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To investigate the pathogenesis of the systemic manifestations of Fabry’s disease, circulating immune complexes (IC) were measured in six patients. Five of these patients were heterozygous for the enzymatic defect, and one patient had Fabry’s disease that was subsequently confirmed by skin biopsy. The latter patient had IC levels of 5,600 micrograms/ml, which was significantly higher than any of the five heterozygous patients (1,400 micrograms/ml). All patients with Fabry’s disease had low serum C4. These observations suggest that autoantibodies may be a cause of immune complex formation in Fabry’s disease and that complement activation may play a role in the pathogenesis of systemic disease
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