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

Abstract and Introduction

Abstract

Nonalcoholic fatty liver disease (NAFLD) describes a range of disorders characterized by excess accumulation of triglyceride within the liver. While simple steatosis may be clinically stable, nonalcoholic steatohepatitis (NASH) can be progressive. Inflammation is believed to be the driving force behind NASH and the progression to fibrosis and subsequent cirrhosis. This article will review and interpret the current literature in an attempt to expand our understanding of the environmental and genetic causes of inflammation and its effects in NAFLD.

Introduction

Nonalcoholic fatty liver disease (NAFLD) is a spectrum of disorders defined by excess accumulation of triglyceride within hepatocytes, ranging from 'simple steatosis', which is often clinically stable, to nonalcoholic steatohepatitis (NASH), which may progress to cirrhosis in a significant proportion of patients.[1] Differentiating simple steatosis from NASH is important in the prognosis and management of patients with NAFLD. Growing evidence indicates that inflammation is the driving force behind the development of NASH and subsequent fibrosis and cirrhosis. This article will review and interpret the current literature in an attempt to expand our understanding of the environmental and genetic causes of inflammation and how this process contributes to NAFLD.

Comments

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