Glucose-6-phosphate dehydrogenase deficiency protects against coronary heart disease

Glucose-6-phosphate dehydrogenase deficiency protects against coronary heart disease
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DOI:
10.1007/s10545-008-0704-5
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发表时间:
2008-06-01
影响因子:
4.2
通讯作者:
Muntoni, Sa.
Muntoni, Sa.
中科院分区:
医学2区
文献类型:
--
作者:
Meloni, L.;Manca, M. R.;Muntoni, Sa.

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先前的研究表明,表达葡萄糖-6-磷酸脱氢酶(G6PD, EC 1.1.1.49)缺陷表型的受试者心血管风险降低。我们的目的是在表达G6PD缺陷型和野生型G6PD的男性受试者中验证这一假设。在一项病例对照研究中,我们检查了因急性心肌梗死或不稳定型心绞痛入院的连续患者,以及因非冠心病(CHD)诊断入院的对照组。G6PD表型是通过测量红细胞中酶活性来确定的,因为NADPH降低导致吸光度变化。采用无条件logistic回归评估与G6PD表型相关的冠心病风险。g6pd缺陷患者在病例中的发生率(11.8%)低于对照组(18.6%,p=0.002)。G6PD缺乏的遗传条件显著降低了冠心病的风险(OR=0.6; 95% CI 0.4 ~ 0.9)。我们证实了g6pd缺陷表型的受试者不容易患冠心病的假设。我们认为,这种保护作用可能归因于3-羟基-3-甲基戊二酰辅酶a还原酶(HMG-CoA R)活性的降低,类似于他汀类药物的作用,以及NADPH氧化酶活性的下调,从而导致氧自由基产生的减少。
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.