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Reliable, easy-to-read patient information on common medical conditions β€” written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.

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POEMS syndrome differential diagnosis

Introduction

Overview

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

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]
Metabolic Syndrome (Axonal pathology)[8]
Vitamin Deficiencies (Axonal Pathology)[10]
      Guillain-Barre Syndrome (Demyelinating)[16]
      • Clinical diagnostic criteria (progressive weakness of more than two limbs, areflexia, and progression for no more than four weeks)[21]
      Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) (Mixed axonal and demyelinatiing)_JAMA_Neurology_|_JAMA_Network-24|[24][25]
        • EFNS/PNS criteria[33]
        • Koski criteria[34]
        Multifocal Motor Neuropathy[35]
        • Progressive, asymmetric, distal and upper limb predominant weakness
        • No significant sensory abnormalities
        • Areflexia
        • 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
          Organ System Involvement Differential Diagnosis Causes Features Laboratory Findings Gold Standard Test Therapy
          O = Organomegaly (Hepatosplenomegaly and Lymphadenopathy) Malaria[37][38][39]
          Kala-azar[40][41]
            Infective Hepatitis[42][43]
            Chronic Myelogenous Leukemia (CML)[44][45][46][47][48][49][50][51][52][51]
            Lymphoma
            Primary (AL) Amyloidosis[54][55]
            • 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]
            Organ System Involvement Differential Diagnosis Causes Features Laboratory Findings Gold Standard Test Therapy
            E = Endocrinopathy (Hypogonadism, Hypothyroidism, Hypopituitarism) Hypogonadism[62][63] Primary Hypogonadism (Hypergonadotrophic)
            Secondary Hypogonadism (Hypogonadotrophic)
            Hypothyroidism[64][65] Primary Hypothyroidism
            Secondary Hypothyroidism
            Tertiary Hypothyroidism
            Hypopituitarism[66][67] Congenital
            • Decreased FSH, LH
            • Decreased TSH
            • Decreased ACTH
            • Decreased GH
            • Decreased ADH
            • Decreased oxytocin
            • Serum hormone levels produced by pituitary
            • Hormone replacement therapy
            Acquired
            Organ System Involvement Differential Diagnosis Causes Features Laboratory Findings Gold Standard Test Therapy
            M = M-protein ( Hematological Abnormality/Plasma Cell Dyscrasias) Multiple myeloma_NEJM-68|[68][69][70]
            • 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
            Monoclonal gammopathy of undetermined significance (MGUS)[71]
            • 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)

            • 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
            • 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
            • Normal serum calcium, phosphate, alkaline phosphatase and parathyroid hormone levels
            • Decreased bone mass
              • T score less than -2.5 on DEXA scan
              Osteomalacia[72]
              • Decreased serum calcium
              • Decreased serum phosphate
              • Increased serum alkaline phosphatase
              • Increased serum parathyroid hormone levels
              • Bone biopsy (increased osteoid and decreased calcification)
              Osteogenesis imperfecta
              • Normal serum calcium
              • Normal serum phosphate
              • Increased serum alkaline phosphatase
              • DNA analysis
              • Collagen analysis
              Skin Changes Scurvy
              Other Differentials

              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

              References

              1. ↑ Gherardi RK, BΓ©lec 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. PMIDΒ 8608236.
              2. ↑ 2.0 2.1 Nozza A (2017). “POEMS SYNDROME: an Update”. Mediterr J Hematol Infect Dis. 9 (1): e2017051. doi:10.4084/MJHID.2017.051. PMCΒ 5584767. PMIDΒ 28894560.
              3. ↑ 3.0 3.1 3.2 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. PMIDΒ 6248720.
              4. ↑ 4.0 4.1 4.2 4.3 4.4 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. PMIDΒ 6315993.
              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. PMIDΒ 19289745.
              6. ↑ GΓΌneş 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. PMIDΒ 25888197.
              7. _International_Myeloma_Working_Group_(IMWG)_Criteria_for_the_Diagnosis_of_Multiple_Myeloma_7-0|↑ “IMWG | International Myeloma Working Group (IMWG) Criteria for the Diagnosis of Multiple Myeloma”.
              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. PMIDΒ 25897354.
              9. ↑ “Diagnosis and classification of diabetes mellitus”. Diabetes Care. 33 Suppl 1: S62–9. January 2010. doi:10.2337/dc10-S062. PMIDΒ 20042775.
              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. PMIDΒ 28129784.
              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. PMIDΒ 2738712.
              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. PMIDΒ 23262189.
              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. PMIDΒ 2339684.
              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. PMCΒ 3573090. PMIDΒ 23262189.
              15. ↑ 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. PMIDΒ 12086562.
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              18. ↑ 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. PMCΒ 1033063. PMIDΒ 3404161.
              19. ↑ Yuki N, Koga M (October 2006). “Bacterial infections in Guillain-BarrΓ© and Fisher syndromes”. Curr. Opin. Neurol. 19 (5): 451–7. doi:10.1097/01.wco.0000245367.36576.e9. PMIDΒ 16969154.
              20. ↑ Kimura J (April 1978). “Proximal versus distal slowing of motor nerve conduction velocity in the Guillain-BarrΓ© syndrome”. Ann. Neurol. 3 (4): 344–50. doi:10.1002/ana.410030412. PMIDΒ 666277.
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              27. ↑ Gabriel CM, Gregson NA, Hughes RA (May 2000). “Anti-PMP22 antibodies in patients with inflammatory neuropathy”. J. Neuroimmunol. 104 (2): 139–46. PMIDΒ 10713353.
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              74. ↑ Nozza, Andrea (2017). “POEMS SYNDROME: AN UPDATE”. Mediterranean Journal of Hematology and Infectious Diseases. 9 (1): e2017051. doi:10.4084/mjhid.2017.051. ISSNΒ 2035-3006.
              75. ↑ 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. PMIDΒ 17342029.
              76. ↑ 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. PMIDΒ 22790102.
              77. ↑ 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. ISSNΒ 1074-7613.

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