HLA antigen frequencies in systemic vasculitis: increase in HLA-DR2 in wegener's granulomatosis

✍ Scribed by Dr. Keith B. Elkon; David C. Sutherland; Andrew J. Rees; Graham R. V. Hughes; J. Richard Batchelor

• Publisher: John Wiley and Sons
• Year: 1983
• Tongue: English
• Weight: 327 KB
• Volume: 26
• Category: Article
• ISSN: 0004-3591
• DOI: 10.1002/art.1780260118

✦ Synopsis

The central feature of a number of connective tissue or "autoimmune" disorders is widespread vascular inflammation. Although many of the resulting clinical and serologic abnormalities nonspecifically reflect tissue injury, sufficient variation exists in the pathology, type of organ involvement, and disease associations that distinctive forms of systemic vasculitis can be recognized ( I ) . The immediate cause or trigger of systemic vasculitis is not usually known, but both virus infection (2) and a number of drugs (3) have been implicated in a proportion of patients with polyarteritis nodosa (4). Not only may diverse agents produce the same disease, but a single agent (the hepatitis B virus) may produce several different forms of vasculitis ( 5 ) . These observations suggest that host factors play a cardinal role in determining susceptibility or expression of systemic vasculitis.

In order to determinc whether serologically defined antigens reflect these host factors, we performed HLA typing on 46 patients with one of three similar but distinctive forms of systemic vasculitis: polyarteritis nodosa. Wegener's griinulomatosis, and Churg-Strauss vasculitis.