Inflammation in Nonalcoholic Steatohepatitis

R Christopher Harmon; Dina G Tiniakos; Curtis K Argo

Disclosures

Expert Rev Gastroenterol Hepatol. 2011;5(2):189-200. 

In This Article

Inflammation: Driving Force of NASH

Previous single-point cross-sectional studies have identified components of the metabolic syndrome to be associated with NASH and fibrosis.[33–39] These prevalence studies identify at-risk populations, but do not clarify cause and effect. In a recent systematic review of serial liver biopsy studies, Argo et al. demonstrated that age and presence of acinar and/or portal inflammation of any type (acute or chronic) on the initial biopsy were the sole independent predictors of the development of advanced fibrosis in NASH.[40] These data imply that inflammation is the key predictor of eventual histological progression to fibrosis and cirrhosis and, thus, potentially a major therapeutic target in NASH. Interestingly, parameters of the metabolic syndrome (BMI, obesity, waist–hip ratio, insulin resistance and Type 2 diabetes) were not statistically significant predictors on multivariate analysis.[40] It is logical to assume that altering the inflammatory injury may modify the clinical course of disease; however, this has yet to be demonstrated. Potential mechanisms driving inflammation in NASH implicate systemic lipotoxicity as a result of overnutrition, lipid metabolites, visceral adipose tissue and production of proinflammatory cytokines and adipokines, gut bacteria and oxidation.

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