Genetic Epidemiology, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
Faculty of Medical Sciences, Newcastle University Medical School, Newcastle upon Tyne, United Kingdom.
Am J Gastroenterol. 2021 Jan 1;116(1):106-115. doi: 10.14309/ajg.0000000000000833.
Sustained high alcohol intake is necessary but not sufficient to produce alcohol-related cirrhosis. Identification of risk factors, apart from lifetime alcohol exposure, would assist in discovery of mechanisms and prediction of risk.
We conducted a multicenter case-control study (GenomALC) comparing 1,293 cases (with alcohol-related cirrhosis, 75.6% male) and 754 controls (with equivalent alcohol exposure but no evidence of liver disease, 73.6% male). Information confirming or excluding cirrhosis, and on alcohol intake and other potential risk factors, was obtained from clinical records and by interview. Case-control differences in risk factors discovered in the GenomALC participants were validated using similar data from 407 cases and 6,573 controls from UK Biobank.
The GenomALC case and control groups reported similar lifetime alcohol intake (1,374 vs 1,412 kg). Cases had a higher prevalence of diabetes (20.5% (262/1,288) vs 6.5% (48/734), P = 2.27 × 10-18) and higher premorbid body mass index (26.37 ± 0.16 kg/m2) than controls (24.44 ± 0.18 kg/m2, P = 5.77 × 10-15). Controls were significantly more likely to have been wine drinkers, coffee drinkers, smokers, and cannabis users than cases. Cases reported a higher proportion of parents who died of liver disease than controls (odds ratio 2.25 95% confidence interval 1.55-3.26). Data from UK Biobank confirmed these findings for diabetes, body mass index, proportion of alcohol as wine, and coffee consumption.
If these relationships are causal, measures such as weight loss, intensive treatment of diabetes or prediabetic states, and coffee consumption should reduce the risk of alcohol-related cirrhosis.
持续大量饮酒是导致酒精相关肝硬化的必要条件,但并非充分条件。除了终生饮酒量之外,确定其他危险因素有助于发现发病机制并预测风险。
我们进行了一项多中心病例对照研究(GenomALC),比较了 1293 例病例(酒精相关肝硬化,75.6%为男性)和 754 例对照(有同等饮酒量但无肝脏疾病证据,73.6%为男性)。通过临床记录和访谈获得确认或排除肝硬化以及饮酒和其他潜在危险因素的信息。在 GenomALC 参与者中发现的病例对照危险因素差异使用来自 UK Biobank 的 407 例病例和 6573 例对照的类似数据进行了验证。
GenomALC 病例组和对照组报告的终生饮酒量相似(1374 与 1412 公斤)。病例组的糖尿病患病率(20.5%(262/1288)比对照组(6.5%(48/734),P=2.27×10-18)和较高的发病前体重指数(26.37±0.16kg/m2)高于对照组(24.44±0.18kg/m2,P=5.77×10-15)。与病例组相比,对照组更有可能是葡萄酒饮用者、咖啡饮用者、吸烟者和大麻使用者。病例组报告父母死于肝病的比例高于对照组(比值比 2.25,95%置信区间 1.55-3.26)。来自 UK Biobank 的数据证实了这些关于糖尿病、体重指数、酒精作为葡萄酒的比例和咖啡消耗的发现。
如果这些关系是因果关系,那么减肥、强化糖尿病或糖尿病前期状态的治疗以及咖啡消费等措施应能降低酒精相关肝硬化的风险。