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Br J Med Med Res ; 2016; 13(11): 1-6
Article in English | IMSEAR | ID: sea-182687

ABSTRACT

Background: Glucose-6-phosphate dehydrogenase (G6PD) is a key enzyme in the pentose phosphate pathway (PPP) and plays an essential role in the oxidative stress response by producing Nicotinamide adenine dinucleotide phosphate (NADPH), the main intracellular reductant. Deficient individuals suffer from mild chronic haemolytic episode which could be exacerbated on exposure to oxidant drugs. Aim: The aim of the study was to determine the prevalence of G-6-PD deficiency in Sokoto, assess liver function, lipid peroxidation and antioxidants status in G-6-PD deficient individuals. Place and Duration of Study: The study was undertaken at the Department of Chemical Pathology, Faculty of Medical Laboratory Sciences, Usmanu Danfodiyo University, Sokoto, Nigeria, between February and April 2015. Methods: G-6-PD screening in 1000 individuals (603 males and 397 females) using Methaemoglobin Reduction Method was carried out, liver function and oxidative stress biomarkers were then evaluated in 60 deficient individuals (30 males and 30 females) and 60 individuals with normal G-6-PD status as controls using standard techniques. Results: 376 (37.6%) subjects were found to be G-6-PD deficient, 128 (12.8%) of the males and 248 (24.8%) of the females screened were deficient. G-6-PD deficient individuals have significantly low (p<0.05) total protein (TP), aspartate transaminase (AST) and alkaline phosphatase activities when compared to control group but the decreases were within the reference range, while albumin (Alb), total bilirubin (TB) and conjugated bilirubin (CB), alanine transaminase (ALT) and alkaline phosphatase (ALP) values showed no significant difference (p > 0.05). Significantly high (p<0.001) malondialdehyde (MDA) and low total antioxidant potential (TAP) values were obtained in G-6-PD deficient individuals compared to controls. Conclusion: The prevalence of G-6-PD deficiency in Sokoto is high, hence screening for G-6-PD deficiency before administration of oxidant drugs in G-6-PD deficient subjects may be necessary. G-6-PD deficient individuals may also be at the risk of developing oxidative stress induced diseases.

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