Abstract
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzymopathy and in Sub-Saharan Africa, is a significant cause of infection- and drug-induced hemolysis and neonatal jaundice. Our goals were to determine the prevalence of G6PD deficiency among Nigerian children of different ethnic backgrounds and to identify predictors of G6PD deficiency by analyzing vital signs and hematocrit and by asking screening questions about symptoms of hemolysis. We studied 1,122 children (561 males and 561 females) aged 1 month to 15 years. The mean age was 7.4±3.2 years. Children of Yoruba ethnicity made up the largest group (77.5%) followed by those Igbo descent (10.6%) and those of Igede (10.2%) and Tiv (1.8%) ethnicity. G6PD status was determined using the fluorescent spot method. We found that the overall prevalence of G6PD deficiency was 15.3% (24.1% in males, 6.6% in females). Yoruba children had a higher prevalence (16.9%) than Igede (10.5%), Igbo (10.1%) and Tiv (5.0%) children. The odds of G6PD deficiency were 0.38 times as high in Igbo children compared to Yoruba children (p = 0.0500). The odds for Igede and Tiv children were not significantly different from Yoruba children (p = 0.7528 and 0.9789 respectively). Mean oxygen saturation, heart rate and hematocrit were not significantly different in G6PD deficient and G6PD sufficient children. The odds of being G6PD deficient were 2.1 times higher in children with scleral icterus than those without (p = 0.0351). In conclusion, we determined the prevalence of G6PD deficiency in Nigerian sub-populations. The odds of G6PD deficiency were decreased in Igbo children compared to Yoruba children. There was no association between vital parameters or hematocrit and G6PD deficiency. We found that a history of scleral icterus may increase the odds of G6PD deficiency, but we did not exclude other common causes of icterus such as sickle cell disease or malarial infection.
Highlights
Glucose-6-phosphate dehydrogenase (G6PD) deficiency affects some 400 million people worldwide and is the most common human enzymopathy [1]
G6PD is found in the cytoplasm of all cells and is responsible for the production of the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH), a coenzyme which maintains the intracellular pool of reduced glutathione and thereby protects cells against oxidative damage
In G6PD deficient children, pro-oxidant exposure can lead to a rapid imbalance in the redox status in red blood cells leading to hemolysis and resultant severe anemia, heart failure, and even death if not recognized early
Summary
Glucose-6-phosphate dehydrogenase (G6PD) deficiency affects some 400 million people worldwide and is the most common human enzymopathy [1]. G6PD is found in the cytoplasm of all cells and is responsible for the production of the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH), a coenzyme which maintains the intracellular pool of reduced glutathione and thereby protects cells against oxidative damage. Deficiency of G6PD impacts red blood cells, as they lack nuclei and mitochondria and must rely solely on G6PD for production of NADPH and reduced glutathione and protection from oxidative challenge. Many children with G6PD deficiency are healthy until they are exposed to a pro-oxidant medication or chemical. In G6PD deficient children, pro-oxidant exposure can lead to a rapid imbalance in the redox status in red blood cells leading to hemolysis and resultant severe anemia, heart failure, and even death if not recognized early
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