The spleen plays an important role in protection against malaria, and asplenic individuals may be at serious risk from P. falciparum infection. Indeed, experienced surgeons in tropical regions
take a conservative approach to management of splenic trauma in the knowledge of the increased mortality from malaria in individuals who have undergone splenectomy. The spleen enlarges with acute malaria, presumably as it functions to remove parasitised erythrocytes (recognised either because of their loss of deformability or propensity to form clumps of sequestered cells) from the peripheral circulation, and splenic macrophages remove dead parasites.
Some individuals have an excessively abnormal immune response to malaria and develop massive splenomegaly and hypergammaglobulinaemia [hyper-reactive malarial splenomegaly (HMS), formerly known as tropical splenomegaly syndrome]. These individuals from genetically predisposed populations have apparently normal clinical immunity to malaria but suffer the effects of hypersplenism (anaemia, leukopenia and thrombocytopenia). Characteristic changes are seen in liver histology. Splenectomy is contra-indicated and the individuals usually have a gratifying response to long-term administration of antimalarial prophylaxis. The pathophysiol-ogy of HMS involves an overproduction of polyclonal IgM in response to repeated infections with P. falciparum, P. malariae or P. vivax. This appears to be due to a depletion of suppressor T cells, leading to a lack of inhibition of B cell activity and failure of maturation of the immune response to IgG production (Piessens et al., 1985; Bates et al., 1991). HMS and splenic lymphoma with villous lymphocytes are clinically indistinguishable and appear to be aetiologically related (Bates and Bedu-Addo, 1997).
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