Hypoprothrombinemia in the compensated form of hepatosplenic schistosomiasis: further studies

Abstract

SUMMARYCoagulation abnormality is frequently observed in schistosomiasis patients but its pathophysiology has not been established. We measured, by immunodiffusion. the prothrombin-antigen concentration in 56 individuals; of these 19 with demonstrated compensated form of hepatosplenic schistosomiasis, 17 with cirrhosis and 20 were control subjects. Transaminases, albumin, transthyretin, prothrombin time, antithrombin III, factor VII, and fibrinogen were also evaluated.All parameters were altered in the cirrhotic group but only albumin, prothrombin and antithrombin III levels were altered in the schistosomiasis group. Ninety percent of the patients with cirrhosis and sixty percent of the patients with schistosomiasis had abnormal plasma levels of albumin, transthyretin, prothrombin-antigen, and/or antithrombin III; an impaired hepatic synthesis was responsible for these results.Conversely forty percent of the schistosomiasis patients with normal plasma concentrations of both albumin and transthyretin had decreased mean plasma levels of both prothrombin and antithrombin III. These results suggest that either proth rombin and antithrombin III are more sensitive markers of impaired hepatic synthesis in schistosomiasis than are levels of albumin and transthyretin combined, or a low grade chronic consumption of clotting proteins also occurs. Considering the latter hypothesis it is possible that the thrombin formed would be inhibited by antithrombin III with the complexed thrombin-antithrombin III being cleared by the liver. Consequently the plasma levels of both prothrombin and antithrombin would be decreased, but the level of fibrinogen would be preserved.

Murine schistosomiasis mansoni: process of blood coagulation at pre-patent, acute and chronic phases, and consequence of chemotherapeutic cure on the reversion of changes

“…Some previous reports show normal levels of albuminemia in advanced stages of S. mansoni infection, indicating an extended and preserved hepatic function, in contrast with the low levels of fibrinogen and the decrease in prothrombin activity [9]. Nevertheless, Manoukian and Borges [12] had already reported a decrease in the albumin levels detected in 60% of patients with the compensated hepato-splenic form of schistosomiasis, which implies an opposing position with more recent data [9]. Reduced levels of transthyrethin, prothrombin antigen and antithrombin, besides albumin, were also described [12].…”

“…Nevertheless, Manoukian and Borges [12] had already reported a decrease in the albumin levels detected in 60% of patients with the compensated hepato-splenic form of schistosomiasis, which implies an opposing position with more recent data [9]. Reduced levels of transthyrethin, prothrombin antigen and antithrombin, besides albumin, were also described [12]. Such conflicting results do not allow one to conclude about a possible reduction in coagulation factor synthesis in the hepatosplenic form of schistosomiasis.…”

Plasma Proteins of Hemostasis in the Hepatointestinal Form of Schistosomiasis Mansoni

“…The hemostatic derangements described in patients with the hepatosplenic form of schistosomiasis are multifactorial in origin, and are attributable to hepatic synthesis impairment, either qualitative or quantitative, enhanced fibrinolysis, or consumption coagulopathy, probably restricted to the portal territory (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18). The pathogenesis of the consumption coagulopathy has not yet been elucidated.…”

“…Prothrombin and antithrombin III were found to be diminished in patients with the hepatosplenic form, either as a consequence of hepatic synthesis impairment or because of consumption coagulopathy ( 11,12,16). The normal plasma concentrations now reported for hepatointestinal patients may reflect that Sm is capable of evading host defense mechanisms in vivo and therefore does not activate the clotting system.…”

Endothelial Markers in Schistosomiasis Patients With or Without Portal Hypertension

“…For the form without portal hypertension, lesion markers and hepatic function are within normal limits. Patients with portal hypertension are characterized by the extent of preservation of hepatic function in relation to the degree of portal hypertension, although some laboratory alterations have been found that characterize organ dysfunction from an early stage [2][3][4][5][6][7][8][9].…”