A new study has found hepatic steatosis – fatty liver disease – in nearly one third of American adults in a large urban population sample. The prevalence of the disease varied significantly among ethnic groups. Hispanics had a higher prevalence than whites, while blacks had a lower prevalence than whites. The study is found in the December 2004 issue of Hepatology, the official journal of the American Association for the Study of Liver Diseases (AASLD). Published by John Wiley & Sons, Inc., Hepatology is available online via Wiley InterScience at http://www.interscience.wiley.com/journal/hepatology.
Nonalcoholic fatty liver disease (NAFLD), the most common cause of abnormal liver function tests among U.S. adults, can range in severity from simple fat accumulation to life-threatening liver disease. It is most commonly associated with obesity, insulin resistance, and hyperlipidemia – all components of metabolic syndrome. However, not everyone with metabolic syndrome develops hepatic steatosis, and the condition does not always progress to severe stages.
Recent retrospective studies have shown that the prevalence of cirrhosis due to NAFLD may vary by ethnic group. Researchers led by Jeffrey D. Browning of the University of Texas, examined a large, ethnically diverse population sample from Dallas, Texas, to determine if ethnic differences in NAFLD-related cirrhosis were associated with underlying differences in susceptibility to hepatic triglyceride (HTGC) accumulation.
They studied 2,287 participants of the Dallas Heart Study in whom HTGC was measured using proton nuclear magnetic resonance spectroscopy (1H-MRS). Each participant filled out a questionnaire on demographics, medical history, other medical conditions and alcohol intake. They also gave a blood sample, blood pressure, body weight and measurements, and underwent H-NMR spectroscopy of liver triglyceride content. The researchers then performed statistical analyses on the collected data.
Nearly one-third of the sample was found to have hepatic steatosis (defined as HTGC greater than 95th percentile of healthy persons, or 5.5 percent liver fat content) and "striking differences in the prevalence of hepatic steatosis were present among the three major ethnic groups," the authors report.
The prevalence of hepatic steatosis was significantly higher in Hispanics than in whites, and significantly lower in blacks than in whites. Furthermore, while the prevalence of hepatic steatosis was similar between the sexes in blacks and Hispanics, in whites, prevalence in men was twice as high than that in women. In all participants, HTGC correlated significantly with components of the metabolic syndrome. Notably, no significant positive correlation was found between daily ethanol intake and HTGC.
The results suggest that there are fundamental differences in lipid homeostasis among ethnic groups. The authors found that while blacks and Hispanics had similar levels of obesity and insulin resistance, blacks had a much lower prevalence of hepatic steatosis. They also found further evidence that a normal serum ALT level offers little diagnostic or prognostic value when assessing patients for NAFLD. Almost 80 percent of the subjects in this study with hepatic steatosis had normal serum ALT levels.
Limitations of this study include possible underestimation of alcohol intake, since this was self-reported by the patients in the study. Also, the researchers could not screen for infectious disease and therefore could not evaluate the impact of hepatitis C virus on hepatic steatosis.
In conclusion, the authors report, "Understanding the mechanisms responsible for the ethnic differences in the prevalence of hepatic steatosis and steatosis-related liver injury may provide clues to the development of new therapeutic approaches for the prevention and treatment of this disorder."
Article: "Prevalence of Hepatic Steatosis in an Urban Population in the United States: Impact of Ethnicity," Jeffrey D. Browning, Lidia S. Szczepaniak, Robert Dobbins, Pamela Nuremberg, Jay D. Horton, Jonathan C. Cohen, Scott M. Grundy, and Helen H. Hobbs, Hepatology; December 2004; 40:6; pp. 1387-1395 (DOI: 10.1002/hep.20466).
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