Endocrine Abstracts

Introduction: The glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzyme deficiency in humans. In red blood cells, the pentose phosphate pathway is the only source of nicotinamide adenine dinucleotide (NADPH), and defense mechanisms against oxidative damage are highly dependent on G6PD activity. The occurrence of acute haemolysis in patient with G6PD deficiency and diabetes has been reported and ascribed to various mechanisms. Her we report a case of patient with G6PD deficiency that his diabetes was revealed by haemolysis crisis.

Case report: A 58-year-old man, who had a G6PD deficiency in its hemizygous form, treated with folic acid, was admitted for acute haemolysis following consumption of beans. He complained of fatigue, polyuria, blurred vision of one month. He had lost a weight and his body mass index was 30 kg/m². Physical examination was unremarkable. Plasma glucose concentration was 18 mmol/l and ketonuria was 2+. G6PD activity was decreased to 7% of the lowest normal value. The patient was treated with fluids and potassium replacement, and intravenous insulin. He rapidly recovered and good glycaemic control was obtained with subcutaneous insulin injection. After a 4-year follow-up, diabetes was controlled (mea capillary blood glucose 6 mmol/l, HbA1C 5.9%) with diet and insulin, and no relapses of haemolysis has occurred (blood haemoglobin 14.6 g/dL, total bilirubin 8 µmol/l). Also, He was treated for arterial hypertension with converting enzyme inhibitor, hydrochlorothiazide and bisoprolol, and for ischemic stroke with salicylic acid and statin.

Conclusion: Experimentally, hyperglycemia decreases the expression of the G6PD gene and the activity of his enzyme. Conversely, G6PD deficiency promotes oxidative stress and disrupts the secretion of insulin by beta cells. In subjects at risk of G6PD deficiency, hemolysis should be sought following diabetes decompensation. These two pathologies can worsen reciprocally. An etiological link between them is plausible.