De Novo nonalcoholic fatty liver disease after liver transplantation

✍ Scribed by Manal F. Abdelmalek; Anna Mae Diehl

• Publisher: John Wiley and Sons
• Year: 2007
• Tongue: English
• Weight: 64 KB
• Volume: 13
• Category: Article
• ISSN: 1527-6465
• DOI: 10.1002/lt.21103

✦ Synopsis

Achieving long-term graft survival and mortality is the primary goal of liver transplantation (LT). However, disease recurrence remains a stumbling block, especially among patients with hepatitis C. In such patients, worse outcomes may be associated with comorbidities (i.e., hyperlipidemia, hypertension, impaired glucose tolerance, type 2 diabetes, and obesity) and immunosuppressive medications that contribute to the development of de novo nonalcoholic fatty liver disease (NAFLD). Although benign steatosis may progress to nonalcoholic steatohepatitis (NASH) and cirrhosis in a minority of individuals, the natural history of de novo hepatic steatosis after LT remains unknown. The significance of de novo hepatic steatosis and its risk of progression to NASH or cirrhosis raise further questions about the pathogenic mechanisms of this condition, and more importantly, about the measures that may be taken to improve associated hepatocellular injury. The article by Seo et al. 1 in this issue of Liver Transplantation addresses this from the vantage point of a single-center experience and concludes that posttransplant weight gain is a positive risk factor for the development of de novo post-LT hepatic steatosis. However, this risk appears to be attenuated by the use of angiotensin converting enzyme inhibitors (ACE-Is), and this suggests that ACE-Is may independently reduce the risk of de novo development of NAFLD in the post-LT setting.

Seo et al. performed a retrospective analysis on a cohort (n ϭ 68) of orthotopic LT patients who had paired donor liver biopsies and a liver biopsy performed after LT for the evaluation of abnormal liver enzymes at the