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Epidemiology, clinical features, and diagnosis of nonalcoholic steatohepatitis
Authors
Sunil G Sheth, MD
Sanjiv Chopra, MD
Section Editor
Marshall M Kaplan, MD
Deputy Editor
Peter A L Bonis, MD
Last literature review version 19.1: January 2011 |This topic last updated: January 4, 2011 (More)
INTRODUCTION — Nonalcoholic steatohepatitis (NASH) is the term used to describe the distinctclinical entity in which patients lack a history of significant alcohol consumption but have liver biopsy findings indistinguishable from alcoholic steatohepatitis [1,2]. Other terms that have infrequently been used to describe this condition include pseudoalcoholic hepatitis, alcohol-like hepatitis, fatty liver hepatitis, steatonecrosis, and diabetic hepatitis. NASH is also considered to be a subsetof nonalcoholic fatty liver disease.
The pathogenesis, clinical features, and diagnosis of NASH will be reviewed here. The natural history and treatment of this disorder are discussed separately. (See "Natural history and treatment of nonalcoholic steatohepatitis".)
DEFINITION — The following criteria have been proposed for the diagnosis of NASH [3,4]:
• A liver biopsy showing steatosis,hepatocyte ballooning degeneration, mild diffuse lobular mixed acute and chronic inflammation, and perivenular, perisinusoidal collagen deposition (picture 1A-C). Zone 3 accentuation may be detected. Other commonly observed features include Mallory's hyaline, vacuolated nuclei in periportal hepatocytes, lobular lipogranulomas, PAS-diastase-resistant Kupffer cells, and pericellular fibrosis (in thosewith advanced stages of fibrosis or cirrhosis). As noted above, these changes are indistinguishable from those of alcoholic steatohepatitis. (See "Clinical manifestations and diagnosis of alcoholic liver disease", section on 'Alcoholic hepatitis'.) It is possible that portal fibrosis alone may represent a variant of NASH [5]. In biopsy specimens from children, portal inflammation may be moreprominent than in adults [3].
• Convincing evidence of negligible alcohol consumption (less than 20 g of ethanol per week) including a detailed history obtained by three physicians independently and interrogation of family members and local medical practitioners. Random blood assays for ethanol estimation should be negative. If performed, assays for the presence of desialylated transferrin in serum, amarker of alcohol consumption, should also be negative [6].
• Absence of serologic evidence of infection with hepatitis B or hepatitis C.
In clinical practice, a meticulous history by three physicians is not usually practical; we therefore feel that this is not mandatory for the diagnosis. In addition, patients with past infection with hepatitis B virus infection should not necessarily beexcluded. On the other hand, patients positive for hepatitis B surface antigen or hepatitis C virus antibody or HCV-RNA should be excluded. (See "Screening for and diagnostic approach to hepatitis C virus infection".)
EPIDEMIOLOGY — The prevalence of NASH in the general population is incompletely understood. A limitation to performing population-based studies is the limited sensitivity of noninvasivemethods for establishing the diagnosis.
Somewhat better understood is the prevalence of nonalcoholic fatty liver disease (NAFLD), which can be detected noninvasively. The major risk factors for nonalcoholic fatty liver disease (NAFLD), central obesity, type 2 diabetes mellitus, dyslipidemia, and metabolic syndrome are common in western societies. NAFLD is the most common liver disorder in Westernindustrialized countries, affecting 20 to 40 percent of the general population [7]. In a prospective study of 400 US military personnel and their families (mean age 55), the prevalence of NAFLD by ultrasound was 46 percent [8]. The prevalence was increased in men, older individuals, and those with hypertension, obesity or diabetes. NASH was confirmed by biopsy in 30 percent of ultrasound-positive...