Methods: Vitamin D 25(OH)D was quantified in serum by liquid chromatographytandem mass spectrometry in 193 adults (>18 yrs) with well characterized, biopsy-proven NAFLD. Vitamin D Deficiency (VDD) was defined as <20ng/mL. Demographics, socioeconomic, and comorbidities (Type 2 DM and metabolic syndrome) were
compared between the VDD and non-VDD groups. Multivariable logistic regression analysis was used to investigate the association of VDD and the presence of definite nonalcoholic steatohepatitis (NASH) and individual features of NAFLD including steatosis, lobular inflammation, portal inflammation, ballooning degeneration and fibrosis, adjusting for age, sex, race, BMI, ALT, and PD98059 nmr diabetes status. Results: VDD was present in 55% of subjects and did not vary significantly among different demographic Natural Product Library concentration or socioeconomic groups or with the presence of comorbidities including diabetes type 2 and metabolic syndrome.
VDD subjects were more likely to have definitive NASH compared to non-VDD subjects (65% vs 35%, respectively, p=0.02). VDD was independently associated with definitive NASH (OR= 3.64, 95%CI=1.80-7.33, p<0.001), increased ballooning (OR= 2.49, CI=1.36-4.57, p=0.003) and a higher lobular inflammation grade (OR= 1.90, CI=1.02-3.51, p=0.042) after controlling for age, sex, diabetes, race, BMI and ALT. VDD subjects were more likely to have fibro-sis, but this failed to reach statistical significance (OR= 1.97, CI=0.94-4.11, p=0.072). Conclusions: VDD is highly prevalent among U.S. patients with NAFLD and is independently associated with a definitive diagnosis of NASH
and increased histological ballooning and inflammation scores. These data support further study of the mechanism for VDD in the pathogenesis of NASH and in dietary and/or lifestyle modifications to increase vitamin D levels in patients with NAFLD. Disclosures: Kris V. Kowdley – Advisory Committees or Review Panels: AbbVie, Gilead, Merck, Novartis, Trio Health, Boeringer Ingelheim, Ikaria, Janssen; Grant/Research Support: AbbVie, Beckman, Boeringer Ingelheim, BMS, Gilead Sciences, Ikaria, Janssen, Merck, selleck Mochida, Vertex The following people have nothing to disclose: James E. Nelson, Laura Wilson, Christian Roth, Matthew M. Yeh Background/aim: Non-alcoholic fatty liver disease (NAFLD) is an increasing health burden in western countries. The pathogenetic mechanisms remain widely unclear. Besides insulin resistance and dietary factors mutations of PNPLA3 (patatin-like phospholipase domain-containing 3 gene) were identified. Since preliminary data suggest that copper deficiency may contribute to the development of NAFLD, the aim of this study was to evaluate the association of hepatic copper content and PNPLA3 with histological features in patients with NAFLD. Methods: One-hundred and eight NAFLD patients (m/f: 75/33, mean age: 49.