作者: Michael Charlton , Paul Angulo , Naga Chalasani , Ralph Merriman , Kimberly Viker
DOI: 10.1002/HEP.22063
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摘要: The biological basis of variability in histological progression nonalcoholic fatty liver disease (NAFLD) is unknown. Dehydroepiandrosterone (DHEA) the most abundant steroid hormone and has been shown to influence sensitivity oxidative stress, insulin sensitivity, expression peroxisome proliferator-activated receptor alpha procollagen messenger RNA. Our aim was determine whether more histologically advanced NAFLD associated with low circulating levels DHEA. Serum samples were obtained prospectively at time biopsy 439 patients (78 an initial 361 validation cohorts) controls cholestatic (n = 44). characterized as mild [simple steatosis or steatohepatitis (NASH) fibrosis stage 0-2] (NASH 3-4). sulfated DHEA (DHEA-S) measured by enzyme-linked immunosorbent assay. Patients had lower plasma DHEA-S than both (0.25 ± 0.07 versus 1.1 0.09 μg/mL, P < 0.001) cohorts (0.47 0.06 0.99 0.04 0.001). A “dose effect” decreasing incremental observed a mean 1.03 0.05, 0.96 0.07, 0.83 0.11, 0.66 0.35 μg/mL for stages 0, 1, 2, 3, 4, respectively. All group levels, majority hypoadrenal range. association between severity persisted after adjusting age. relationship disease/fibrosis not seen diseases. Conclusion: More NAFLD, indicated presence NASH stage, strongly DHEA-S. These data provide novel evidence relative deficiency NASH. (HEPATOLOGY 2008;47:484–492.)