Plasma proteins of hemostasis in the hepatointestinal form of schistosomiasis mansoni

The hepatosplenic form of schistosomiasis mansoni is associated with impairment of blood coagulation, a result of reduced synthesis of clotting factors and inhibitors, enhanced fibrinolytic activity, or ''consumption'' of plasma clotting proteins. The pathogenesis of the latter mechanism has not been elucidated. Schistosoma mansoni (Sm) has a long lifespan as an intravascular fluke, probably a consequence of its ability to evade host immunologic defense mechanisms. In order to determine 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 the hepatointestinal form of the disease, with viable Sm ova in stools, and 10 were healthy volunteers (control group). Blood specimens were drawn by a two-syringe technique for both the performance of liver tests and determination of hemostasis proteins (prothrombin, antithrombin III, protein C, protein S, high-molecular-weight kininogen, and plasminogen). The latter proteins were assayed immunologically in plasma using 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 synthesis in the mild form of the disease and that Sm probably escapes host defense mechanisms in vivo, and does not contribute to the consumption coagulopathy described in the hepatosplenic form of the disease.