Multicentric Castleman's disease with an increased serum level of macrophage colony-stimulating factor

Lee, Muneyasu; Hirokawa, Makoto; Matuoka, Satoru; Hasegawa, Hitoshi; Nanjo, Hiroshi; Mizutani, Takashi; Imatani, Hideo; Miura, Akira B.

doi:10.1002/(sici)1096-8652(199704)54:4<321::aid-ajh11>3.0.co;2-e

Cited by 9 publications

(3 citation statements)

References 15 publications

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“…[54][55][56] VEGF, which promotes cell survival, angiogenesis, and vascular permeability, is often elevated in parallel with iMCD symptoms. 56 Elevated systemic VEGF levels typically decrease in iMCD cases following anti-IL-6 treatment, suggesting that VEGF release is downstream of IL-6.…”

Section: Key Imcd Cytokinesmentioning

confidence: 99%

HHV-8-negative, idiopathic multicentric Castleman disease: novel insights into biology, pathogenesis, and therapy

Fajgenbaum

Rhee

Nabel

2014

Blood

272

265

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Multicentric Castleman's disease (MCD) describes a heterogeneous group of disorders involving proliferation of morphologically benign lymphocytes due to excessive proinflammatory hypercytokinemia, most notably of interleukin-6. Patients demonstrate intense episodes of systemic inflammatory symptoms, polyclonal lymphocyte and plasma cell proliferation, autoimmune manifestations, and organ system impairment. Human herpes virus-8 (HHV-8) drives the hypercytokinemia in all HIV-positive patients and some HIV-negative patients. There is also a group of HIV-negative and HHV-8-negative patients with unknown etiology and pathophysiology, which we propose referring to as idiopathic MCD (iMCD). Here, we synthesize what is known about iMCD pathogenesis, present a new subclassification system, and propose a model of iMCD pathogenesis. MCD should be subdivided into HHV-8-associated MCD and HHV-8-negative MCD or iMCD. The lymphocyte proliferation, histopathology, and systemic features in iMCD are secondary to hypercytokinemia, which can occur with several other diseases. We propose that 1 or more of the following 3 candidate processes may drive iMCD hypercytokinemia: systemic inflammatory disease mechanisms via autoantibodies or inflammatory gene mutations, paraneoplastic syndrome mechanisms via ectopic cytokine secretion, and/or a non-HHV-8 virus. Urgent priorities include elucidating the process driving iMCD hypercytokinemia, identifying the hypercytokine-secreting cell, developing consensus criteria for diagnosis, and building a patient registry to track cases.

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Section: Key Imcd Cytokinesmentioning

confidence: 99%

HHV-8-negative, idiopathic multicentric Castleman disease: novel insights into biology, pathogenesis, and therapy

Fajgenbaum

Rhee

Nabel

2014

Blood

272

265

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“…Most patients with localized forms have no systemic symptoms (15,16,18,19). In the contrast, patients with multicentric forms are older and have systemic symptoms such as fatigue, fever, weight loss, night sweats, nausea, and physical abnormalities such as splenomegaly, hepatomegaly, edema, polyneuropathy and skin rash (15,16,(19)(20)(21)(22)(23), and laboratory abnormalities such as anemia, hypergammaglobulinemia, elevated IL-6, hypoalbuminemia, elevated erythrocyte sedimentation rate, proteinuria, elevated creatinine, elevated liver function tests and thrombocytopenia (16,(19)(20)(21)(22)(23). In this case, general fatigue before ARF, hepatomegaly and edema (after correction of dehydration) were observed.…”

Section: Discussionmentioning

confidence: 99%

Acute Interstitial Nephritis with Polyclonal B Cell Infiltration and Development of Mantle Cell Lymphoma.

Jinde

Yanagi

et al. 2002

Intern. Med.

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A 69-year-old man with proteinuria, hematuria and abnormal renal and hepatic function developed acute renal failure. His clinical and laboratory examinations showed splenomegaly, edema, anemia and polyclonal hypergammaglobulinemia with high IgG levels. Renal biopsy showed interstitial nephritis with predominant B cell and plasma cell infiltration without monoclonality. After corticosteroid treatment, the patient showed remission in clinical symptoms and laboratory findings. However, one year later, he developed mantle cell lymphoma (MCL) with typical lymphocyte markers of cyclin Dl and CD5. Whenevaluated retrospectively, this patient appeared to have multicentric Castleman's disease initially and developed MCLlater.

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“…1996), vascular endothelial growth factor (VEGF) (Foss et al. 1997), and macrophage colony‐stimulating factor (Lee et al. 1997).…”

Section: Discussionmentioning

confidence: 99%

Hyaline‐vascular type Castleman's disease involving both orbits

Park¹,

Choi²,

Song³

2002

Acta Ophthalmologica Scandinavica

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Multicentric Castleman's disease with an increased serum level of macrophage colony-stimulating factor

Cited by 9 publications

References 15 publications

HHV-8-negative, idiopathic multicentric Castleman disease: novel insights into biology, pathogenesis, and therapy

HHV-8-negative, idiopathic multicentric Castleman disease: novel insights into biology, pathogenesis, and therapy

Acute Interstitial Nephritis with Polyclonal B Cell Infiltration and Development of Mantle Cell Lymphoma.

Hyaline‐vascular type Castleman's disease involving both orbits

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