Dynamic Alteration in Splenic Function during Acute falciparum Malaria

Abstract

Plasmodium-infected erythrocytes lose their normal deformability and become susceptible to splenic filtration. In animal models, this is one mechanism of antimalarial defense. To assess the effect of acute falciparum malaria on splenic filtration, we measured the clearance of heated 51 Cr-labeled autologous erythrocytes in 25 patients with acute falciparum malaria and in 10 uninfected controls. Two groups of patients could be distinguished. Sixteen patients had splenomegaly, markedly accelerated clearance of the labeled erythrocytes (clearance half-time, 8.4±4.4 minutes [mean ±SD] vs. 62.5±36.5 minutes in controls; P < 0.001), and a lower mean hematocrit than did the patients without splenomegaly (P < 0.001). In the nine patients without splenomegaly, clearance was normal. After institution of antimalarial chemotherapy, however, the clearance in this group accelerated to supernormal rates similar to those in the patients with splenomegaly, but without the development of detectable splenomegaly. Clearance was not significantly altered by treatment in the group with splenomegaly. Six weeks later, normal clearance rates were reestablished in most patients in both groups. We conclude that splenic clearance of labeled erythrocytes is enhanced in patients with malaria if splenomegaly is present and is enhanced only after treatment if splenomegaly is absent. Whether this enhanced splenic function applies to parasite-infected erythrocytes in patients with malaria and has any clinical benefit will require further studies. (N Engl J Med 1987; 317:675–9.) ERYTHROCYTES infected with plasmodia lose deformability and become susceptible to filtration by the spleen. 1,2 A role for splenic filtration in antimalarial host defense is suggested by the deleterious effects of splenectomy, 3 the apparent requirement of an intact splenic architecture in this defense, 4 and the close relation between splenic filtration and parasite attrition recently observed in a rodent model of malaria (Plasmodium berghei infection in rats). 5 These studies demonstrated that early in P. berghei infection, the capacity of the spleen to remove infected erythrocytes and rigid (heat-damaged) uninfected cells was diminished to subnormal levels, permitting parasitemia to increase. In contrast,. © 1987, Massachusetts Medical Society. All rights reserved.