BACKGROUND: TGFbeta(1) has a confirmed role in liver fibrosis and its antiproliferative, proapoptotic, and immunosuppressive activities can play important roles in the pathogenesis of viral hepatitis. MATERIAL/ METHODS: The concentrations of transforming growth factor-beta(1) (TGFbeta(1)) was measured with enzyme immunoassay in the plasma of 70 patients with acute viral hepatitis types A, B, and C to evaluate an association with the course and severity of the disease. RESULTS: The highest concentrations of TGFbeta(1) were observed in the first week of acute viral hepatitis types A and B (52.8+/-7.4 and 50.0+/-7.7, respectively). They were significantly higher than normal values or levels in patients with hepatitis type C. Significant correlation was observed between TGFbeta(1) concentrations and alanine aminotransferase in all groups, whereas with aspartate aminotransferase only hepatitis A and B. A four-week follow-up showed a gradual decrease in TGFbeta(1) levels in hepatitis A and B patients. In patients with acute C hepatitis, the relatively low initial TGFbeta(1) concentrations increased in the second and third weeks of follow-up. Among HBV-infected patients the highest TGFbeta(1) concentrations (75+/-17 ng/ml) were observed in the severe form of the disease. CONCLUSIONS: These results support an important role of TGF-beta(1) in the pathogenesis of acute viral hepatitis that seems to be connected with the degree of hepatocyte damage, but not with its mechanism or etiology.
BACKGROUND:TGFbeta(1) has a confirmed role in liver fibrosis and its antiproliferative, proapoptotic, and immunosuppressive activities can play important roles in the pathogenesis of viral hepatitis. MATERIAL/ METHODS: The concentrations of transforming growth factor-beta(1) (TGFbeta(1)) was measured with enzyme immunoassay in the plasma of 70 patients with acute viral hepatitis types A, B, and C to evaluate an association with the course and severity of the disease. RESULTS: The highest concentrations of TGFbeta(1) were observed in the first week of acute viral hepatitis types A and B (52.8+/-7.4 and 50.0+/-7.7, respectively). They were significantly higher than normal values or levels in patients with hepatitis type C. Significant correlation was observed between TGFbeta(1) concentrations and alanine aminotransferase in all groups, whereas with aspartate aminotransferase only hepatitis A and B. A four-week follow-up showed a gradual decrease in TGFbeta(1) levels in hepatitis A and B patients. In patients with acute C hepatitis, the relatively low initial TGFbeta(1) concentrations increased in the second and third weeks of follow-up. Among HBV-infectedpatients the highest TGFbeta(1) concentrations (75+/-17 ng/ml) were observed in the severe form of the disease. CONCLUSIONS: These results support an important role of TGF-beta(1) in the pathogenesis of acute viral hepatitis that seems to be connected with the degree of hepatocyte damage, but not with its mechanism or etiology.