PLASMA-PROTEINS OF HEMOSTASIS IN THE HEPATOINTESTINAL FORM OF SCHISTOSOMIASIS-MANSONI

The hepatosplenic form of schistosomiasis mansoni is associated with i mpairment of blood coagulation, a result of reduced synthesis of clott ing factors and inhibitors, enhanced fibrinolytic activity, or ''consu mption'' of plasma clotting proteins. The pathogenesis of the latter m echanism has not been elucidated. Schistosoma mansoni (Sm) has a long lifespan as an intravascular fluke, probably a consequence of its abil ity to evade host immunologic defense mechanisms. In order to determin e if the parasite is able to disturb hemostasis in vivo, we studied 21 non-alcoholics with normal body mass index, and HBsAg, anti-HBc, and anti-HCV negative adult males, who were not using drugs. Eleven had th e hepatointestinal form of the disease, with viable Sm ova in stools, and 10 were healthy volunteers (control group). Blood specimens were d rawn by a two-syringe technique for both the performance of liver test s and determination of hemostasis proteins (prothrombin, antithrombin III, protein C, protein S, high-molecular-weight kininogen, and plasmi nogen). The latter proteins were assayed immunologically in plasma usi ng specific antibodies. Statistical analysis of the results failed to demonstrate any significant difference between the two groups. We may therefore conclude that there is no derangement of hepatic protein syn thesis in the mild form of the disease and that Sm probably escapes ho st defense mechanisms in vivo, and does not contribute to the consumpt ion coagulopathy described in the hepatosplenic form of the disease.