Aim: Non-alcoholic steatohepatitis is one of the most common causes of chronic liver disease and the incidence in the population varies from %1024. TGF- β 1 is the most important TGF- β isoform responsible for fibrosis and its effect on hepatic fibrosis was demonstrated in-vitro and in chronic viral hepatitis. Besides TGF- β is an immunsuppresive cytokine and it is known that low TGF- β activity can trigger autoimmune diseases and inflammation.
However, studies about serum TGF- β -1 levels in patients with NASH failed to show a direct relationship between NASH and TGF- β -1. The aim of this study is to demonstrate serum TGF- β -1 levels in NASH and to determine the possible correlations between serum TGF-β-1, and other laboratory and antropometric parameters.
Materials and methods: 31 patients with NASH (diagnosed with liver biopsy) and 31 healthy subjects were included. The mean age of the patient group (17 men, 14 women) and healthy subjects (17 men, 14 women) was 51.7 and 50.6 respectively. The metabolic, antropometric and laboratuary parameters were recorded.
Results: The mean body mass index of the patient group was significantly higher than the healthy subjects (P=0.009). The mean serum TGF- β -1 level of patients was significantly lower than the control group (8.17 ng/ml and 11.07 ng/ml respectively, P=0.018). In the patient group serum TGF- β 1 levels were found to be correlated with fasting insulin (r=0.531 P<0.05). In the multiple regression analysis fasting insulin was found to be the most important parameter effecting serum TGF- β -1 levels in NASH.
Conclusion: In the literature there is a small number of human studies present determining the serum TGF- β -1 levels in NASH and the results are contradictory. In our study in spite of their high BMI the patient group had low serum TGF- β -1 levels. It is known that TGF- β has immunsuppresive properties and low TGF-beta activity can trigger autoimmune diseases. It was demonstrated that TGF- β knock-out mice developed multi-organ inflamatory changes. Thats why the low serum TGF- β -1 levels in NASH may be responsible as a trigger for the inflammatuary process.