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. 2020 Sep 25;26(4):662–669. doi: 10.3350/cmh.2020.0163

Table 2.

Detrimental effect of moderate alcohol intake in NAFLD

Study Type of study Patient Outcome measure Result
Åberg et al. [5] (2018) Cohort study 6,732 patients Liver disease progression, HCC, liver-related death Alcohol use (HR, 1.002; 95% CI, 1.001–1.002)
Alcohol was significant even when average alcohol consumption was within the limits currently defining nonalcoholic fatty liver disease.
Bellentani et al. [23] (2000) Cross-sectional cohort study 257 patients Ultrasonography Risk for steatosis was higher by 2.8-fold (95% CI, 1.4–7.1)
Hézode et al. [21] (2003) Cohort study 260 patients with chronic hepatitis C Liver biopsy The proportion of patients with moderate (F2) or marked (F3) fibrosis or cirrhosis (F4) gradually increased from 29.0% in abstinent patients to 67.6% for an intake between 31 and 50 g/day (P<0.001)
Becker et al. [26] (1996) Cohort study 13,285 patients Death certificates and the hospital discharge register A dose‐dependent increase in relative risk of developing alcohol‐induced liver disease for both men and women, with the steepest increase among women.

NAFLD, nonalcoholic fatty liver disease; HCC, hepatocellular carcinoma; HR, hazard ratio; CI, confidence interval.