Department of Diabetology, hôpital Cochin, AP-HP, université Paris Descartes, France.
Diabetes Metab. 2011 Feb;37(1):79-82. doi: 10.1016/j.diabet.2010.09.004. Epub 2010 Dec 13.
Epidemiological data suggest that glucose-6-phosphate dehydrogenase (G6PD) deficiency may be a risk factor for diabetes. Also, the occurrence of haemolysis in the context of diabetes crises has been reported in patients with G6PD deficiency. A unifying hypothesis could explain these associations.
We report two patients in whom haemolytic crises occurred soon after acute diabetes decompensation, and revealed G6PD deficiency. We have reviewed the mechanisms that may link the two diseases.
One patient was admitted for decompensated ketosis-prone type-2 diabetes (KPT2D), but no acidosis, and was treated with insulin, then metformin and glibenclamide. The second patient had type-1 diabetes and ketoacidosis treated with insulin. Haemolytic crises were recognized 8 and 4 days after admission, respectively, and G6PD deficiency was confirmed in both patients. These patients and the other published cases share, as a unique characteristic, the occurrence of haemolysis after diabetes decompensation, whatever the treatment or associated conditions. Experimental data show that hyperglycaemia can reduce expression of the G6PD gene and activity of the enzyme. Conversely, G6PD deficiency can promote oxidative stress and impairment of insulin secretion by beta cells.
In patients at risk of G6PD deficiency, the possibility of haemolysis should be explored in case of diabetes crisis. In African patients with KPT2D diabetes, potentially oxidative hypoglycaemic agents should be avoided in the remission phase of the disease. G6PD deficiency and diabetes can aggravate each other, and diabetes could be aetiologically associated with G6PD deficiency.
流行病学数据表明葡萄糖-6-磷酸脱氢酶(G6PD)缺乏可能是糖尿病的一个风险因素。此外,在 G6PD 缺乏症患者的糖尿病危象中也有溶血的发生报道。一个统一的假说可以解释这些关联。
我们报告了两例患者,他们在急性糖尿病失代偿后不久发生了溶血性危象,并发现了 G6PD 缺乏症。我们回顾了可能将这两种疾病联系起来的机制。
一名患者因酮症倾向 2 型糖尿病(KPT2D)失代偿入院,但没有酸中毒,并用胰岛素治疗,然后用二甲双胍和格列本脲治疗。第二例患者患有 1 型糖尿病和酮症酸中毒,用胰岛素治疗。溶血性危象分别在入院后 8 天和 4 天被发现,两名患者均被证实存在 G6PD 缺乏症。这些患者和其他已发表的病例有一个共同的特点,即在糖尿病失代偿后发生溶血,无论治疗或相关情况如何。实验数据表明,高血糖可降低 G6PD 基因的表达和酶的活性。相反,G6PD 缺乏可促进氧化应激和β细胞胰岛素分泌受损。
在 G6PD 缺乏症风险患者中,如果发生糖尿病危象,应探讨发生溶血的可能性。在 KPT2D 糖尿病的非洲患者中,在疾病缓解期应避免使用可能引起氧化的低血糖药物。G6PD 缺乏症和糖尿病可以相互加重,糖尿病可能与 G6PD 缺乏症有病因学关联。