Abstract

Glucose 6 phosphate dehydrogenase (G6PD) is a housekeeping enzyme critical in the redox metabolism. In red blood cells, it is the only source of Nicotinamide adenine dinucleotide phosphate hydrogen(NADPH) that act directly and via glutathione defends these cells against oxidative stress. Dengue infection as like other infections can trigger intravascular haemolysis in G6PD deficiency patients. We have reported a 17 year old boy with G6PD deficiency presented with dengue fever which was complicated by acute haemolysis, methaemoglobinemia, hepatitis and rhabdomyolysis.

Highlights

  • Glucose 6 phosphate dehydrogenase (G6PD) is a housekeeping enzyme critical in the redox metabolism[1]

  • Severe intravascular haemolysis in G6PD deficiency can lead to acute renal failure via a multitude of mechanisms including deposition of iron in the kidneys[6,7]

  • There is no clear association between G6PD deficiency and dengue severity or viral replication in general[8], dengue infection, like other infections, can trigger intravascular haemolysis in patients with G6PD deficiency

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Summary

Introduction

Glucose 6 phosphate dehydrogenase (G6PD) is a housekeeping enzyme critical in the redox metabolism[1]. A 17-year-old Sri Lankan Tamil boy with G6PD deficiency was referred to the medical casualty on day two of a febrile illness with positive Nonstructural protein 1(NS1) antigen for dengue. The patient developed cyanosis of his nail beds with headache and oxygen saturation on ambient air was noted to be low (88%) without any lung signs., A possibility of methaemoglobinaemia was considered and spectroscopic examination of blood for methaemoglobin levels confirmed methaemoglobinaemia with a value of. The disproportionate rise of AST compared to ALT, could be explained by tissue hypoxia possibly due to methaemoglobinaemia Even though he had ultrasonographic evidence of fluid leakage into the pleural space on day 4 of the illness his blood pressure, pulse pressure and urine output were well within normal range throughout the course of the illness. Indicating a reduction of metheamoglobineamia and it was confirmed by a repeat methaemoglobin level of 2%

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