Peripheral neuropathy associated with Castleman's disease

Donaghy, Michael; Hall, Peter A.; Gawler, J; Gregson, N. A.; Leibowitz, Sidney; Jitpimolmard, Suthipun; King, R. H. M.; Thomas, P K

doi:10.1016/0022-510x(89)90027-0

Cited by 66 publications

(41 citation statements)

References 34 publications

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“…Only anecdotal cases treated with a variety of single agents or combination regimens were found in the literature 19,20,[51][52][53][54][55][56][57][58] (Table 6). The use of high dose corticosteroids alone is associated with incomplete responses in most patients.…”

Section: Discussionmentioning

confidence: 99%

The management of unicentric and multicentric Castleman's disease

Bowne

Lewis

Filippa

et al. 1999

Cancer

394

335

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Section: Discussionmentioning

confidence: 99%

The management of unicentric and multicentric Castleman's disease

Bowne

Lewis

Filippa

et al. 1999

Cancer

394

335

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“…Multicentric Castleman disease with and without peripheral neuropathy tend to be different; it has even been proposed that the presence or absence of peripheral neuropathy should be part of the multicentric Castleman disease classification system [134]. Those patients with peripheral neuropathy are more likely to have edema and impaired peripheral circulation [131,[135][136][137][138][139][140], and they are also more likely to have a monoclonal lambda protein in their serum and/or urine [141].…”

Section: Relationship To Castleman Disease and Castleman Disease Varimentioning

confidence: 99%

“…At its worst, however, it is a mixture of demyelination and axonal degeneration with normal myelin spacing on electron microscopy [139], and abnormal capillary proliferation, similar to what is seen in the affected lymph nodes, has been described [139]. In contrast to the osteosclerotic myeloma variant of POEMS in which VEGF is the most consistently elevated cytokine, in Castleman disease IL-6 is the dominant aberrantly overexpressed cytokine.…”

Section: Relationship To Castleman Disease and Castleman Disease Varimentioning

confidence: 99%

POEMS syndrome: Update on diagnosis, risk‐stratification, and management

2015

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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 three 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 3–6 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. 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. The benefit of anti‐VEGF antibodies is conflicting. Prompt recognition and institution of both supportive care measures and therapy directed against the plasma cell result in the best outcomes. Am. J. Hematol. 90:951–962, 2015. © 2015 Wiley Periodicals, Inc.

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“…At its worst, however, it is a mixture of demyelination and axonal degeneration with normal myelin spacing on electron microscopy, [118,123] and abnormal capillary proliferation, similar to what is seen in the affected lymph nodes, has been described [126]. In contrast to the osteosclerotic myeloma variant of POEMS in which VEGF is the most consistently elevated cytokine, in Castleman disease IL-6 is the dominant aberrantly overexpressed cytokine.…”

Section: Relationship To Castleman Disease and Castleman Disease Varimentioning

confidence: 99%

“…Multicentric Castleman disease with and without peripheral neuropathy tend to be different; it has even been proposed that the presence or absence of peripheral neuropathy should be part of the multicentric Castleman disease classification system [116]. Those patients with peripheral neuropathy are more likely to have edema and impaired peripheral circulation, [117][118][119][120][121][122][123][124] and they are also more likely to have a monoclonal lambda protein in their serum and/or urine [125].…”

Section: Relationship To Castleman Disease and Castleman Disease Varimentioning

confidence: 99%

POEMS syndrome: 2011 update on diagnosis, risk‐stratification, and management

Dispenzieri

2011

American J Hematol

120

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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. Diagnosis: The diagnosis of POEMS syndrome is made with three 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. 86:592–601, 2011. © 2011 Wiley‐Liss, Inc.

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Peripheral neuropathy associated with Castleman's disease

Cited by 66 publications

References 34 publications

The management of unicentric and multicentric Castleman's disease

The management of unicentric and multicentric Castleman's disease

POEMS syndrome: Update on diagnosis, risk‐stratification, and management

POEMS syndrome: 2011 update on diagnosis, risk‐stratification, and management

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