0 vs.17.5 IU/L), alkaline phosphatase (165.0 vs.146.8 IU/L), total-cholesterol (200.0 vs.186.2 mg/dL), and LDL-cholesterol (155.3 vs.80.5 mg/dL) were significantly different (P<0.05). However, baseline glucose level and diabetes were not statistically significant for tamoxifen-induced steatosis (P>0.05). BMI was the only independent risk factor of tamoxifen-induced steatosis (Hazard ratio: 1.227, 95% confidence interval: 1.039-1.448; P=0.016).

Furthermore, of excluded 36 patients with NASH at baseline, the levels of aminotransferase of 19 patients were normalized after tamoxifen therapy (52.8%). The normalization of aminotransferases took 108.6±66.8 days after administration of tamoxifen. DMXAA Conclusions: Our study showed that tamoxifeninduced hepatotoxicity might be associated with BMI, and tamoxifen could cause hepatoprotective effect as well as liver injury. Disclosures: The following people have nothing to disclose: Myung Jin Oh, Heon Ju Lee, Si Hyung Lee, Sung Bum

Kim, Yeoun Su Jung, Jung Woo Lee BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a common cause of hepatic steatosis in patients with inflammatory bowel disease (IBD). Both metabolic syndrome (MetS) and intestinal inflammation are implicated in NAFLD pathogenesis. In our see more hospital population of patients with dual diagnosis of NAFLD and IBD, the prevalence of MetS parallels national trends. We examined whether MetS and IBD severity increase the risk of NAFLD severity in patients with NAFLD and IBD. METHODS: A retrospective medical record review was performed for all patients entered into the electronic medical record of a tertiary care university hospital from January 1997December 2011. Patients with a dual diagnosis Tacrolimus (FK506) of

IBD and NAFLD were included. We excluded patients with viral, alcoholic, autoimmune or genetic etiology of hepatic steatosis. Patients were grouped according to “MetS” (>3 of the following: hypertension, hyperlipidemia, BMI>30, and diabetes/insulin resistance) or “non-MetS. ” BARD score or liver pathology was used to grade NAFLD severity. Physician global assessment and Montreal classification were used to determine IBD severity/pattern. Patient demographics, medications, and serology were analyzed. Statistical analysis was performed using Fisher Exact test or Mann-Whitney U test. RESULTS: 84 pts were included in our analysis (25 UC, 59 Crohn’s). Pts were predominantly female (57%) and Caucasian (85%). The majority of UC pts had ulcerative proctitis; most Crohn’s pts had ileocolonic disease. Pts were diagnosed with NAFLD a mean of 12 years after the time of IBD diagnosis.25% of pts had MetS. Pts with IBD and MetS were diagnosed with NAFLD at older age than IBD and non-MetS pts (54.8 vs 45.8, p=0.015). Mean BMI at NAFLD diagnosis was 34.4 and 28.8 kg/m2 in MetS and non-MetS pts (p<0.001).30% of pts were referred to hepatology independent of MetS diagnosis. Compared with nonMetS, MetS pts had higher ALT (57 vs 38, p=0.007); AST (56 vs 36, p=0.