Thirty-eight patients with essential mixed cryoglobulinemia (EMC: 16 type II and 22 type III) were evaluated. Almost all patients had clinical manifestations which could be related to a cutaneous and/or visceral vasculitic process. No significant clinical or laboratory differences were found between type II and type III EMC patients. Kidney biopsy performed in 9 patients showed membranoproliferative glomerulonephritis in 6 cases, diffuse proliferative glomerulonephritis in 2 cases and mesangioproliferative glomerulonephritis in one case. Skin biopsy performed in 11 patients showed typical leukocytoclastic vasculitis as the most common finding. A picture consistent with overlapping vasculitis was found in 2 cases (one type II and one type III) and thrombus-like deposits were observed in 3 cases (2 type II and one type III). These thrombotic lesions, not associated with vessel wall necrosis and inflammatory infiltrate, were indistinguishable from those observed in one case of type I cryoglobulinemia. Our data emphasize the complexity of blood vessel involvement in cryoglobulinemia and point out the possible existence of multiple pathogenetic mechanisms.

The cryoglobulinemic vasculitis

Facchetti, F
1986-01-01

Abstract

Thirty-eight patients with essential mixed cryoglobulinemia (EMC: 16 type II and 22 type III) were evaluated. Almost all patients had clinical manifestations which could be related to a cutaneous and/or visceral vasculitic process. No significant clinical or laboratory differences were found between type II and type III EMC patients. Kidney biopsy performed in 9 patients showed membranoproliferative glomerulonephritis in 6 cases, diffuse proliferative glomerulonephritis in 2 cases and mesangioproliferative glomerulonephritis in one case. Skin biopsy performed in 11 patients showed typical leukocytoclastic vasculitis as the most common finding. A picture consistent with overlapping vasculitis was found in 2 cases (one type II and one type III) and thrombus-like deposits were observed in 3 cases (2 type II and one type III). These thrombotic lesions, not associated with vessel wall necrosis and inflammatory infiltrate, were indistinguishable from those observed in one case of type I cryoglobulinemia. Our data emphasize the complexity of blood vessel involvement in cryoglobulinemia and point out the possible existence of multiple pathogenetic mechanisms.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11379/501130
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