Background/aims: Liver dysfunction is said to occur only late in the course of schistosomiasis. As albumin levels tend to be normal, the observed prolonged prothrombin time is thought to arise from subclinical consumption coagulopathy. The aim of this study was to further evaluate this matter by studying the role of Schistosoma mansoni and liver function in the genesis of the compromised haemostasis tests in chronic "pure" schistosomiasis patients.
Methods: Twenty-five adults with chronic "pure" schistosomiasis were selected: 12 with the hepatointestinal form (group 2) and 13 with the compensated hepatosplenic form (group 3), as well as 10 matched control individuals (group 1). Alcoholism, viral hepatitis B and C, malnutrition (BMI<20 kg/m2), use of anticoagulant or anti-aggregant drugs and chronic diseases apart from schistosomiasis were carefully excluded. All patients were submitted to abdominal ultrasound and upper digestive endoscopy. Blood samples were used for routine hepatic tests and for transthyretin, prothrombin, antithrombin and protein C antigen determinations by immunodiffusion. Laboratory markers of coagulation activation (prothrombin fragment1+2(F1+2), serine esterases-antithrombin complexes (ATM) and plasminogen activator, tissue type activity (t-PA) were also assayed by ELISA and photometric determination, respectively.
Results: Decreased plasma levels of transthyretin (p<0.001), protein C (p:0.006), prothrombin (p:0.022) and antithrombin (p:0.008) contrasted with normal albuminaemia (p:0.094), F1+2 (p:0.061) and ATM (p:0.714) plasma levels in group 3 patients; t-PA activity (p:0.001) on the other hand, were increased in this group.
Conclusions: These results suggest impairment of liver clearance and protein synthesis capacity rather than consumption coagulopathy. They also indicate that changes in liver function are not a late event in the course of schistosomiasis.