Department of Internal Medicine, Boston Medical Center, Boston University School of Medicine, Boston, MA.
School of Public Health and Social Policy, University of Victoria, Victoria, British Columbia, Canada.
Clin Gastroenterol Hepatol. 2023 Oct;21(11):2854-2863.e2. doi: 10.1016/j.cgh.2022.10.039. Epub 2022 Dec 8.
While heavy alcohol use consistently associates with liver disease, the effects of nonheavy alcohol consumption are less understood. We aimed to investigate the relationship between nonheavy alcohol use and chronic liver disease.
This cross-sectional study included 2629 current drinkers in the Framingham Heart Study who completed alcohol use questionnaires and transient elastography. We defined fibrosis as liver stiffness measurement (LSM) ≥8.2 kPa. We defined at-risk nonalcoholic steatohepatitis (NASH) as FibroScan-aspartate aminotransferase (FAST) score >0.35 (90% sensitivity) or ≥0.67 (90% specificity). We performed logistic regression to investigate associations of alcohol use measures with fibrosis and NASH, adjusting for sociodemographic and metabolic factors. Subgroup analysis excluded heavy drinkers (>14 drinks per week for women or >21 for men).
In this sample (mean age 54.4 ± 8.9 years, 53.3% women), mean LSM was 5.6 ± 3.4 kPa, 8.2% had fibrosis, 1.9% had NASH by FAST ≥0.67, and 12.4% had NASH by FAST >0.35. Participants drank 6.2 ± 7.4 drinks per week. Total drinks per week and frequency of drinking associated with increased odds of fibrosis (adjusted odds ratio [aOR], 1.18; 95% confidence interval [CI], 1.04-1.33; and aOR, 1.08; 95% CI, 1.01-1.16, respectively). Risky weekly drinking, present in 17.4%, also associated with fibrosis (aOR, 1.49; 95% CI, 1.03-2.14). After excluding 158 heavy drinkers, total drinks per week remained associated with fibrosis (aOR, 1.16; 95% CI, 1.001-1.35). Multiple alcohol use measures positively associated with FAST >0.35.
In this community cohort, we demonstrate that nonheavy alcohol use associates with fibrosis and NASH, after adjustment for metabolic factors. Longitudinal studies are needed to determine the benefits of moderating alcohol use to reduce liver-related morbidity and mortality.
尽管大量饮酒与肝病密切相关，但对于非大量饮酒与慢性肝病的关系，我们的了解仍不够深入。本研究旨在探讨非大量饮酒与慢性肝病的关系。
本横断面研究纳入了Framingham 心脏研究中的 2629 名当前饮酒者，他们完成了饮酒问卷和瞬时弹性成像检查。我们将纤维化定义为肝脏硬度测量值（LSM）≥8.2kPa。我们将风险性非酒精性脂肪性肝炎（NASH）定义为 FibroScan-天门冬氨酸氨基转移酶（FAST）评分>0.35（90%灵敏度）或≥0.67（90%特异性）。我们通过逻辑回归分析，调整社会人口学和代谢因素后，探讨饮酒量与纤维化和 NASH 的相关性。亚组分析排除了大量饮酒者（女性每周饮酒>14 杯或男性每周饮酒>21 杯）。
在该样本中（平均年龄 54.4±8.9 岁，53.3%为女性），平均 LSM 为 5.6±3.4kPa，8.2%的人存在纤维化，1.9%的人通过 FAST≥0.67 诊断为 NASH，12.4%的人通过 FAST>0.35 诊断为 NASH。参与者每周饮酒 6.2±7.4 杯。每周总饮酒量和饮酒频率与纤维化的患病风险增加相关（校正比值比[aOR]，1.18；95%置信区间[CI]，1.04-1.33；aOR，1.08；95%CI，1.01-1.16）。17.4%的人存在风险性每周饮酒，也与纤维化相关（aOR，1.49；95%CI，1.03-2.14）。排除 158 名大量饮酒者后，每周总饮酒量仍与纤维化相关（aOR，1.16；95%CI，1.001-1.35）。多种饮酒指标与 FAST>0.35 呈正相关。
在本社区队列中，我们发现非大量饮酒与纤维化和 NASH 相关，且在调整代谢因素后仍然如此。需要进行前瞻性研究来确定适量饮酒以降低与肝脏相关的发病率和死亡率的获益。
