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A 73-year-old man with hydatid disease developed autoimmune hemolytic anemia due to IgM cold agglutinin with anti-I specificity. Hemolysis decreased after initiating mebendazole therapy. The cysts notably diminished in size and the red cell autoantibodies disappeared at the end of this treatment. On the basis of these observations, 44 patients with hydatid disease were investigated. One patient showed IgM cold autoantibody with no signs of anemia. In addition, cleavage fragments of C3 were detected on the erythrocyte membranes of 6 patients, following chronic activation of the complement system. We suggest that parasitic antigens may evoke antibodies cross-reacting with the red blood cells of the host.

A case of warm autoimmune hemolytic anemia due to IgA antibody is described. The patient had clinical and hematologic signs of hyperhemolysis, but all specific tests were negative. The direct antiglobulin test was positive only when it was performed with anti-IgA monospecific antiserum. The autoantibody eluted from the patient's red cells showed anti-e specificity. The sensitivity of broad-spectrum antiglobulin serum and the possible hemolytic mechanisms of IgA-coated red cells are discussed.