Galen called the spleen the "organ of mystery," and in the 19th century both Banti and Gretsel believed that the spleen could exert harmful effects by the exaggeration of its normal function (138). Chauffard coined the term hypersplenism in 1907 (138), but it was made popular by Dameshek 40 yr later (139). The term defined a condition associating splenomegaly with pancytopenia. A debate ensued between Dameshek and Doan. Dameshek held that the spleen exerted an influence on the bone marrow, inhibiting the production of blood cells, whereas Doan's position was that the pancytopenia was caused by the sequestration and destruction of cells in the spleen. After a demonstration in his own laboratory that transfused platelets failed to emerge in the splenic vein, Dameshek conceded defeat, "Well, it looks as though Charley Doan is right" (140).
The anemia of hypersplenism has two causes. There is an expansion of the total plasma volume as well as a pooling of red cells. In very large spleens, up to 40% of red cells may be sequestered there (141,142). The neutropenia of hypersplenism is usually only moderate and asymptomatic. It is caused by an increase in the marginated pool, some of which may be located within the spleen (143,144). On the other hand, the thrombocytopenia of hypersplenism is caused by splenic pooling (144,145). In massively enlarged spleens, up to 90% of platelets can be sequestered there. Nevertheless, the splenic transit time for platelets remains normal at about 10 min, and the splenic platelets remain part of the exchangeable pool (145).
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