POSTERS 1.017; 95% confidence interval, CI 1.012–1.021, p < 0.001). Moreover, FLI had the best discriminative ability to identify patients with fatty liver than other clinical markers with a highest AUROC value of 0.827 (95%CI, 0.822–0.831). By comparing the Youden’s index (sensitivity + specificity − 1), the cut-off values of FLI in predicting fatty liver were set as 30 for males and 15 for females, respectively. Conclusions: FLI could accurately identify fatty liver in a large- scale population in Taiwan. However, the cut-off value was lower in females than that in males. P794 NON ALCOHOLIC FATTY LIVER DISEASE (NAFLD) MAY INDUCE PORTAL HYPERTENSION WITHOUT ASSOCIATED LIVER FIBROSIS I. Kapnikov 1,2 , R. Farah 3 , N. Gibstein 4 , A. Djibre 1 , M. Grosovski 5 , N. Assy 2,6 . 1 Liver Unit, Ziv Medical Center, 2 Faculty of Medicine at Galilee, Bar Ilan University, 3 Department of Medicine B, 4 Radiology, Ziv Medical Center, Safed, 5 Biotechnology, Ort Braude, Carmiel, 6 Ziv Medical Center, Safed, Israel E-mail: assy.n@ziv.health.gov.il Background and Aims: It is unknown whether NAFLD per se may induce portal hypertension. Our aim was to study portal hypertension in NAFLD patients and to identify clinical predictors. Methods: 61 Patients with NAFLD underwent Transient Elastography (Fibroscan, nl < 6 kPa) with Controlled Attenuation Parameter (CAP; nl (170–230) dB/m and Ultrasound Doppler. Portal hypertension was defined as PV >13 mm, and/or spleen size >13 cm, and/or portal flow velocity <15 cm/s. Degree of steatosis was defined as a CAP >300 dB/m for severe or <300 for mild steatosis. Results: Mean age was 48±13 years; 67% were male. Liver stiffness was normal in 41 patients (68%), moderate in 10 (16%) and severe in 10 (16%). Significant portal hypertension was seen in 46% of patients with NAFLD in which 30% were with severe steatosis and 16% with mild steatosis. Portal hypertension was present in 18/41 (30%) of patients with NAFLD but without fibrosis. While Portal flow velocity (32±6 cm/s vs. 29±10, P = 0.03), and liver stiffness 5.8±2.2 kPa vs. 8.6±9, P = 0.007) were significantly different between NAFLD with mild or severe steatosis; PV diameter (10.7±3 mm vs. 11.1±2, P = 0.29), spleen size (11.2±2 cm vs. 12±2, p = 0.08), and platelets count (239,000±107 vs 221,000±57, P = 0.3) were not different. CAP values correlate with liver stiffness (r = 0.35, p < 0.01). By multivariate analysis, Albumin, Triglyceride, PV diameter and liver size were independent predictors of fat accumulation. Conclusions: Nonalcoholic fatty liver disease may induce portal hypertension in the absence of significant fibrosis. The mechanism has yet to be determined. P795 POLYMORPHISMS AT THE ADIPOR1, ADIPOR2 ARE ASSOCIATED WITH LIVER FUNCTION TEST IN OBESITY PATIENTS WITH NONALCOHOLIC FATTY LIVER DISEASE O. Kolesnikova 1 , V. Nemtsova 2 . 1 Hepatology, GI ‘Institute of Therapy named after Acad. L.T. Malaya’ NAMS, Kharkiv, 2 Hepatology, National Medical Unversity, Kharkov, Ukraine E-mail: igorchupin@yandex.ru Background and Aims: Adiponectin protects against liver dysfunction in insulin-resistant states such as obesity, type 2 diabetes and nonalcoholic fatty liver disease (NAFLD) but the role of adiponectin receptors in this disorder is largely unknown. We studied whether common single-nucleotide polymorphisms (SNPs) in ADIPOR1 and ADIPOR2 are associated with liver function tests (LFTs) in NAFLD’s patients. Methods: Serum alanine (ALT) and aspartate (AST) aminotrans- ferases, homeostasis model assessment of insulin resistance (HOMA-IR), −8503 G/A (rs6666089) and +5843 A/G (rs1342387) SNPs in ADIPOR1, −64241 T/C (rs767870) and +33447 C/T (rs1044471) SNPs in ADIPOR2 were assessed in 340 Ukraine with NAFLD. Genotyping was performed using Allele Specific Primer Extension method. Results: In nonobesity subjects, the alleles rs1342387 C/T SNPs in ADIPOR1 and rs1044471 C/T SNPs in ADIPOR2 were associated with increased circulating adiponectin (P< 0.05 to P< 0.005), but not with LFT. Conversely, in obesity patients with NAFLD, the same alleles were associated with increased serum ALT and AST (P< 0.05 to P< 0.0001), but not with circulating adiponectin. No significant associations with these parameters were evident for the common rs6666089 G/A SNPs in ADIPOR1 and rs767870 T/C SNPs in ADIPOR2. In a replication study, the (rs1342387 C/T SNPs in ADIPOR1 and rs1044471 C/T SNPs in ADIPOR2 were associated with ALT and AST (P< 0.05 to P< 0.0001) in patients with NAFLD. Conclusions: Common SNPs in ADIPOR1, ADIPOR2 are associated with LFT in obesity patients with NAFLD, which suggests a possible role of this receptor in liver dysfunction. P796 NADPH OXIDASE (NOX 4) AND P22PHOX GENE POLYMORPHISMS ARE ASSOCIATED WITH HUMAN NON-ALCOHOLIC FATTY LIVER DISEASE (NAFLD) F. Rabelo 1 , J.T. Stefano 1 , R.V. Lima 1 , M. Seixas 1 , T. Patente 2 , D. Vanni 1 , A.M. Cavaleiro 2 , D.C. Mazo 1 , F.J. Carrilho 1 , M.L. Corrˆ ea-Giannella 2 , C. Oliveira 1 . 1 Department of Gastroenterology, Clinical Division, (LIM-07), 2 Laboratory for Cellular and Molecular Endocrinology (LIM-25), University of S˜ao Paulo School of Medicine, S˜ao Paulo, Brazil E-mail: cpm@usp.br Background and Aims: Oxidative stress has been implicated in progression to severe forms of non-alcoholic fatty liver disease (NAFLD). NADPH oxidase appears to be an important source of production of reactive oxygen species. We investigated by the first time two single nucleotide polymorphisms (SNPs) in the regulatory region of genes encoding the NADPH oxidase 4 (Nox4) and p22phox (CYBA) in NAFLD. Methods: 188 biopsy-proven NAFLD patients (47 = steatosis; 141= NASH) were evaluated. Genomic DNA was extracted from peripheral blood cells and on Nox4 and CYBA polymorphisms were determined by direct sequencing of PCR. All the patients were negative for markers of viral hepatitis, Metabolic diseases, autoimmune diseases and had daily intake of alcohol <100 g/week. Results: The presence of A allele in the CYBA SNP was independently associated with NASH (OR = 5.6, 95% CI (1.03–24.82), p = 0.0455), while the presence of A allele in the Nox4 SNP conferred protection for the development of NASH (OR = 12.38, 95% CI (0.15– 0.94) p = 0.0374). On the other hand, the CC genotype in Nox4 SNP was associated with NASH. The presence of diabetes, higher concentration of ALT and gGT also, conferred risk for developing NASH. Conclusions: 1. The presence of the A allele in the CYBA SNP was associated with risk of developing NASH; 2. The CC genotype frequency in the Nox4 SNP was associated with the presence of NASH, while the presence of the allele A conferred protection to the development of NASH in this study. Journal of Hepatology 2014 vol. 60 | S215–S359 S335