Antiviral therapy against HCV did not appear to influence the findings of the study. However, some patients who achieved a sustained virological response decompensated, raising the possibility of a concurrent liver condition such as nonalcoholic steatohepatitis or alcoholism. The quantification of alcohol use during the study was not entirely clear. The effect of beta-blocker use during the study was also not addressed, which may affect the interpretation of the findings. Patients may have also experienced different management of cirrhosis-related complications

which could affect their prognosis. For example, the use of different types of bridging therapy for transplant-listed Selleckchem Roxadustat patients with HCC or the use of variceal ligation for primary prophylaxis against variceal hemorrhage in patients intolerant to beta-blockers. Findings from Gomez et al.[9] confirm that there are two distinct stages of compensated selleck products cirrhosis (with and without varices) where the near-term risks and complications differ. Patients with stage 1 cirrhosis without varices are more likely to have mild portal hypertension (HVPG <10 mmHg) and their near-term risks may be related to HCC and comorbid nonhepatic

conditions. In contrast, patients with compensated stage 2 cirrhosis with varices will be at higher near-term risk for portal hypertensive complications as well as HCC in addition to any risk from nonhepatic conditions. As the two stages of compensated cirrhosis are now well defined, further studies should appropriately stage patients, which may result in better treatment strategies and outcomes. Studies using beta-blockers in preprimary prophylaxis against varices with timolol and primary

prophylaxis against variceal hemorrhage with nadolol and propranolol are examples of such a strategy. Amir Ahmed Qamar, M.D. “
“We read with great interest the article by Orellana-Gavalda etal. about the ameliorating effects of long-term hepatic gene transfer of carnitine palmitoyltransferase 1A (CPT1A) on obesity-induced hepatic steatosis, diabetes, and insulin resistance.1 The authors observed increased lipid oxidation mediated by a significant up-regulation of liver CPT1A messenger RNA (mRNA). This effect not only improved lipid and glucose metabolism, but also had direct impact on liver inflammatory stress triggered Celastrol by high-fat diet (HFD) feeding. Orellana-Gavalda etal. suggest that increasing hepatic CPT1A expression is a valid in vivo strategy to reduce obesity-related complications. In a rat model of nonalcoholic fatty liver disease (NAFLD), we observed fairly similar results with indomethacin, a dual pharmacological inhibitor of cyclooxygenase 1 (COX1) (prostaglandin H synthase 1 [PTGS1]) and COX2 (PTGS2). We evaluated the effect of the drug on reversing fatty liver, and we also explored the impact on liver mRNA expression of several lipogenic and glucogenic genes, and nuclear receptors.