Home > Journals > Giornale Italiano di Dermatologia e Venereologia > Past Issues > Giornale Italiano di Dermatologia e Venereologia 1998 February;133(1) > Giornale Italiano di Dermatologia e Venereologia 1998 February;133(1):23-49

CURRENT ISSUE
 

ARTICLE TOOLS

Reprints

GIORNALE ITALIANO DI DERMATOLOGIA E VENEREOLOGIA

A Journal on Dermatology and Sexually Transmitted Diseases


Official Journal of the Italian Society of Dermatology and Sexually Transmitted Diseases
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,014


eTOC

 

REVIEWS  


Giornale Italiano di Dermatologia e Venereologia 1998 February;133(1):23-49

language: Italian

Cutaneous necrotizing vasculitis

Comacchi C. 1, Ghersetich I. 1, Lotti T. 2

1 Università degli Studi - Firenze, Clinica Dermatologica;
2 Università degli Studi - Siena, Clinica Dermatologica


PDF  


Cutaneous necrotizing vasculitis (CNV) is a clinical disorder comprising a large spectrum of cutaneous lesions usually presenting as palpable purpura. The skin is often the only organ apparently involve, but clinically relevant systemic involvment may occur. In many cases the cause of CNV remains unknown (idiopathic CNV), in others CNV has been reported in association with chronic diseases, malignant neoplasms and precipitating causes (drugs, chemicals, infections, food allergens). Histologically CNV is characterized by angiocentric segmental inflammation, endothelial cells swelling and fibrinoid necrosis of blood vessel walls. Although blood vessels of any size may be affected in systemic vasculitis, CNV occurs in the small venules (postcapillary venules), being characterized by two main histological patterns: a leukocytoclastic form, with a presumed immune complex mediated pathogenesis and a lymphomonocytic form in which a cell-mediated pathogenesis is proposed. More recent data also seem to suggest the participation of a secondary cell mediated immune response in the late phase of the leukocytoclastic form. The cutaneous fibrinolytic activity is increased in the early phase and reduced in the late phase of the leukocytoclastic form. γ/δ T lymphocytes and heat shock proteins are strongly represented only in lesional skin of cases of leukocytoclastic vasculitis with documented infective etiology, suggesting that the investigation of γ/δ T cells and heat shock proteins in CNV might represent a clue to the infective etiology of CNV. Therapeutic approach requires elimination of the cause (drugs, chemicals, infections, food allergens) when possible. In other cases local and systemic antinflammatory or immunosuppressive therapies are recommended.

top of page

Publication History

Cite this article as

Corresponding author e-mail