{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T05:58:33Z","timestamp":1780379913102,"version":"3.54.1"},"reference-count":45,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2008,4,4]],"date-time":"2008-04-04T00:00:00Z","timestamp":1207267200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Inher Metab Disea"],"published-print":{"date-parts":[[2008,6]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Previous studies suggest a reduction in cardiovascular risk among subjects expressing the glucose\u20106\u2010phosphate dehydrogenase (G6PD, EC 1.1.1.49) deficient phenotype. We aimed to test this hypothesis in male subjects expressing the G6PD\u2010deficient phenotype vs wild type G6PD. In a case\u2013control 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\u2010deficient subjects were less frequently represented among cases (11.8%) than among controls (18.6%, <jats:italic>p<\/jats:italic>=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\u2010deficient phenotype are less prone to CHD. We suggest that such a protective effect may be ascribable to a reduced 3\u2010hydroxy\u20103\u2010methylglutaryl\u2010coenzyme A reductase (HMG\u2010CoA R) activity, a statin\u2010like effect, as well as to a downregulation in NADPH oxidase activity with a consequent reduction in oxygen\u2010free radical production.<\/jats:p>","DOI":"10.1007\/s10545-008-0704-5","type":"journal-article","created":{"date-parts":[[2008,4,7]],"date-time":"2008-04-07T01:28:26Z","timestamp":1207531706000},"page":"412-417","source":"Crossref","is-referenced-by-count":59,"title":["Glucose\u20106\u2010phosphate dehydrogenase deficiency protects against coronary heart disease"],"prefix":"10.1002","volume":"31","author":[{"given":"L.","family":"Meloni","sequence":"first","affiliation":[{"name":"Department of Cardiovascular and Neurological Sciences, Heart Unit University School of Cagliari Cagliari Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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