Body Fat Distribution and Risk Factors for Fibrosis in Patients with Alcoholic Liver Disease
Article first published online: 7 SEP 2012
Copyright © 2012 by the Research Society on Alcoholism
Alcoholism: Clinical and Experimental Research
Volume 37, Issue 2, pages 332–338, February 2013
How to Cite
Naveau, S., Dobrin, A.-S., Balian, A., Njiké-Nakseu, M., Nohra, P., Asnacios, A., Prévot, S. and Perlemuter, G. (2013), Body Fat Distribution and Risk Factors for Fibrosis in Patients with Alcoholic Liver Disease. Alcoholism: Clinical and Experimental Research, 37: 332–338. doi: 10.1111/j.1530-0277.2012.01927.x
- Issue published online: 1 FEB 2013
- Article first published online: 7 SEP 2012
- Manuscript Accepted: 5 JUN 2012
- Manuscript Received: 24 FEB 2012
- Alcoholic Liver Disease;
- HDL Cholesterol;
- Body Mass Index;
- Metabolic Syndrome;
- Abdominal Height
Only a small proportion of alcoholic patients develop advanced liver disease, suggesting that factors other than alcohol intake may influence alcoholic liver disease (ALD) progression. We have shown that body mass index (BMI) is an independent risk factor for fibrosis in alcohol-induced liver disease and that adipose tissue inflammation is correlated with liver lesions in alcoholic patients. The aim of this study was to determine whether visceral adipose tissue, as assessed by abdominal height measurement, affected individual susceptibility to fibrosis in alcoholic patients.
We included 127 consecutive alcoholic patients with abnormal liver test findings for whom liver histology data were available. Abdominal height was measured with a Holtain-Kahn abdominal caliper. We carried out univariate comparisons followed by multivariate regression analysis, to investigate the relationship between abdominal height and fibrosis score.
Abdominal height (p < 0.005), waist circumference (p < 0.05), fasting blood glucose concentration (p < 0.05), serum triglyceride concentration (p < 0.05), serum bilirubin (p < 0.005), and BMI (p = 0.05) were higher, whereas high-density lipoprotein (HDL) cholesterol level (p < 0.01) was lower in the 72 patients with significant (F2–F4) fibrosis than in the 55 patients with F0–F1 fibrosis. In multivariate regression analysis, only abdominal height (β = 7.2, p < 0.002) was independently and positively correlated with fibrosis score, which was also negatively correlated with HDL cholesterol level (β = −1.04, p < 0.05).
We provide the first demonstration that abdominal height may be a predictor of significant fibrosis in patients with ALD. Our findings support a role for visceral fat accumulation, independent of BMI and of metabolic syndrome criteria, in the onset of alcoholic liver damage.