Clark M, Root R K
Yale J Biol Med. 1979 Mar-Apr;52(2):169-79.
The Mediterranean variant of glucose-6-phosphate dehydrogenase (G6PD) is functionally deficient and found in a variety of cell types of affected individuals, including both erythocytes and neutrophils. To determine if the presence of this sex-linked gene is associated to any degree with the occurrence of severe bacterial infection, a study of hospitalized male patients in Iran was undertaken. As determined by erythrocyte assay, allele prevalence in male patients with infection was 22% vs. 12% in a patient group matched for the absence of other risk factors for infection and 6% in a second group who had additional risk factors for infection. When the control and patient groups were considered together the difference between the frequency of G6PD deficiency (10.2%) was significantly different from that found in the infected patients (p less than .05). Furthermore, the mean age of infected patients with G6PD deficiency was significantly less than that of infected patients without G6PD deficiency or non-infected control groups. These data suggest that host defenses may be altered in G6PD deficiency so that bacterial infections are more severe. Alternatively, G6PD deficiency and infection might represent concomittant risk factors which lead to hospitalization during bacterial infection. Potential mechanisms by which host defenses might be altered in G6PD deficiency are discussed.
葡萄糖-6-磷酸脱氢酶(G6PD)的地中海变体功能存在缺陷,在受影响个体的多种细胞类型中都有发现,包括红细胞和中性粒细胞。为了确定这种性连锁基因的存在是否在任何程度上与严重细菌感染的发生有关,对伊朗住院男性患者进行了一项研究。通过红细胞检测确定,感染男性患者的等位基因患病率为22%,而在没有其他感染风险因素的匹配患者组中为12%,在有额外感染风险因素的第二组中为6%。当将对照组和患者组合并考虑时,G6PD缺乏症的频率差异(10.2%)与感染患者中的频率差异显著不同(p小于0.05)。此外,患有G6PD缺乏症的感染患者的平均年龄明显低于没有G6PD缺乏症的感染患者或未感染的对照组。这些数据表明,G6PD缺乏症可能会改变宿主防御,从而使细菌感染更严重。或者,G6PD缺乏症和感染可能代表导致细菌感染期间住院的伴随风险因素。文中讨论了G6PD缺乏症中宿主防御可能改变的潜在机制。