A total of 32 patients with Plasmodium falciparum malaria were studied. Of these, 23 had benign infections, and 9 had typical cerebral malaria. Cryoglobulins, circulating immune complexes detected by a C1q-binding assay, and hypocomplementemia were found in eight of nine patients with cerebral malaria. Raised levels of complement component 3 breakdown products (C3d) were found in the seven patients tested. Peak levels of circulating immune complexes and C3d were associated with thrombocytopenia. In contrast, in patients with benign Plasmodium falciparum malaria, cryoglobulins and circulating immune complexes were found only in 3 of 23 patients. Similarly, hypocomplementemia was detected only in 5 of 23 patients. These observations suggest that the intensity of the immune response and of the associated complement activation may be important factors in the pathogenesis of cerebral malaria.

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Using the Raji cell radioimmune assay, we found low levels of circulating immune complexes (IC) in a small percentage of patients with schistosomiasis and filariasis. C3d levels, measured by immunoprecipitation, were elevated in a large number of these patients, whereas complement levels were within normal limits. Proteinuria was not found in any of the 55 patients studied. Circulating IC or elevated C3d levels were not found in any of the 19 patients with hydatidosis. The increased C3d levels, apparently not related to circulating IC, may be due to direct complement activation by parasite antigens or to sequestered IC. The latter hypothesis appears more attractive because the highest levels of C3d were found in schistosomiasis whereas schistosome antigens were unable to activate complement in vitro.