The spectrum of vasculitis in human immunodeficiency virus–infected patients. a clinicopathologic evaluation
Article first published online: 9 DEC 2005
Copyright © 1993 American College of Rheumatology
Arthritis & Rheumatism
Volume 36, Issue 8, pages 1164–1174, September 1993
How to Cite
Gherardi, R., Belec, L., Mhiri, C., Gray, F., Lescs, M.-C., Sobel, A., Guillevin, L. and Wechsler, J. (1993), The spectrum of vasculitis in human immunodeficiency virus–infected patients. a clinicopathologic evaluation. Arthritis & Rheumatism, 36: 1164–1174. doi: 10.1002/art.1780360818
- Issue published online: 9 DEC 2005
- Article first published online: 9 DEC 2005
- Manuscript Accepted: 17 FEB 1993
- Manuscript Received: 6 OCT 1992
Objective. To delineate the different types of inflammatory vascular diseases (IVD) occurring in patients with human immunodeficiency virus (HIV) infection.
Methods. Muscle, nerve, or skin biopsy specimens from 148 symptomatic HIV-infected individuals were reviewed, and subgroups of vasculitis were identified using the American College of Rheumatology (ACR) 1990 clinicopathologic criteria for the classification of vasculitis.
Results. IVD was documented in 34 patients (23%) and included necrotizing arteritis (3 patients), non-necrotizing arteritis (1 patient), neutrophilic IVD (7 patients), mononuclear IVD (17 patients), and other small vessel inflammatory changes (6 patients). According to the ACR criteria, 11 patients could be classified as having a distinct category of vasculitis, including polyarteritis nodosa (4 patients), Henoch-Schönlein purpura (1 patient), and drug-induced hypersensitivity vasculitis (6 patients), and 23 were classified in the group ‘other vasculitis, type unspecified.’ One patient had hepatitis B virus surface antigenemia, 2 had cryoglobulinemia, and 2 were coinfected by human T lymphotropic virus type I. Cytomegalovirus inclusions and antigens were found in endothelial cells in 1 patient. HIV antigens and genome were detected in perivascular cells of 2 of the 3 patients with necrotizing arteritis; in 1, HIV-like particles were seen by electron microscopy. Immune deposits were found in small vessel walls in 5 skin biopsy samples showing small vessel vasculitis and in the muscle of the 3 patients with necrotizing arteritis.
Conclusion. A wide range of inflammatory vascular diseases may occur in HIV-infected individuals. Vascular inflammation appears multifactorial and may result from HIV-induced immunologic abnormalities and exposure to a variety of xenoantigens, such as HIV itself, other infectious agents, and drugs.