Behçet's syndrome and autoimmunity.

The aetiology of Behget's syndrome has long been disputed. Behget (1937) first suggested a viral hypothesis on the basis of finding inclusion bodies in scrapings from the ulcers. Sezer (1953, 1956) claimed to have isolated a virus from these patients and to have reproduced the disease, and showed a strongly positive complement-fixation reaction in other patients with Behget's syndrome. Evans et al. (1957) also grew a virus, and they showed the presence of neutralizing antibodies in the serum of patients with this disease, but not in control sera. Recently Mortada and Imam (1964) also grew a virus from one patient, but numerous other workers have failed to do so. The literature has been reviewed by Dudgeon (1961) and Dowling (1961). Oshima et al. (1963) and Shimizu et al. (1965) have raised the possibility that an autoimmune mechanism may play a part in the pathogenesis of Behget's syndrome. They showed convincingly in a large series of patients that there is a rise of serum globulin and sialic acid. They have also demonstrated the presence of autoantibodies against oral mucosa by the tanned red cell haemagglutination technique. In an immunofluorescent investigation they claim to have shown significant fluorescence of the cytoplasm of peripheral blood leucocytes and of cells from the oral ulcers. While evidence of an autoimmune reaction does not disprove the viral hypothesis it could be important not only from the aetiological point of view but also in understanding the pattern of the disease and of its response to treatment. The aim of this investigation was to carry out the haemagglutination, complement-fixation, andOuchterlony'sprecipitation test against foetal oral mucosa in 21 patients with Behget's syndrome, as described by Lehner (1964, 1965) for a series of patients with recurrent oral ulceration. Furthermore, an attempt was made to differentiate the oral ulcers in Behget's syndrome and to compare them with those of recurrent focal oral ulceration.