Lower levels of dehydroepiandrosterone sulfate are associated with more advanced liver fibrosis in chronic hepatitis C

Abstract

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 dis ease. Recently, an inverse association between serum levels of dehydroepiandroster one 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 fibro sis 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 vari ables associated to fibrosis. We included 287 patients (43.9% male). According to fi brosis 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 signifi cant (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 associ ated with more advanced stages of liver fibrosis in hepatitis C patients.