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Plasma exchange has been used to investigate the function fo anti-acetylcholine receptor (anti-AChR) antibody in seven patients with acquired myasthenia gravis (MG) who had elevated antibody titers and in one patient with congenital MG who had normal titers. There was an inverse association between clinical indices of muscle strength and anti-AChR titers, with a minimum time lag of 2 days for the clinical response. The inverse association of the clinical state with anti-AChR antibody titers was closer than that with total immunoglobulin G or other immunoglobulins, and is consistent with the view that the anti-AChR antibody is the principal factor interfering with neuromuscular transmission in acquired MG.

Summary and conclusionsOut of 20 relapses that occurred in patients with Wegener's granulomatosis, nine were provoked by bacterial or viral infection. Seven of these occurred during maintenance treatment in response to infection with common pathogens, and treatment of the infection alone was insufficient to produce remission. Circulating immune complexes were seen only in relapses due to infection and rarely in infections that occurred without relapse. A possible mechanism for infection-provoked relapses is that infection-derived complexes reactivate disease; alternatively, the acute-phase or cellular response to infection may enhance quiescent disease.Infection may exacerbate Wegener's granulomatosis and other autoallergic diseases, but whether it does so by a common mechanism is not known and further study is required. Introduction A study of patients being treated for antiglomerular basementmembrane disease identified intercurrent infection as an important cause of relapse and led to the recognition of infectioninduced enhancement of antibody-mediated injury.' Although its cause is still not clear, several mechanisms have been considered, including activation of inflammatory cells in response to infection, increased concentrations of acute-phase proteins such as fibrinogen and C-reactive protein, and the superimposition of infection-derived immune complexes. We report here on part of a prospective analysis of the effect of infection in autoallergic diseases, which investigated the importance of infection in relapses of Wegener's granulomatosis, a condition of uncertain aetiology but probably having an allergic pathogenesis of immune complex type. Enhanced tissue injury after infection has also been noted in other immunologically mediated diseases,2-8 and the possibility arises that exacerbation of allergic tissue damage by infection might be a more general phenomenon. Patients and methodsWe studied 18 patients with Wegener's granulomatosis. Three died early in the course of their disease, and the remainder were followed up for periods ranging from three months to three years; eight are still alive. Treatment was generally started with a regimen including cyclophosphamide, azathioprine, and prednisolone and in some cases plasma exchange (referred to later as the "induction

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