Chronic infection with the hepatitis C virus induces liver fibrosis, but it is unknown why some patients progress to advanced fibrosis while others remain with mild disease. Recently, an inverse association between serum levels of dehydroepiandrosterone sulphate (DHEA-S) and liver fibrosis in patients with nonalcoholic fatty liver disease was described, and it was postulated that dehydroepiandrosterone (DHEA) has antifibrotic effects. Our aim was to compare serum DHEA-S levels with liver fibrosis in hepatitis C patients. We collected serum samples from hepatitis C patients at the same day they underwent a liver biopsy. S-DHEA was compared to different stages of fibrosis. Binary logistic regression models were applied to evaluate independent variables associated to fibrosis. We included 287 patients (43.9% male). According to fibrosis stages 0, 1, 2, 3 and 4, median serum DHEA-S levels were 103 (26-462), 73 (5-391), 46 (4-425), 35 (6-292) and 28 (2-115) μg/dL, respectively (P < .001). Median serum DHEA-S levels were 74 (5-462) vs 36 (2-425) μg/dL for mild (F0-1) vs significant (F2-4) fibrosis, respectively (P < .001). Median serum DHEA-S levels were 64 (4-462) vs 31 (2-292) μg/dL for non advanced (F0-2) vs advanced fibrosis (F3-4), respectively (P < .001). The same association was found when the subgroup of HCV patients with and without steatosis or steatohepatitis was analysed. The association between lower DHEA-S levels and advanced fibrosis was independent of age, gender, diabetes mellitus, obesity and steatosis. Lower circulating DHEA-S levels are associated with more advanced stages of liver fibrosis in hepatitis C patients.
Keywords: S-DHEA; dehydroepiandrosterone sulphate; fibrogenesis; hepatitis C; liver fibrosis.
© 2017 John Wiley & Sons Ltd.