Subacute cutaneous lupus erythematosus in a patient with inherited deficiency of the third component of complement

To the Editor.— A genetic deficiency of one of the complement proteins, though distinctly uncommon in the general population, is a well-known predisposing factor for clinical disease. The most prominent manifestation of classic pathway component deficiencies is autoimmune disease, such as lupus erythematosus (LE). Alternative pathway component deficiencies lead to recurrent and fulminant pyogenic infections, while patients lacking terminal complement components have an increased risk of acquiring neisserial infections and, less often, have autoimmune disease. The central role of C3 in both complement-activation pathways and the multiple biologic functions of its fragments make it such that no homozygous C3-deficient patient has been described as being free of disease. Recurrent infections, autoimmune disease, vasculitic syndromes, and glomerulonephritis have been reported in these patients. Some of these symptoms may be explained by periodically present immune complexes that are difficult to clear in the absence of a normally functioning complement system. Report of