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γ-Glutamyltransferase decreases in patients with the chronic form of schistosomiasis mansoni treated with ursodeoxycholic acid
  1. P de J Ribeiro,
  2. J L Narciso,
  3. C F de Toledo,
  4. D R Borges
  1. Gastroenterology Division, Department of Medicine, Universidade Federal de São Paulo, São Paulo, 04023–900 Brazil;

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    Schistosomiasis mansoni is a chronic parasitic liver disease characterised by a relative preservation of hepatic function, but there are early alterations in laboratory test results.1–4 The rise in serum γ-glutamyltransferase (γGT) activity in patients with schistosomiasis does not correlate with either parasite load or ultrasonographic alterations.5,6 We now report the effect of ursodeoxycholic acid in these patients.

    Eleven adults (nine men) with raised serum γGT activity and the “pure” form of schistosomiasis participated in the prospective study (eutrophic patients; body mass index > 20 and < 30 kg/m2; abstemious or with alcohol ingestion less than 160 g/week; non-users of hepatotoxic and/or cholestatic drugs; and hepatitis B surface antigen, anti-hepatitis B core antigen, and anti-hepatitis C negative). All patients were previously treated for the parasitosis. Echographic examinations were interpreted as described previously.7 Upper digestive endoscopy revealed the presence of oesophageal and/or oesophagogastric varices and/or hypertensive gastropathy. The patients were treated with ursodeoxycholic acid at a dose of 10 mg/kg/day, divided into two daily portions for a period of six weeks. Before treatment, during treatment, and 30–45 days after drug discontinuation, the patients underwent clinical and laboratory evaluation.

    At the beginning of the treatment γGT was 3.1 (SEM, 0.4) times the upper normal limit, whereas alkaline phosphatase was normal (mean, 1.1 times the upper normal limit; SEM, 0.2). There was a progressive and significant decrease in γGT to near normal values at the end of treatment and an increase again after drug discontinuation, whereas alkaline phosphatase remained unaltered. Aminotransferases also decreased during treatment and increased again after drug discontinuation (table 1). Prothrombin index (mean international normalised ratio at the beginning, 1.2; SEM, 0.1) and platelet count (mean, 96 × 109/litre at the beginning; SEM, 23) remained unaltered.

    Table 1

     Laboratory parameters in patients with schistosomiasis mansoni at the beginning and end of treatment with ursodeoxycholic acid and 30–45 days after discontinuation of the drug

    Ursodeoxycholic acid is widely used for the treatment of primary biliary cirrhosis and other chronic cholestatic liver diseases.8,9 We now report that the increased serum γGT activity seen in patients with the chronic form of schistosomiasis is ursodeoxycholic sensitive. The mechanism of this increase in γGT seems to be different from that which occurs in alcoholism, and is compatible with the existence of changes in the biliary tree.6,10

    Further studies are required to understand the role of ursodeoxycholic acid in the molecular and cellular mechanisms of bile secretion and its ability to reduce γGT activity in schistosomiasis mansoni (for example whether it acts on the evolutionary stage of the disease), and to determine whether γGT could be used as a prognostic marker for this disease.


    This research was supported by FAPESP Fundação de Amparo à Pesquisa do Estado de São Paulo, Proc. 02/0562.