Growth factors and proinflammatory cytokines in the renal involvement of POEMS syndrome

Soubrier, Martin; Sauron, C.; Souweine, Bertrand; Larroche, Claire; Wechsler, B.; Guillevin, Loı̈c; Piette, Jean Charles; Rousset, H.; Deteix, P

doi:10.1016/s0272-6386(99)70386-0

Cited by 83 publications

(47 citation statements)

References 27 publications

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“…To date, VEGF is the cytokine that correlates best with disease activity, [10][11][12][13][14][15][16][17][18] although it may not be the driving force of the disease based on the mixed results seen with anti-VEGF therapy [19][20][21][22][23][24][25]. VEGF is known to target endothelial cells, induce a rapid and reversible increase in vascular permeability, and be important in angiogenesis.…”

Section: Annual Clinical Updates In Hematological Malignancies: a Conmentioning

confidence: 99%

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

Dispenzieri

2011

American J Hematol

119

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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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Section: Annual Clinical Updates In Hematological Malignancies: a Conmentioning

confidence: 99%

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

Dispenzieri

2011

American J Hematol

119

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show abstract

“…To date, VEGF is the cytokine that correlates best with disease activity [11][12][13][14][15][16][17][18][19][20], although it may not be the driving force of the disease based on the mixed results seen with anti-VEGF therapy [21][22][23][24][25][26][27][28]. VEGF is known to target endothelial cells, induce a rapid and reversible increase in vascular permeability, and be important in angiogenesis.…”

mentioning

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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“…Other studies have suggested that the pathogenic roles of systemic IL-6 and VEGF in POEMS syndrome should be respected particularly in regards to intrarenal pathological changes such as hyperpermiability, known as systemic capillary leak syndrome (Teelucksingh et al 1990;Takazoe et al 1997;Nakamoto et al 1999;Soubrier et al 1999;Dispenzieri et al 2003). Therefore, we hypothesize that the A. Immunohistochemical analysis by using anti human CD34 antibody demonstrated that abundant numbers of CD34-positive endocapillaries were found in the expanded mesangial lesion showing both mature and immature (arrow) capillary formations.…”

Section: Discussionmentioning

confidence: 82%

A Patient with POEMS Syndrome: The Pathology of Glomerular Microangiopathy

Nakamura

Nishimura

Terano

et al. 2013

Tohoku J. Exp. Med.

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POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin changes) is potentially fatal multisystem disorder but its renal complication has often been overlooked because renal involvement is not necessarily included in the diagnostic criteria of POEMS. This report documents the patient with POEMS syndrome with long-term renal histopathological changes evaluated by renal biopsy. A 32-year-old Japanese woman presented with symptoms consistent with POEMS syndrome associated with proteinuria and IgA-λ type monoclonal gammopathy. Initial renal biopsy for confirmation of diagnosis revealed the proliferation of glomerular capillary loops located in the expanded mesangial matrices associated with glomerular enlargement. Electron microscopy examination of the renal biopsy revealed the presence of double contoured glomerular basement membrane containing peculiar fibrillary structure. The patient was therefore initially diagnosed as membranoproliferative glomerulonephritis (MPGN)-like lesion without any significant immunoglobulins and complements deposition. The patient was subsequently admitted to hospital on five occasions due to renal dysfunction and anasarca for the next four years of her clinical course. The severity of anasarca was correlated mainly with serum titer of vascular endothelial growth factor (VEGF) during this period. Acute renal failure occurred at the last admission and the second biopsy was performed. An increased mesangial matrix and frequent global sclerosis of the glomeruli with arteriolosclerosis was noted in this second biopsy compared to the first one. These findings of renal biopsies suggest that the glomerular microangiopathy of POEMS syndrome may occur in the context of systemic capillary leak syndrome superimposed on chronic endothelial injury.

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Growth factors and proinflammatory cytokines in the renal involvement of POEMS syndrome

Cited by 83 publications

References 27 publications

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

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

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

A Patient with POEMS Syndrome: The Pathology of Glomerular Microangiopathy

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