Consecutive patients with compensated cirrhosis and without hepatocellular carcinoma (HCC) were prospectively

enrolled. Baseline LSM was assessed at enrollment, then at a 6-12-month interval. Esophagogastroduodenoscopy and ultrasonography were performed regularly for surveillance Midostaurin molecular weight of varices and HCC. Liver disease progression (LDP) was defined as portal hypertension (PHT) progression (development of varices, varices growth, variceal bleeding, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy), HCC occurrence and liver-related death. Hepatic decompensation was defined as variceal bleeding, ascites, spontaneous bacterial peritonitis, or hepatic encephalopathy. Clinical event included hepatic decompensation and SB203580 price HCC development. Two hundred and twenty patients were enrolled. In a median follow-up period of 36.9 months, LDP were detected in 49 patients including 30 PHT progression (10 variceal development, 11 variceal growth, 9 hepatic decompensation) and 19 HCC developments. The cumulative incidence of LDP, PHT progression and HCC development at 3 years was 20.7%, 12.8% and 9.1% respectively. Multivariate analyses showed baseline

LSM is an independent predictor of PHT progression (HR: 1.05, 95% Cl: 1.02-1.09) and LDP (HR: 1.04, 95% Cl: 1.01-1.07); however, not of HCC occurrence. Assessed with area under receiver operating characteristic curve, the performance of baseline LSM in predicting PHT progression and hepatic decompensation was 0.744 and 0.929 respectively. With 17 and 21.1 kilopascal as the cut-offs, the negative predictive value was 92% and 99% respectively. Patients with baseline LSM≥17kPa and 14kPa without serial changes had higher risk of MCE PHT progression

and LDP respectively. Conclusions: For patients with compensated hepatic cirrhosis, LSM was an independent predictor of PHT and LDP, but not of HCC occurrence. Baseline LSM was useful to exclude PHT progression and hepatic decompensation. Patients with baseline LSM≥17 kilopascal without serial change had higher risk of PHT progression. Disclosures: The following people have nothing to disclose: JIng-Houng Wang, Seng-Kee Chuah, Sheng-Nan Lu, Chao-Hung Hung, Chung-Mou Kuo, Wei-Chen Tai, ShueShian Chiou Background Gastroesophageal variceal hemorrhage is an important complication of cirrhosis. We investigated the in-hospital mortality and its risk factors after variceal hemorrhage in a large sample, using a nationwide Japanese database. Methods Data on the patients with variceal hemorrhage were collected for a total of 39 months from a nationwide administrative database covering approximately 1,000 hospitals. The risk factors for fatal outcome due to variceal hemorrhage was analyzed with receiver operating characteristics (ROC) curves and univariate and multivariate logistic regression. Comorbidities were assessed by using Charlson Comorbidity index.