Predictive factors for pure steatosis in alcoholic patients

Bearing in mind the mechanisms involved in nonalcoholic fatty liver disease, this study aims to verify whether metabolic syndrome or its various individual components are independent predictive factors for steatosis > or =10% in alcoholic patients.

This study included 281 consecutive alcoholic patients with abnormal liver tests and either normal liver histology or steatosis <10% (n = 119) or steatosis > or =10% (n = 162). Logistic regression analysis was used to study the relationship between metabolic syndrome components and various risk factors and the presence of steatosis > or =10%. We assessed apolipoprotein A1 (ApoA-1) levels, a major protein component of plasma high-density lipoprotein (HDL), rather than HDL-cholesterol levels.

Plasma ApoA-1 levels (p < 0.01), body mass index (BMI) (p < 0.01), and waist circumference (p < 0.05) were significantly higher in patients with steatosis > or =10% than in patients with normal liver histology or steatosis <10%. A higher percentage of patients with steatosis > or =10% had high blood pressure (p = 0.003) than patients with normal liver histology or steatosis <10%. In the logistic regression, ApoA-1 [odds ratio (OR) = 1.57 (1.10-2.22)], BMI [OR = 1.10 (1.01-1.23)], and high blood pressure [OR = 1.84 (1.10-3.06)] were positively and independently correlated with the presence of steatosis > or =10%. In the multivariate regression high blood pressure was independently and positively correlated with steatosis score (r = 0.55 +/- 0.26; p < 0.05). On the other hand, when the presence of high blood pressure was the dependent variable, the presence of steatosis > or =10% positively and independently correlated with it [OR = 1.82 (1.05-3.15)].

In alcoholic patients without fibrosis, ApoA-1, BMI, and high blood pressure on the next morning after the admission were predictive of steatosis > or =10%. High blood pressure was the only metabolic syndrome component associated with the presence of alcoholic steatosis >/=10% and was not correlated with other metabolic syndrome components. These findings suggest that steatosis mechanisms are different in alcoholic and nonalcoholic fatty liver.