SARS-CoV-2 Trigger in Severe Insulin Resistance With Acute Haemolytic Crisis in Diabetes and Glucose-6-phosphate Dehydrogenase Deficiency

Background: We report a case of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection as trigger for increased insulin resistance and severe haemolytic crisis in a male with type 2 diabetes mellitus and glucose-6-phosphate dehydrogenase (G6PD) deficiency. Clinical Case: A 64-year-old man (BMI 25kg/m2, weight 75kg) with past medical history of type 2 diabetes mellitus (on metformin and sitagliptin; glycated haemoglobin 51 mmol/mol, n<42mmol/mol), hypertension, G6PD deficiency and gout was admitted to hospital with COVID pneumonitis and type 1 respiratory failure giving 5 days’ history of cough, shortness of breath, fatigue and tiredness. As per hospital guidelines, the patient was treated with amoxicillin/clavulanate 625mg three times daily and doxycycline 100mg once daily. Hydroxycholoroquine was not given in view of G6PD deficiency. There was no evidence of diabetic ketoacidosis and a short-acting insulin sliding scale was initiated at 2U/hr. Continuous positive pressure ventilation was offered for next 72 hours, however the patient failed to improve and required transfer to intensive care unit for intubation and mechanical ventilation. Computer tomography scan of pulmonary artery excluded embolism. The patient was fed via nasogastric tube post intubation. On day 8, the patient experienced a sudden drop in haemoglobin levels from 132 g/dl on day 1 to 68 g/dl, requiring multiple blood transfusions. The blood results demonstrated evidence of haemolysis with a rise in total and direct bilirubin and lactate dehydrogenase levels. The peripheral blood smear showed numerous bite cells with polychromasia suggesting an acute haemolytic crisis in the context of G6PD deficiency. A medication review revealed no evidence of drug-induced haemolysis. Later the patient was started on dexamethasone 6mg once daily (day 11) and on remdesivir 100mg once daily (day 15). During this time, the patient’s insulin infusion requirements had progressively increased from 2U/hr to 8U/hr (equivalent to 192 units/24 hr). On day 22, the patient’s clinical condition deteriorated with septicaemia requiring extended course of antibiotics. At this time, continuous insulin infusion was stopped and intermediate acting insulin (insulatard 36U twice daily; later increased to 48U twice daily) was started. In the next 10 days, the patient made good clinical recovery from sepsis with stable haemoglobin and blood sugar levels. He was extubated and transferred for rehabilitation. The patient was successfully weaned off insulin in the community with optimal diabetes control. Conclusion: This is a case demonstrating the possible role of SARS-CoV-2 in increased insulin resistance and severe haemolytic crisis on background of diabetes and G6PD deficiency.