Health Insurance Review and Assessment Service, Wonju-si, Republic of Korea.
Chungbuk National University, Chungcheongbuk-do, Republic of Korea.
Arthritis Care Res (Hoboken). 2023 Sep;75(9):1955-1966. doi: 10.1002/acr.25095. Epub 2023 Mar 7.
Population-based studies of the familial aggregation of gout are scarce, and gene/environment interactions are not well studied. This study was undertaken to evaluate the familial aggregation of gout as well as assess interactions between family history and obesity or alcohol consumption on the development of gout.
Using the Korean National Health Insurance database, which includes information regarding familial relationships and risk factor data, we identified 5,524,403 individuals from 2002 to 2018. Familial risk was calculated using hazard ratios (HRs) with 95% confidence intervals (95% CIs) to compare the risk in individuals with and those without affected first-degree relatives. Interactions between family history and obesity/alcohol consumption were assessed on an additive scale using the relative excess risk due to interaction (RERI).
Individuals with a gout-affected first-degree relative had a 2.42-fold (95% CI 2.39, 2.46) increased risk of disease compared to those with unaffected first-degree relatives. Having both a family history of gout and being either overweight or having moderate alcohol consumption was associated with a markedly increased risk of disease, with HRs of 4.39 (95% CI 4.29, 4.49) and 2.28 (95% CI 2.22, 2.35), respectively, which exceeded the sum of their individual risks but was only statistically significant in overweight individuals (RERI 0.96 [95% CI 0.85, 1.06]). Obese individuals (RERI 1.88 [95% CI 1.61, 2.16]) and heavy drinkers (RERI 0.36 [95% CI 0.20, 0.52]) had a more prominent interaction compared to overweight individuals and moderate drinkers, suggesting a dose-response interaction pattern.
Our findings indicate the possibility of an interaction between gout-associated genetic factors and obesity/alcohol consumption.
基于人群的痛风家族聚集性研究较为匮乏，基因-环境相互作用也尚未得到充分研究。本研究旨在评估痛风的家族聚集性，并评估家族史与肥胖或饮酒之间的相互作用对痛风发病的影响。
我们利用韩国国家健康保险数据库（该数据库包含家族关系和风险因素数据），从 2002 年至 2018 年期间确定了 5524403 名个体。使用风险比（HR）及其 95%置信区间（95%CI）来计算家族风险，以比较有和无受影响一级亲属的个体的发病风险。使用交互作用归因超额相对危险度（RERI）在加性尺度上评估家族史与肥胖/饮酒之间的相互作用。
与一级亲属无痛风病史的个体相比，一级亲属有痛风病史的个体患病风险增加了 2.42 倍（95%CI 2.39，2.46）。同时具有痛风家族史和超重或中度饮酒史与疾病风险显著增加相关，HR 分别为 4.39（95%CI 4.29，4.49）和 2.28（95%CI 2.22，2.35），这两个风险超过了它们各自的风险总和，但仅在超重个体中具有统计学意义（RERI 0.96[95%CI 0.85，1.06]）。肥胖个体（RERI 1.88[95%CI 1.61，2.16]）和重度饮酒者（RERI 0.36[95%CI 0.20，0.52]）与超重个体和中度饮酒者相比，相互作用更为显著，提示存在剂量-反应交互作用模式。
我们的研究结果表明，痛风相关遗传因素与肥胖/饮酒之间可能存在相互作用。
