Nonheavy Alcohol Use Associates With Liver Fibrosis and Nonalcoholic Steatohepatitis in the Framingham Heart Study.
Nonheavy Alcohol Use Associates With Liver Fibrosis and Nonalcoholic Steatohepatitis in the Framingham Heart Study.
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弗雷明汉心脏研究中，非重度饮酒与肝纤维化和非酒精性脂肪性肝炎有关。
DOI：
10.1016/j.cgh.2022.10.039
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发表时间：
2023
期刊：
影响因子：
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通讯作者：
Long,MichelleT
中科院分区：
文献类型：
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作者：
Rice,BrookeA;Naimi,TimothyS;Long,MichelleT
背景和目的虽然大量饮酒与肝病相关，但对非大量饮酒的影响了解较少。我们的目的是调查之间的关系nonheavy酒精使用和慢性liver diseases.MethodsThis横断面研究包括2629当前饮酒者在心脏研究谁完成了酒精使用问卷和瞬态弹性成像。我们将肝纤维化定义为肝硬度测量值（LSM）≥8.2 kPa。我们将风险非酒精性脂肪性肝炎（NASH）定义为FibroScan天冬氨酸转氨酶（FAST）评分>0.35（90%灵敏度）或≥0.67（90%特异性）。我们进行了逻辑回归，以调查酒精使用措施与纤维化和NASH的关联，调整社会人口统计学和代谢因素。亚组分析排除了重度饮酒者（女性每周饮酒>14次，男性每周饮酒>21次）。结果在该样本中（平均年龄54.4 ± 8.9岁，53.3%为女性），平均LSM为5.6 ± 3.4 kPa，8.2%有纤维化，1.9%有FAST ≥0.67的NASH，12.4%有FAST >0.35的NASH。参与者每周喝6.2 ± 7.4杯饮料。每周总饮酒量和饮酒频率与纤维化几率增加相关（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%的患者每周饮酒，也与纤维化相关（aOR，1.49; 95% CI，1.03-2.14）。排除158名重度饮酒者后，每周饮酒总量仍与纤维化相关（aOR，1.16; 95%CI，1.001-1.35）。多次饮酒与FAST > 0.35呈正相关。结论在这个社区队列中，我们证明了在调整代谢因素后，非重度饮酒与纤维化和NASH相关。需要进行纵向研究以确定适度饮酒对降低肝脏相关发病率和死亡率的益处。
Background and AimsWhile 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.MethodsThis 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).ResultsIn 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.ConclusionsIn 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.