Negative antineutrophil cytoplasmic antibodies in Behçet's disease.

Sir: Antineutrophil cytoplasmic antibodies have been detected in patients with idiopathic necrotising and crescentic glomerulonephritis, active Wegener's granulomatosis, and microscopic polyarteritis nodosa.' Behcet's disease, an inflammatory disorder of unknown cause, is characterised by oral and genital ulcerations associated with systemic manifestations due to large and small vessel vasculitis. Ocular, cutaneous, and central nervous system involvement are often the translation of small vessel vasculitis.2 Crescentic glomerulonephritis has also been reported.3 Polymorphonuclear leucocytes have been incriminated in the physiopathology of Behcet's disease. Lesions are characterised histologically by acute inflammation and an intense infiltration of polymorphonuclear leucocytes with small vessel necrosis, especially at mucosal and cutaneous sites.4 The increased chemotaxis and random motility of polymorphonuclear leucocytes in Behcet's disease have been confirmed in several studies, and it has been suggested that a cytoplasmic polymorphonuclear leucocyte factor, serum or lymphocytic factor is responsible for this increased activity.5 To appreciate better the role of polymorphonuclear leucocytes in this disease we looked for the presence of antineutrophil cytoplasmic antibodies in patients with active and inactive Behcet's disease. Twenty eight patients (27 male, one female) with a mean (SD) age of 40 (3) years (range 29-56) were studied. Disease durati .n was 6-8 (1-9) years (range 2-25). All patients had buccal aphthosis associated with at least two of the following criteria: genital aphthosis, cutaneous lesions, uveitis, and positive pathergy testing. The incidence of clinical manifestations with reported vasculitis is as follows: uveitis (12 cases), central nervous system disease (six cases), thrombophlebitis (six cases), erythema nodosum-like lesions (five cases), and arterial aneurysm (one case). The disease was active in 15 patients and inactive in 13. Indirect immunofluorescence on human neutrophils was used to detect antineutrophil cytoplasmic antibodies, according to the method of Van der Woude.6 None of the 28 serum samples from the patients with Behcet's disease was positive for these antibodies (titres >1/10). The fluorescence was negative in 27 patients and positive in one at a titre of 1/10. This study strongly suggests that antineutrophil cytoplasmic antibodies cannot be incriminated as contributing to the abnormalities of polymorphonuclear leucocytes in Behqet's disease. M HAMZA Semice de Rhumatologie HOpital la Rabta Tunis, and Faculti Medicine de Tunis Tunisia