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Glucose‐6‐phosphate dehydrogenase deficiency protects against coronary heart disease
Author(s) -
Meloni L.,
Manca M. R.,
Loddo I.,
Cioglia G.,
Cocco P.,
Schwartz A.,
Muntoni S.,
Muntoni Sa.
Publication year - 2008
Publication title -
journal of inherited metabolic disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 102
eISSN - 1573-2665
pISSN - 0141-8955
DOI - 10.1007/s10545-008-0704-5
Subject(s) - medicine , unstable angina , myocardial infarction , endocrinology , reductase , nadph oxidase , heart disease , phenotype , cardiology , biology , enzyme , biochemistry , oxidative stress , gene
Summary Previous studies suggest a reduction in cardiovascular risk among subjects expressing the glucose‐6‐phosphate dehydrogenase (G6PD, EC 1.1.1.49) deficient phenotype. We aimed to test this hypothesis in male subjects expressing the G6PD‐deficient phenotype vs wild type G6PD. In a case–control study we examined consecutive patients admitted for acute myocardial infarction or unstable angina, and controls admitted for diagnoses other than coronary heart disease (CHD). The G6PD phenotype was determined by measuring the enzyme activity in erythrocytes, as the absorbance rate change due to NADPH reduction. The CHD risk associated with the G6PD phenotype was assessed with unconditional logistic regression. G6PD‐deficient subjects were less frequently represented among cases (11.8%) than among controls (18.6%, p =0.002). The genetic condition of G6PD deficiency conveyed a significant reduction in CHD risk (OR=0.6; 95% CI 0.4 to 0.9). We confirm the hypothesis that subjects with the G6PD‐deficient phenotype are less prone to CHD. We suggest that such a protective effect may be ascribable to a reduced 3‐hydroxy‐3‐methylglutaryl‐coenzyme A reductase (HMG‐CoA R) activity, a statin‐like effect, as well as to a downregulation in NADPH oxidase activity with a consequent reduction in oxygen‐free radical production.