Showing papers by "Mary E. Rinella published in 2014"

Liraglutide-induced autoimmune hepatitis.

Abstract: Importance Use of incretin-based hypoglycemic agents is increasing, but safety data remain limited We treated a woman with marker-negative autoimmune hepatitis associated with the glucagon-like peptide 1 agonist liraglutide Observations A young woman with type 2 diabetes mellitus and vitiligo presented with a 10-day history of acute hepatitis Other than starting liraglutide therapy 4 months prior, she reported no changes in medication therapy and no use of supplements At admission, aspartate aminotransferase level was 991 U/L; alanine aminotransferase level, 1123 U/L; total bilirubin level, 95 mg/dL; and international normalized ratio, 13 Results of a liver biopsy demonstrated interface hepatitis with prominent eosinophils and rare plasma cells The patient’s liraglutide therapy was withheld at discharge but her symptoms worsened A second biopsy specimen revealed massive hepatic necrosis She started oral prednisone therapy for presumed liraglutide-induced marker-negative autoimmune hepatitis Conclusions and Relevance This case represents, to our knowledge, the first report of liraglutide-induced autoimmune hepatitis Hepatotoxicity may be an incretin analogue class effect with a long latency period This case raises prescriber awareness about the potential adverse effects of glucagon-like peptide 1 agonists Postmarketing studies are needed to define the hepatotoxic potential of these agents

NAFLD and Cardiovascular Disease: Can the Real Association Be Determined?

Abstract: Non-alcoholic fatty liver disease (NAFLD) represents a spectrum of liver diseases ranging from isolated hepatic steatosis (IHS) to non-alcoholic steatohepatitis (NASH) defined by the presence of hepatocellular injury, and may progress to end-stage liver disease and its complications. Mounting evidence also suggests that direct effects on the heart may explain why cardiovascular disease (CVD), comprising coronary artery disease and cerebrovascular disease, is the leading cause of death among individuals with NASH. CVD and NASH share common risk factors, however NASH may increase atherogenic risk or alter cardiac function independent of these commonalities. A complex interplay between an inflamed visceral fat compartment, the liver and the endothelium creates a pro-inflammatory, pro-coagulant and pro-atherogenic milieu that can contribute to accelerated atherosclerosis and cardiac dysfunction. While new evidence is accumulating that might help close the gap in our understanding of the putative role of NASH in CVD, more prospective data are still needed.