Department of Preventive Medicine, Korea University, Seoul, South Korea.
Health and Wellness College, Sungshin Women's University Woonjung Green Campus, Seoul, South Korea.
Rheumatology (Oxford). 2023 Sep 1;62(9):3006-3013. doi: 10.1093/rheumatology/kead048.
We evaluated the familial risk of seropositive rheumatoid arthritis (RA) and examined interactions between family history and smoking.
Using the National Health Insurance and Health Screening Program databases, which include information on familial relationships and lifestyle factors, we identified 5 524 403 individuals with first-degree relatives (FDRs) from 2002-2018. We calculated familial risk using hazard ratios (HRs) with 95% CIs which compare the risk of individuals with and without affected FDRs. Interactions between smoking and family history were assessed on an additive scale using the relative excess risk due to interaction (RERI).
Individuals with affected FDR had 4.52-fold (95% CI 3.98, 5.12) increased risk of disease compared with those with unaffected FDR. Familial risk adjusted for lifestyle factors decreased slightly (HR 4.49), suggesting that a genetic contribution is the predominant driver in the familial aggregation of RA. Smoking was associated with an increased risk of disease that was more pronounced among heavy (HR 1.92 95% CI 1.70, 2.18) compared with moderate (HR 1.15 95% CI 1.04, 1.28) smoking. In the interaction analysis, the risk associated with the combined effect of smoking and family history was higher than the sum of their individual effects, though statistically non-significant (RERI 1.30 95% CI ‒0.92, 3.51). Heavy smokers with a positive family history showed a prominent interaction (RERI 4.13 95% CI ‒0.88, 9.13) which exceeded moderate smokers (RERI 0.61 95% CI ‒1.90, 3.13), suggesting a dose-response interaction pattern.
Our findings indicate the possibility of an interaction between RA-associated genes and smoking.
我们评估了阳性类风湿关节炎(RA)的家族发病风险,并研究了家族史与吸烟之间的相互作用。
利用包括家族关系和生活方式因素信息的国家健康保险和健康筛查计划数据库,我们从 2002 年至 2018 年确定了 5524403 名一级亲属(FDR)的个体。我们使用风险比(HR)和 95%置信区间(CI)计算家族风险,将患有和不患有受影响 FDR 的个体的风险进行比较。使用交互作用归因超额相对危险度(RERI),以加性尺度评估吸烟与家族史之间的相互作用。
与不伴有受影响 FDR 的个体相比,伴有受影响 FDR 的个体疾病风险增加了 4.52 倍(95%CI 3.98,5.12)。调整生活方式因素后的家族风险略有下降(HR 4.49),这表明遗传因素是 RA 家族聚集的主要驱动因素。吸烟与疾病风险增加相关,且在重度吸烟(HR 1.92,95%CI 1.70,2.18)中比在中度吸烟(HR 1.15,95%CI 1.04,1.28)中更为明显。在交互作用分析中,吸烟和家族史共同作用的风险高于其各自作用的总和,但统计学上无显著性差异(RERI 1.30,95%CI-0.92,3.51)。具有阳性家族史的重度吸烟者表现出明显的交互作用(RERI 4.13,95%CI-0.88,9.13),超过了中度吸烟者(RERI 0.61,95%CI-1.90,3.13),表明存在剂量-反应交互作用模式。
我们的研究结果表明,RA 相关基因与吸烟之间可能存在相互作用。