POEMS syndrome: Update on diagnosis, risk-stratification, and management
Disease overview: POEMS syndrome is a paraneoplastic syndrome due to an underlying plasma cell neoplasm. The major criteria for the syndrome are polyradiculoneuropathy, clonal plasma cell disorder (PCD), sclerotic bone lesions, elevated vascular endothelial growth factor, and the presence of Castlem...
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Published in | American journal of hematology Vol. 87; no. 8; pp. 804 - 814 |
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Main Author | |
Format | Journal Article |
Language | English |
Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.08.2012
Wiley-Liss Wiley Subscription Services, Inc |
Subjects | |
Online Access | Get full text |
ISSN | 0361-8609 1096-8652 1096-8652 |
DOI | 10.1002/ajh.23288 |
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Abstract | Disease overview: POEMS syndrome is a paraneoplastic syndrome due to an underlying plasma cell neoplasm. The major criteria for the syndrome are polyradiculoneuropathy, clonal plasma cell disorder (PCD), sclerotic bone lesions, elevated vascular endothelial growth factor, and the presence of Castleman disease. Minor features include organomegaly, endocrinopathy, characteristic skin changes, papilledema, extravascular volume overload, and thrombocytosis. Diagnoses are often delayed because the syndrome is rare and can be mistaken for other neurologic disorders, most commonly chronic inflammatory demyelinating polyradiculoneuropathy. POEMS syndrome should be distinguished from the Castleman disease variant of POEMS syndrome, which has no clonal PCD and typically little to no peripheral neuropathy but has several of the minor diagnostic criteria for POEMS syndrome.
Diagnosis: The diagnosis of POEMS syndrome is made with 3 of the major criteria, two of which must include polyradiculoneuropathy and clonal plasma cell disorder, and at least one of the minor criteria.
Risk stratification: Because the pathogenesis of the syndrome is not well understood, risk stratification is limited to clinical phenotype rather than specific molecular markers. The number of clinical criteria is not prognostic, but the extent of the plasma cell disorder is. Those patients with an iliac crest bone marrow biopsy that does not reveal a plasma cell clone are candidates for local radiation therapy; those with a more extensive or disseminated clone will be candidates for systemic therapy.
Risk‐adapted therapy: For those patients with a dominant sclerotic plasmacytoma, first line therapy is irradiation. Patients with diffuse sclerotic lesions or disseminated bone marrow involvement and for those who have progression of their disease 3 to 6 months after completing radiation therapy should receive systemic therapy. Corticosteroids are temporizing, but alkylators are the mainstay of treatment, either in the form of low dose conventional therapy or high dose with stem cell transplantation. The benefit of anti‐VEGF antibodies is conflicting. Lenalidomide shows promise with manageable toxicity. Thalidomide and bortezomib also have activity, but their benefit needs to be weighed against their risk of exacerbating the peripheral neuropathy. Prompt recognition and institution of both supportive care measures and therapy directed against the plasma cell result in the best outcomes. Am. J. Hematol. 2012. © 2012 Wiley Periodicals, Inc. |
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AbstractList | Disease overview: POEMS syndrome is a paraneoplastic syndrome due to an underlying plasma cell neoplasm. The major criteria for the syndrome are polyradiculoneuropathy, clonal plasma cell disorder (PCD), sclerotic bone lesions, elevated vascular endothelial growth factor, and the presence of Castleman disease. Minor features include organomegaly, endocrinopathy, characteristic skin changes, papilledema, extravascular volume overload, and thrombocytosis. Diagnoses are often delayed because the syndrome is rare and can be mistaken for other neurologic disorders, most commonly chronic inflammatory demyelinating polyradiculoneuropathy. POEMS syndrome should be distinguished from the Castleman disease variant of POEMS syndrome, which has no clonal PCD and typically little to no peripheral neuropathy but has several of the minor diagnostic criteria for POEMS syndrome.
Diagnosis: The diagnosis of POEMS syndrome is made with 3 of the major criteria, two of which must include polyradiculoneuropathy and clonal plasma cell disorder, and at least one of the minor criteria.
Risk stratification: Because the pathogenesis of the syndrome is not well understood, risk stratification is limited to clinical phenotype rather than specific molecular markers. The number of clinical criteria is not prognostic, but the extent of the plasma cell disorder is. Those patients with an iliac crest bone marrow biopsy that does not reveal a plasma cell clone are candidates for local radiation therapy; those with a more extensive or disseminated clone will be candidates for systemic therapy.
Risk‐adapted therapy: For those patients with a dominant sclerotic plasmacytoma, first line therapy is irradiation. Patients with diffuse sclerotic lesions or disseminated bone marrow involvement and for those who have progression of their disease 3 to 6 months after completing radiation therapy should receive systemic therapy. Corticosteroids are temporizing, but alkylators are the mainstay of treatment, either in the form of low dose conventional therapy or high dose with stem cell transplantation. The benefit of anti‐VEGF antibodies is conflicting. Lenalidomide shows promise with manageable toxicity. Thalidomide and bortezomib also have activity, but their benefit needs to be weighed against their risk of exacerbating the peripheral neuropathy. Prompt recognition and institution of both supportive care measures and therapy directed against the plasma cell result in the best outcomes. Am. J. Hematol. 2012. © 2012 Wiley Periodicals, Inc. Disease overview: POEMS syndrome is a paraneoplastic syndrome due to an underlying plasma cell neoplasm. The major criteria for the syndrome are polyradiculoneuropathy, clonal plasma cell disorder (PCD), sclerotic bone lesions, elevated vascular endothelial growth factor, and the presence of Castleman disease. Minor features include organomegaly, endocrinopathy, characteristic skin changes, papilledema, extravascular volume overload, and thrombocytosis. Diagnoses are often delayed because the syndrome is rare and can be mistaken for other neurologic disorders, most commonly chronic inflammatory demyelinating polyradiculoneuropathy. POEMS syndrome should be distinguished from the Castleman disease variant of POEMS syndrome, which has no clonal PCD and typically little to no peripheral neuropathy but has several of the minor diagnostic criteria for POEMS syndrome. Diagnosis: The diagnosis of POEMS syndrome is made with 3 of the major criteria, two of which must include polyradiculoneuropathy and clonal plasma cell disorder, and at least one of the minor criteria. Risk stratification: Because the pathogenesis of the syndrome is not well understood, risk stratification is limited to clinical phenotype rather than specific molecular markers. The number of clinical criteria is not prognostic, but the extent of the plasma cell disorder is. Those patients with an iliac crest bone marrow biopsy that does not reveal a plasma cell clone are candidates for local radiation therapy; those with a more extensive or disseminated clone will be candidates for systemic therapy. Risk‐adapted therapy: For those patients with a dominant sclerotic plasmacytoma, first line therapy is irradiation. Patients with diffuse sclerotic lesions or disseminated bone marrow involvement and for those who have progression of their disease 3 to 6 months after completing radiation therapy should receive systemic therapy. Corticosteroids are temporizing, but alkylators are the mainstay of treatment, either in the form of low dose conventional therapy or high dose with stem cell transplantation. The benefit of anti‐VEGF antibodies is conflicting. Lenalidomide shows promise with manageable toxicity. Thalidomide and bortezomib also have activity, but their benefit needs to be weighed against their risk of exacerbating the peripheral neuropathy. Prompt recognition and institution of both supportive care measures and therapy directed against the plasma cell result in the best outcomes. Am. J. Hematol. 2012. © 2012 Wiley Periodicals, Inc. Disease overview: POEMS syndrome is a paraneoplastic syndrome due to an underlying plasma cell neoplasm. The major criteria for the syndrome are polyradiculoneuropathy, clonal plasma cell disorder (PCD), sclerotic bone lesions, elevated vascular endothelial growth factor, and the presence of Castleman disease. Minor features include organomegaly, endocrinopathy, characteristic skin changes, papilledema, extravascular volume overload, and thrombocytosis. Diagnoses are often delayed because the syndrome is rare and can be mistaken for other neurologic disorders, most commonly chronic inflammatory demyelinating polyradiculoneuropathy. POEMS syndrome should be distinguished from the Castleman disease variant of POEMS syndrome, which has no clonal PCD and typically little to no peripheral neuropathy but has several of the minor diagnostic criteria for POEMS syndrome. Diagnosis: The diagnosis of POEMS syndrome is made with 3 of the major criteria, two of which must include polyradiculoneuropathy and clonal plasma cell disorder, and at least one of the minor criteria. Risk stratification: Because the pathogenesis of the syndrome is not well understood, risk stratification is limited to clinical phenotype rather than specific molecular markers. The number of clinical criteria is not prognostic, but the extent of the plasma cell disorder is. Those patients with an iliac crest bone marrow biopsy that does not reveal a plasma cell clone are candidates for local radiation therapy; those with a more extensive or disseminated clone will be candidates for systemic therapy. Risk-adapted therapy: For those patients with a dominant sclerotic plasmacytoma, first line therapy is irradiation. Patients with diffuse sclerotic lesions or disseminated bone marrow involvement and for those who have progression of their disease 3 to 6 months after completing radiation therapy should receive systemic therapy. Corticosteroids are temporizing, but alkylators are the mainstay of treatment, either in the form of low dose conventional therapy or high dose with stem cell transplantation. The benefit of anti-VEGF antibodies is conflicting. Lenalidomide shows promise with manageable toxicity. Thalidomide and bortezomib also have activity, but their benefit needs to be weighed against their risk of exacerbating the peripheral neuropathy. Prompt recognition and institution of both supportive care measures and therapy directed against the plasma cell result in the best outcomes. Am. J. Hematol. 2012. © 2012 Wiley Periodicals, Inc. [PUBLICATION ABSTRACT] POEMS syndrome is a paraneoplastic syndrome due to an underlying plasma cell neoplasm. The major criteria for the syndrome are polyradiculoneuropathy, clonal plasma cell disorder (PCD), sclerotic bone lesions, elevated vascular endothelial growth factor, and the presence of Castleman disease. Minor features include organomegaly, endocrinopathy, characteristic skin changes, papilledema, extravascular volume overload, and thrombocytosis. Diagnoses are often delayed because the syndrome is rare and can be mistaken for other neurologic disorders, most commonly chronic inflammatory demyelinating polyradiculoneuropathy. POEMS syndrome should be distinguished from the Castleman disease variant of POEMS syndrome, which has no clonal PCD and typically little to no peripheral neuropathy but has several of the minor diagnostic criteria for POEMS syndrome. The diagnosis of POEMS syndrome is made with 3 of the major criteria, two of which must include polyradiculoneuropathy and clonal plasma cell disorder, and at least one of the minor criteria. Because the pathogenesis of the syndrome is not well understood, risk stratification is limited to clinical phenotype rather than specific molecular markers. The number of clinical criteria is not prognostic, but the extent of the plasma cell disorder is. Those patients with an iliac crest bone marrow biopsy that does not reveal a plasma cell clone are candidates for local radiation therapy; those with a more extensive or disseminated clone will be candidates for systemic therapy. For those patients with a dominant sclerotic plasmacytoma, first line therapy is irradiation. Patients with diffuse sclerotic lesions or disseminated bone marrow involvement and for those who have progression of their disease 3 to 6 months after completing radiation therapy should receive systemic therapy. Corticosteroids are temporizing, but alkylators are the mainstay of treatment, either in the form of low dose conventional therapy or high dose with stem cell transplantation. The benefit of anti-VEGF antibodies is conflicting. Lenalidomide shows promise with manageable toxicity. Thalidomide and bortezomib also have activity, but their benefit needs to be weighed against their risk of exacerbating the peripheral neuropathy. Prompt recognition and institution of both supportive care measures and therapy directed against the plasma cell result in the best outcomes. POEMS syndrome is a paraneoplastic syndrome due to an underlying plasma cell neoplasm. The major criteria for the syndrome are polyradiculoneuropathy, clonal plasma cell disorder (PCD), sclerotic bone lesions, elevated vascular endothelial growth factor, and the presence of Castleman disease. Minor features include organomegaly, endocrinopathy, characteristic skin changes, papilledema, extravascular volume overload, and thrombocytosis. Diagnoses are often delayed because the syndrome is rare and can be mistaken for other neurologic disorders, most commonly chronic inflammatory demyelinating polyradiculoneuropathy. POEMS syndrome should be distinguished from the Castleman disease variant of POEMS syndrome, which has no clonal PCD and typically little to no peripheral neuropathy but has several of the minor diagnostic criteria for POEMS syndrome.DISEASE OVERVIEWPOEMS syndrome is a paraneoplastic syndrome due to an underlying plasma cell neoplasm. The major criteria for the syndrome are polyradiculoneuropathy, clonal plasma cell disorder (PCD), sclerotic bone lesions, elevated vascular endothelial growth factor, and the presence of Castleman disease. Minor features include organomegaly, endocrinopathy, characteristic skin changes, papilledema, extravascular volume overload, and thrombocytosis. Diagnoses are often delayed because the syndrome is rare and can be mistaken for other neurologic disorders, most commonly chronic inflammatory demyelinating polyradiculoneuropathy. POEMS syndrome should be distinguished from the Castleman disease variant of POEMS syndrome, which has no clonal PCD and typically little to no peripheral neuropathy but has several of the minor diagnostic criteria for POEMS syndrome.The diagnosis of POEMS syndrome is made with 3 of the major criteria, two of which must include polyradiculoneuropathy and clonal plasma cell disorder, and at least one of the minor criteria.DIAGNOSISThe diagnosis of POEMS syndrome is made with 3 of the major criteria, two of which must include polyradiculoneuropathy and clonal plasma cell disorder, and at least one of the minor criteria.Because the pathogenesis of the syndrome is not well understood, risk stratification is limited to clinical phenotype rather than specific molecular markers. The number of clinical criteria is not prognostic, but the extent of the plasma cell disorder is. Those patients with an iliac crest bone marrow biopsy that does not reveal a plasma cell clone are candidates for local radiation therapy; those with a more extensive or disseminated clone will be candidates for systemic therapy.RISK STRATIFICATIONBecause the pathogenesis of the syndrome is not well understood, risk stratification is limited to clinical phenotype rather than specific molecular markers. The number of clinical criteria is not prognostic, but the extent of the plasma cell disorder is. Those patients with an iliac crest bone marrow biopsy that does not reveal a plasma cell clone are candidates for local radiation therapy; those with a more extensive or disseminated clone will be candidates for systemic therapy.For those patients with a dominant sclerotic plasmacytoma, first line therapy is irradiation. Patients with diffuse sclerotic lesions or disseminated bone marrow involvement and for those who have progression of their disease 3 to 6 months after completing radiation therapy should receive systemic therapy. Corticosteroids are temporizing, but alkylators are the mainstay of treatment, either in the form of low dose conventional therapy or high dose with stem cell transplantation. The benefit of anti-VEGF antibodies is conflicting. Lenalidomide shows promise with manageable toxicity. Thalidomide and bortezomib also have activity, but their benefit needs to be weighed against their risk of exacerbating the peripheral neuropathy. Prompt recognition and institution of both supportive care measures and therapy directed against the plasma cell result in the best outcomes.RISK-ADAPTED THERAPYFor those patients with a dominant sclerotic plasmacytoma, first line therapy is irradiation. Patients with diffuse sclerotic lesions or disseminated bone marrow involvement and for those who have progression of their disease 3 to 6 months after completing radiation therapy should receive systemic therapy. Corticosteroids are temporizing, but alkylators are the mainstay of treatment, either in the form of low dose conventional therapy or high dose with stem cell transplantation. The benefit of anti-VEGF antibodies is conflicting. Lenalidomide shows promise with manageable toxicity. Thalidomide and bortezomib also have activity, but their benefit needs to be weighed against their risk of exacerbating the peripheral neuropathy. Prompt recognition and institution of both supportive care measures and therapy directed against the plasma cell result in the best outcomes. |
Author | Dispenzieri, Angela |
Author_xml | – sequence: 1 givenname: Angela surname: Dispenzieri fullname: Dispenzieri, Angela email: dispenzieri.angela@mayo.edu organization: Professor of Medicine (Division of Hematology) and Laboratory Medicine |
BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26173315$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/22806697$$D View this record in MEDLINE/PubMed |
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Keywords | Endocrinopathy Immunopathology Skin disease Nervous system diseases Immunoglobulinopathy Hematology Diagnosis Risk management POEMS syndrome |
Language | English |
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Notes | NIH - No. CA125614; No. CA107476; No. CA111345 Robert A. Kyle Hematologic Malignancies Fund Conflict of interest: Research dollars from Celgene, Travel compensation from Binding Site and Celgene, and unpaid advisory board to Onyx and Millenium ark:/67375/WNG-F9JLVNM1-4 ArticleID:AJH23288 istex:1966649A89CB35A853225682DE879095DA159D6B the Predolin Foundation, JABBS Foundation ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
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Discrepancy between disease activity and levels of vascular endothelial growt 1968; 69 1982; 57 1997; 40 1991; 114 2011; 118 2011; 117 1976; 66 2006; 35 2009; 83 1977; 27 1983; 6 2002; 13 1997; 47 2002; 99 2008; 32 1998; 157 1983; 13 2009; 114 2006; 210 1996; 75 1989; 34 1987; 117 1984; 311 1989; 185 2005; 106 1991; 90 1988; 84 1978; 69 2008; 112 1992; 42 1994; 307 2001; 56 2009; 19 2010; 5 2003; 42 1994; 74 1985; 16 2003; 44 2005; 79 1992; 5 2007; 17 2010; 31 1990; 125 1990; 35 1997; 20 1999; 28 1988; 15 2005; 116 2004; 45 2007; 92 1996; 243 2001; 28 2012; 36 1999; 104 1994; 87 1980; 59 2010; 43 2010; 42 2009; 73 2009; 72 2011; 91 2011; 90 1999; 39 1984; 34 2006; 47 2005; 128 1967; 30 1999; 34 1994; 16 2007; 82 1994; 15 2008; 42 2008; 133 1990; 113 2006; 107 2003; 102 2003; 101 1994; 97 1986; 409 1989; 89 2009; 43 1991; 59 1990; 14 1990; 17 1989; 80 2010; 146 1984; 24 1995; 76 2008; 79 2011; 18 2008; 142 2008; 71 1992; 94 1996; 347 1996; 105 2004; 76 2002; 41 1986; 142 1993; 71 2006; 66 2003; 8 1987; 316 2002; 100 1999; 14 1998; 126 1998; 128 1999; 93 2007; 21 1985; 56 1992; 83 1988; 413 2012; 83 2010; 76 2004; 104 2004; 103 2002; 30 2012 2006; 13 2000; 23 1991; 30 1985; 9 2008; 19 2004; 89 2006; 7 2007 1996; 58 1998; 21 1998; 20 2010; 85 2010; 84 1998; 25 1983; 33 1991; 6 1972; 27 1994; 42 2008; 181 1994; 9 2004; 10 2010; 89 1989; 96 2002; 26 2006; 85 1993; 18 1980; 208 2000; 39 2006; 84 2004; 19 1991; 21 2007; 110 1988; 66 1992; 69 1988; 64 2012; 88 2007; 46 2012; 87 2001; 115 2008; 80 1992; 62 1987; 27 e_1_2_11_70_2 Carcaterra A (e_1_2_11_97_2) 1990; 125 Hineman VL (e_1_2_11_129_2) 1982; 57 e_1_2_11_55_2 e_1_2_11_78_2 Bhatia M (e_1_2_11_110_2) 1994; 42 e_1_2_11_118_2 e_1_2_11_51_2 e_1_2_11_32_2 e_1_2_11_74_2 e_1_2_11_148_2 e_1_2_11_4_2 e_1_2_11_25_2 e_1_2_11_121_2 e_1_2_11_144_2 e_1_2_11_167_2 e_1_2_11_48_2 e_1_2_11_29_2 e_1_2_11_140_2 e_1_2_11_163_2 e_1_2_11_81_2 Zhang B (e_1_2_11_7_2) 2010; 31 Myers BM (e_1_2_11_102_2) 1991; 90 e_1_2_11_20_2 e_1_2_11_43_2 e_1_2_11_89_2 Schliamser LM (e_1_2_11_137_2) 2003; 102 e_1_2_11_24_2 e_1_2_11_62_2 e_1_2_11_85_2 e_1_2_11_8_2 Badros A (e_1_2_11_27_2) 2006; 107 e_1_2_11_17_2 Forster A (e_1_2_11_116_2) 1998; 128 e_1_2_11_113_2 e_1_2_11_159_2 e_1_2_11_136_2 e_1_2_11_36_2 e_1_2_11_155_2 e_1_2_11_59_2 Tanaka O (e_1_2_11_68_2) 1984; 24 e_1_2_11_151_2 e_1_2_11_174_2 Jaccard A (e_1_2_11_150_2) 2009; 114 Menke DM (e_1_2_11_132_2) 1992; 5 e_1_2_11_170_2 Takatsuki K (e_1_2_11_3_2) 1983; 13 e_1_2_11_92_2 e_1_2_11_31_2 e_1_2_11_54_2 Anonymous (e_1_2_11_125_2) 1984; 311 e_1_2_11_50_2 e_1_2_11_73_2 e_1_2_11_96_2 e_1_2_11_12_2 e_1_2_11_119_2 e_1_2_11_28_2 e_1_2_11_5_2 e_1_2_11_149_2 e_1_2_11_126_2 e_1_2_11_168_2 e_1_2_11_47_2 e_1_2_11_145_2 e_1_2_11_122_2 e_1_2_11_164_2 e_1_2_11_141_2 Coto V (e_1_2_11_103_2) 1991; 6 e_1_2_11_160_2 e_1_2_11_65_2 e_1_2_11_46_2 e_1_2_11_88_2 e_1_2_11_9_2 e_1_2_11_23_2 e_1_2_11_61_2 e_1_2_11_107_2 Hineman VL (e_1_2_11_120_2) 1982; 57 e_1_2_11_42_2 e_1_2_11_84_2 e_1_2_11_114_2 e_1_2_11_16_2 De Roma I (e_1_2_11_49_2) 2004; 19 e_1_2_11_58_2 e_1_2_11_133_2 e_1_2_11_156_2 e_1_2_11_39_2 e_1_2_11_152_2 e_1_2_11_171_2 e_1_2_11_91_2 e_1_2_11_30_2 e_1_2_11_76_2 e_1_2_11_57_2 e_1_2_11_99_2 e_1_2_11_72_2 e_1_2_11_11_2 e_1_2_11_139_2 e_1_2_11_53_2 e_1_2_11_95_2 e_1_2_11_6_2 Dispenzieri A (e_1_2_11_41_2) 2008; 142 e_1_2_11_104_2 e_1_2_11_127_2 e_1_2_11_146_2 e_1_2_11_169_2 e_1_2_11_2_2 e_1_2_11_69_2 e_1_2_11_100_2 e_1_2_11_123_2 e_1_2_11_142_2 e_1_2_11_165_2 Soubrier M (e_1_2_11_33_2) 2004; 89 Nakaseko C (e_1_2_11_34_2) 2007; 110 e_1_2_11_161_2 Del Rio R (e_1_2_11_109_2) 1994; 74 Navis GJ (e_1_2_11_77_2) 1994; 9 e_1_2_11_60_2 e_1_2_11_45_2 e_1_2_11_87_2 Soubrier M (e_1_2_11_13_2) 1998; 25 e_1_2_11_22_2 e_1_2_11_64_2 e_1_2_11_83_2 e_1_2_11_108_2 e_1_2_11_138_2 e_1_2_11_15_2 e_1_2_11_157_2 e_1_2_11_134_2 e_1_2_11_19_2 e_1_2_11_38_2 e_1_2_11_153_2 e_1_2_11_111_2 Lapresle J (e_1_2_11_93_2) 1986; 142 e_1_2_11_130_2 e_1_2_11_172_2 e_1_2_11_71_2 e_1_2_11_90_2 e_1_2_11_56_2 e_1_2_11_79_2 e_1_2_11_98_2 Takazoe K (e_1_2_11_80_2) 1997; 47 e_1_2_11_117_2 e_1_2_11_52_2 e_1_2_11_75_2 e_1_2_11_94_2 e_1_2_11_10_2 e_1_2_11_124_2 e_1_2_11_26_2 Aravamudan B (e_1_2_11_35_2) 2008; 112 e_1_2_11_105_2 e_1_2_11_147_2 Arimura K (e_1_2_11_66_2) 1999; 39 e_1_2_11_101_2 e_1_2_11_143_2 Takai K (e_1_2_11_166_2) 2004; 45 e_1_2_11_82_2 Chang YJ (e_1_2_11_115_2) 1996; 58 e_1_2_11_44_2 Nakazawa K (e_1_2_11_106_2) 1992; 42 e_1_2_11_67_2 e_1_2_11_40_2 e_1_2_11_86_2 e_1_2_11_128_2 e_1_2_11_21_2 e_1_2_11_63_2 e_1_2_11_135_2 e_1_2_11_158_2 e_1_2_11_14_2 e_1_2_11_37_2 e_1_2_11_131_2 e_1_2_11_112_2 e_1_2_11_18_2 e_1_2_11_154_2 e_1_2_11_173_2 Arima F (e_1_2_11_162_2) 1992; 83 |
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Snippet | Disease overview: POEMS syndrome is a paraneoplastic syndrome due to an underlying plasma cell neoplasm. The major criteria for the syndrome are... Disease overview: POEMS syndrome is a paraneoplastic syndrome due to an underlying plasma cell neoplasm. The major criteria for the syndrome are... POEMS syndrome is a paraneoplastic syndrome due to an underlying plasma cell neoplasm. The major criteria for the syndrome are polyradiculoneuropathy, clonal... |
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SubjectTerms | Biological and medical sciences Education, Medical, Continuing Hematologic and hematopoietic diseases Hematology Humans Medical sciences POEMS Syndrome - diagnosis POEMS Syndrome - therapy Risk Factors |
Title | POEMS syndrome: Update on diagnosis, risk-stratification, and management |
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