Dipartimento di Scienze Mediche, Chirurgiche e Sperimentali, University of Sassari.
Baylor College of Medicine.
J Atheroscler Thromb. 2021 Jun 1;28(6):604-610. doi: 10.5551/jat.56531. Epub 2020 Sep 10.
Recent studies suggest that glucose-6-phosphate dehydrogenase (G6PD) deficiency, a genetically inherited condition causing hemolytic anemia, may be a risk factor for cardiovascular disease (CVD). We aimed to perform a retrospective case-control study in Sardinia taking advantage from clinical records of patients undergoing upper digestive endoscopy and screened for H. pylori infection.
A total of 9,604 patients with a known G6PD status and a complete clinical history, encompassing CVD, and leading CVD risk factors, including H. pylori infection, undergoing upper endoscopy between 2002 and 2017 were enrolled in this study.
Multivariate logistic regression analysis confirmed an increased CVD risk in subjects with G6PD deficiency [odd ratio (OR), 3.24; 95% confidence interval (CI) 2.44-4.30] after adjusting for potential confounders and effect modifiers, including H. pylori infection. Cardiovascular risk was similar in subjects with and without G6PD deficiency before age 60 (OR, 1.26; 95% CI 0.78-2.04, P=0.562), whereas it increased after age 60 in the former group (OR, 3.05; 95% CI 2.22-4.19, P＜0.0001) especially in males (OR 3.67; 95% CI 2.19-6.14) compared with females (OR, 2.96; 95% CI 1.89-4.64) by sex-specific logistic regression analysis.
The risk of CVD was greater in G6PD-deficient subjects after age 60, both in males and females, than those with normal enzyme activity, after adjusting for conventional CVD risk factors and H. pylori infection. The reduction of important protective mechanisms against oxidative stress in the elderly might explain the study findings.
最近的研究表明，葡萄糖-6-磷酸脱氢酶（G6PD）缺乏症是一种遗传性溶血性贫血病，可能是心血管疾病（CVD）的一个危险因素。我们旨在利用在 2002 年至 2017 年间接受上消化道内镜检查并筛查幽门螺杆菌感染的患者的临床记录，在撒丁岛进行一项回顾性病例对照研究。
共纳入 9604 例已知 G6PD 状态且具有完整临床病史的患者，包括 CVD 以及包括幽门螺杆菌感染在内的主要 CVD 危险因素，并接受了上消化道内镜检查。
多变量逻辑回归分析确认，在调整了潜在混杂因素和效应修饰剂（包括幽门螺杆菌感染）后，G6PD 缺乏症患者的 CVD 风险增加[比值比（OR），3.24；95%置信区间（CI）2.44-4.30]。在 60 岁之前，G6PD 缺乏症患者和无 G6PD 缺乏症患者的心血管风险相似（OR，1.26；95%CI 0.78-2.04，P=0.562），但前者在 60 岁后增加（OR，3.05；95%CI 2.22-4.19，P＜0.0001），尤其是男性（OR 3.67；95%CI 2.19-6.14）与女性（OR，2.96；95%CI 1.89-4.64）相比，通过性别特异性逻辑回归分析。
在调整了常规 CVD 危险因素和幽门螺杆菌感染后，与具有正常酶活性的患者相比，60 岁以上的 G6PD 缺乏症患者的 CVD 风险更高，无论男女均如此。在老年人中，对抗氧化应激的重要保护机制减少可能解释了研究结果。
