4.4 ^4.5 ^4.6 ^4.7 ^4.8 Takatsuki K, Sanada I (September 1983). "Plasma cell dyscrasia with polyneuropathy and endocrine disorder: clinical and laboratory features of 109 reported cases". Jpn. J. Clin. Oncol. 13 (3): 543–55. PMID 6315993.
↑ Nobile-Orazio E, Terenghi F, Giannotta C, Gallia F, Nozza A (March 2009). "Serum VEGF levels in POEMS syndrome and in immune-mediated neuropathies". Neurology. 72 (11): 1024–6. doi:10.1212/01.wnl.0000344569.13496.ff. PMID 19289745.
↑ Güneş HN, Bilecenoğlu NT, Şener U, Yoldaş TK (April 2015). "POEMS syndrome with peripheral and central nervous system demyelination: case report". Neurologist. 19 (4): 101–3. doi:10.1097/NRL.0000000000000017. PMID 25888197.
↑ "IMWG | International Myeloma Working Group (IMWG) Criteria for the Diagnosis of Multiple Myeloma".
↑ Schreiber AK, Nones CF, Reis RC, Chichorro JG, Cunha JM (April 2015). "Diabetic neuropathic pain: Physiopathology and treatment". World J Diabetes. 6 (3): 432–44. doi:10.4239/wjd.v6.i3.432. PMID 25897354.
↑ "Diagnosis and classification of diabetes mellitus". Diabetes Care. 33 Suppl 1: S62–9. January 2010. doi:10.2337/dc10-S062. PMID 20042775.
↑ Ekabe CJ, Kehbila J, Abanda MH, Kadia BM, Sama CB, Monekosso GL (January 2017). "Vitamin B12 deficiency neuropathy; a rare diagnosis in young adults: a case report". BMC Res Notes. 10 (1): 72. doi:10.1186/s13104-017-2393-3. PMID 28129784.
↑ Doi T, Kawata T, Tadano N, Iijima T, Maekawa A (February 1989). "Effect of vitamin B12 deficiency on S-adenosylmethionine metabolism in rats". J. Nutr. Sci. Vitaminol. 35 (1): 1–9. PMID 2738712.
↑ Berg RL, Shaw GR (February 2013). "Laboratory evaluation for vitamin B12 deficiency: the case for cascade testing". Clin Med Res. 11 (1): 7–15. doi:10.3121/cmr.2012.1112. PMID 23262189.
↑ Lindenbaum J, Savage DG, Stabler SP, Allen RH (June 1990). "Diagnosis of cobalamin deficiency: II. Relative sensitivities of serum cobalamin, methylmalonic acid, and total homocysteine concentrations". Am. J. Hematol. 34 (2): 99–107. PMID 2339684.
↑ Berg RL, Shaw GR (February 2013). "Laboratory evaluation for vitamin B12 deficiency: the case for cascade testing". Clin Med Res. 11 (1): 7–15. doi:10.3121/cmr.2012.1112. PMC 3573090. PMID 23262189.
↑ Lane LA, Rojas-Fernandez C (2002). "Treatment of vitamin b(12)-deficiency anemia: oral versus parenteral therapy". Ann Pharmacother. 36 (7–8): 1268–72. doi:10.1345/aph.1A122. PMID 12086562.
↑ Winer JB (December 2001). "Guillain Barré syndrome". MP, Mol. Pathol. 54 (6): 381–5. PMC 1187127. PMID 11724912.
↑ Rees JH, Gregson NA, Hughes RA (November 1995). "Anti-ganglioside GM1 antibodies in Guillain-Barré syndrome and their relationship to Campylobacter jejuni infection". Ann. Neurol. 38 (5): 809–16. doi:10.1002/ana.410380516. PMID 7486873.
↑ Winer JB, Hughes RA, Anderson MJ, Jones DM, Kangro H, Watkins RP (May 1988). "A prospective study of acute idiopathic neuropathy. II. Antecedent events". J. Neurol. Neurosurg. Psychiatry. 51 (5): 613–8. PMC 1033063. PMID 3404161.
↑ Yuki N, Koga M (October 2006). "Bacterial infections in Guillain-Barré and Fisher syndromes". Curr. Opin. Neurol. 19 (5): 451–7. doi:10.1097/01.wco.0000245367.36576.e9. PMID 16969154.
↑ Kimura J (April 1978). "Proximal versus distal slowing of motor nerve conduction velocity in the Guillain-Barré syndrome". Ann. Neurol. 3 (4): 344–50. doi:10.1002/ana.410030412. PMID 666277.
↑ Winer JB (December 2001). "Guillain Barré syndrome". MP, Mol. Pathol. 54 (6): 381–5. PMC 1187127. PMID 11724912.
↑ "Randomised trial of plasma exchange, intravenous immunoglobulin, and combined treatments in Guillain-Barré syndrome. Plasma Exchange/Sandoglobulin Guillain-Barré Syndrome Trial Group". Lancet. 349 (9047): 225–30. January 1997. PMID 9014908.
↑ "Plasmapheresis and acute Guillain-Barré syndrome. The Guillain-Barré syndrome Study Group". Neurology. 35 (8): 1096–104. August 1985. PMID 4022342.
↑ "Chronic Inflammatory Demyelinating Polyradiculoneuropathy: Clinical Characteristics, Course, and Recommendations for Diagnostic Criteria | JAMA Neurology | JAMA Network".
↑ "onlinelibrary.wiley.com".
↑ Milner P, Lovelidge CA, Taylor WA, Hughes RA (July 1987). "P0 myelin protein produces experimental allergic neuritis in Lewis rats". J. Neurol. Sci. 79 (3): 275–85. PMID 2440998.
↑ Gabriel CM, Gregson NA, Hughes RA (May 2000). "Anti-PMP22 antibodies in patients with inflammatory neuropathy". J. Neuroimmunol. 104 (2): 139–46. PMID 10713353.
↑ Bouchard C, Lacroix C, Planté V, Adams D, Chedru F, Guglielmi JM, Said G (February 1999). "Clinicopathologic findings and prognosis of chronic inflammatory demyelinating polyneuropathy". Neurology. 52 (3): 498–503. PMID 10025777.
↑ Yan WX, Archelos JJ, Hartung HP, Pollard JD (September 2001). "P0 protein is a target antigen in chronic inflammatory demyelinating polyradiculoneuropathy". Ann. Neurol. 50 (3): 286–92. PMID 11558784.
↑ Barohn RJ, Kissel JT, Warmolts JR, Mendell JR (August 1989). "Chronic inflammatory demyelinating polyradiculoneuropathy. Clinical characteristics, course, and recommendations for diagnostic criteria". Arch. Neurol. 46 (8): 878–84. PMID 2757528.
↑ Barohn RJ, Kissel JT, Warmolts JR, Mendell JR (August 1989). "Chronic inflammatory demyelinating polyradiculoneuropathy. Clinical characteristics, course, and recommendations for diagnostic criteria". Arch. Neurol. 46 (8): 878–84. PMID 2757528.
↑ Dimachkie MM, Barohn RJ (June 2013). "Chronic inflammatory demyelinating polyneuropathy". Curr Treat Options Neurol. 15 (3): 350–66. doi:10.1007/s11940-013-0229-6. PMC 3987657. PMID 23564314.
↑ "onlinelibrary.wiley.com".
↑ 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 (February 2009). "Derivation and validation of diagnostic criteria for chronic inflammatory demyelinating polyneuropathy". J. Neurol. Sci. 277 (1–2): 1–8. doi:10.1016/j.jns.2008.11.015. PMID 19091330.
↑ Robbins, Nathaniel M; Lawson, Victoria (2018). "The Potential Misdiagnosis of Multifocal Motor Neuropathy as Amyotrophic Lateral Sclerosis—A Case Series". US Neurology. 14 (2): 102. doi:10.17925/USN.2018.14.2.102. ISSN 1758-4000.
↑ "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". J. Peripher. Nerv. Syst. 15 (4): 295–301. December 2010. doi:10.1111/j.1529-8027.2010.00290.x. PMID 21199100.
↑ 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.

[pmid8608236-1] Gherardi RK, Bélec L, Soubrier M, Malapert D, Zuber M, Viard JP, Intrator L, Degos JD, Authier FJ (February 1996). "Overproduction of proinflammatory cytokines imbalanced by their antagonists in POEMS syndrome". Blood. 87 (4): 1458–65. PMID 8608236.

[pmid28894560-2] 2.0 ^2.1 ^2.2 Nozza A (2017). "POEMS SYNDROME: an Update". Mediterr J Hematol Infect Dis. 9 (1): e2017051. doi:10.4084/MJHID.2017.051. PMC 5584767. PMID 28894560.

[pmid6248720-3] 3.0 ^3.1 ^3.2 ^3.3 ^3.4 Bardwick PA, Zvaifler NJ, Gill GN, Newman D, Greenway GD, Resnick DL (July 1980). "Plasma cell dyscrasia with polyneuropathy, organomegaly, endocrinopathy, M protein, and skin changes: the POEMS syndrome. Report on two cases and a review of the literature". Medicine (Baltimore). 59 (4): 311–22. PMID 6248720.

[pmid6315993-4] 4.0 ^4.1 ^4.2 ^4.3 ^4.4 ^4.5 ^4.6 ^4.7 ^4.8 Takatsuki K, Sanada I (September 1983). "Plasma cell dyscrasia with polyneuropathy and endocrine disorder: clinical and laboratory features of 109 reported cases". Jpn. J. Clin. Oncol. 13 (3): 543–55. PMID 6315993.

[pmid19289745-5] Nobile-Orazio E, Terenghi F, Giannotta C, Gallia F, Nozza A (March 2009). "Serum VEGF levels in POEMS syndrome and in immune-mediated neuropathies". Neurology. 72 (11): 1024–6. doi:10.1212/01.wnl.0000344569.13496.ff. PMID 19289745.

[pmid25888197-6] Güneş HN, Bilecenoğlu NT, Şener U, Yoldaş TK (April 2015). "POEMS syndrome with peripheral and central nervous system demyelination: case report". Neurologist. 19 (4): 101–3. doi:10.1097/NRL.0000000000000017. PMID 25888197.

[urlIMWG_|_International_Myeloma_Working_Group_(IMWG)_Criteria_for_the_Diagnosis_of_Multiple_Myeloma-7] "IMWG | International Myeloma Working Group (IMWG) Criteria for the Diagnosis of Multiple Myeloma".

[pmid25897354-8] Schreiber AK, Nones CF, Reis RC, Chichorro JG, Cunha JM (April 2015). "Diabetic neuropathic pain: Physiopathology and treatment". World J Diabetes. 6 (3): 432–44. doi:10.4239/wjd.v6.i3.432. PMID 25897354.

[pmid20042775-9] "Diagnosis and classification of diabetes mellitus". Diabetes Care. 33 Suppl 1: S62–9. January 2010. doi:10.2337/dc10-S062. PMID 20042775.

[pmid28129784-10] Ekabe CJ, Kehbila J, Abanda MH, Kadia BM, Sama CB, Monekosso GL (January 2017). "Vitamin B12 deficiency neuropathy; a rare diagnosis in young adults: a case report". BMC Res Notes. 10 (1): 72. doi:10.1186/s13104-017-2393-3. PMID 28129784.

[pmid2738712-11] Doi T, Kawata T, Tadano N, Iijima T, Maekawa A (February 1989). "Effect of vitamin B12 deficiency on S-adenosylmethionine metabolism in rats". J. Nutr. Sci. Vitaminol. 35 (1): 1–9. PMID 2738712.

[pmid23262189-12] Berg RL, Shaw GR (February 2013). "Laboratory evaluation for vitamin B12 deficiency: the case for cascade testing". Clin Med Res. 11 (1): 7–15. doi:10.3121/cmr.2012.1112. PMID 23262189.

[pmid2339684-13] Lindenbaum J, Savage DG, Stabler SP, Allen RH (June 1990). "Diagnosis of cobalamin deficiency: II. Relative sensitivities of serum cobalamin, methylmalonic acid, and total homocysteine concentrations". Am. J. Hematol. 34 (2): 99–107. PMID 2339684.

[pmid232621892-14] Berg RL, Shaw GR (February 2013). "Laboratory evaluation for vitamin B12 deficiency: the case for cascade testing". Clin Med Res. 11 (1): 7–15. doi:10.3121/cmr.2012.1112. PMC 3573090. PMID 23262189.

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Primary amyloidosis differential diagnosis

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Differentiating Primary amyloidosis from Other Diseases

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