Aim: 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.
Methods: 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.
Results: 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.
Conclusion: 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.
Keywords: Antioxidant defense; Cardiovascular disease; Glucose-6-phosphate dehydrogenase; Helicobacter pylori.