Both alcoholic and non-alcoholic steatohepatitis association with cardiovascular risk and liver fibrosis

Title
Both alcoholic and non-alcoholic steatohepatitis association with cardiovascular risk and liver fibrosis
Publication type
Journal Article
Year of Publication
2018
Journal
Alcohol
Volume
69
Pagination
63 - 67
Date published
2018
Abstract

Background: Non-alcoholic fatty liver disease (NAFLD) is the most common cause of liver disease worldwide. Mortality in NAFLD is mainly related to cardiovascular disease (CVD) and cancer. NAFLD and its association with both CVD and liver disease risk have been well evaluated, but the association of NAFLD with alcohol, known as “both alcoholic and non-alcoholic steatohepatitis” (BASH), remains uncertain. The objective of this study was to assess the influence of alcohol and obesity in the development of liver and cardiovascular disease risk. Methods: This was a case-control study that included patients from a regular check-up. Alcohol consumption was evaluated with MAST, AUDIT, and CAGE. Cardiovascular risk was evaluated using the Framingham score, and liver fibrosis was evaluated with APRI and NAFLD score. Patients were classified in five groups: healthy patients, steatosis with obesity, steatosis with alcoholism, BASH, and idiopathic steatosis. Results: A total of 414 patients were included. The BASH group represented 16% of patients, and showed a greater proportion of patients with high cardiovascular risk with 17% (p = 0.001), and liver fibrosis with 9%, according to the APRI score (p = 0.10). A multivariate logistic regression showed that alcohol consumption >140 g/week (OR 2.546, 95% CI 1.11–5.81, p = 0.003) and BMI >25 kg/m2 (OR 12.64, 95% CI 1.66 96.20, p = 0.001) were related to high cardiovascular risk. Liver fibrosis according to APRI was only related to alcohol consumption >140 g/week (OR 2.74, 95% CI 1–7.48, p = 0.03). Conclusions: BASH remains an area not well explored, and of great implication given the increasing number of patients affected. We observed an additive effect of both etiologies in the development of high cardiovascular and liver disease risk.