Department of Medicine, Comprehensive Transplant Center, Cedars-Sinai Medical Center, 8900 Beverly Boulevard, Suite 250, Los Angeles, CA 90048, USA.
Gastroenterology Section, VA Long Beach Healthcare System, 5901 East Seventh Street - 11G, Long Beach, CA 90822, USA. Electronic address: Timothy.email@example.com.
Hepatic steatosis and steatohepatitis have several etiologies; the most common are alcoholic steatohepatitis (ASH) and obesity/metabolic syndrome-induced steatohepatitis, also known as nonalcoholic steatohepatitis (NASH). Although the etiology of these 2 conditions is different, they share pathways to disease progression and severity. They also have differences in physiologic pathways, and shared and divergent mechanisms can be therapeutic targets. There is no approved pharmacologic therapy for NASH, but several molecules are under study. Focus remains on modulation of insulin resistance, oxidative stress, the inflammatory cascade, hepatic fibrosis, and cell death. This review provides an overview of pathophysiologic similarities and differences between ASH and NASH.