GLUCOSE-6-PHOSPHATE DEHYDROGENASE LEVELS IN ICTERIC NEONATES IN JOS

GLUCOSE-6-PHOSPHATE DEHYDROGENASE LEVELS IN ICTERIC NEONATES IN JOS

Abstract

Background: Glucose-6-phosphate dehydrogenase (G6PD) is a key regulatory enzyme in the
hexose monophosphate shunt with the major role of generating reduced nicotinamide adenine
dinucleotide phosphate (NADPH) to meet cellular needs for reductive biosynthesis and
maintenance of the cellular redox status. G6PD deficiency is a common inherited enzyme
disorder of mankind known to be associated with severe neonatal hyperbilirubinaemia that can
result in permanent neurologic damage or death. This study was aimed at estimating the level
of G6PD activity among icteric neonates, identifying G6PD deficient neonates, other associated
risks factors for development of hyperbilirubinaemia and its attendant complications in Jos.
Patients and Methods: One hundred and fifty icteric neonates made up of 92 (61.3%) males
and 58 (38.7%) females whose parents consented were consecutively enrolled as they presented
at the Special Care Baby Units (SCBU) of the Jos University Teaching Hospital (JUTH),
Bingham University Teaching Hospital (BhUTH), and the Plateau State Specialist Hospital
(PSSH), Jos, from March 2013 to February 2014. These subjects had their G6PD activity levels
assayed using the Pointe Quantitative Diagnostic Kit (USA). In addition, relevant clinical
information was obtained using a questionnaire, while relevant laboratory investigations were
carried out on the neonates and their mothers.
Results: The G6PD activity of the neonates studied ranged from 0.54-24.18 IU/gHb with a
mean activity of 8.02 ± 4.87 IU/gHb and a median activity of 7.19 IU/gHb. Sixty-one (40.7 %),
comprising of 45 males and 16 female neonates were G6PD deficient with mean G6PD activity
of 3.79 ± 1.37 IU/gHb while eighty-nine (59.3%) were G6PD normal with a mean G6PD
activity of 10.92 ± 4.24 IU/gHb. The mean haemoglobin concentration, haematocrit,
reticulocyte counts and mean serum bilirubin of the G6PD deficient neonates compared with
the G6PD normal neonates did not differ significantly. (P= 0.06, 0.56, 0.86 and 0.27
respectively). Treatment modality for hyperbilirubinaemia and the outcome showed no
significant difference between G6PD deficient and G6PD normal icteric neonates (P= 0.94,
0.97). ABO and Rh incompatibility in the proportion of 22.7% and 2.0% respectively, were the
other major haematological risk factors for neonatal hyperbilirubinaemia in this study after
G6PD deficiency.
Conclusion: The G6PD activity levels in icteric neonates in Jos vary widely with a relatively
high prevalence of G6PD deficiency. Determination of G6PD activity levels in icteric neonates
is therefore important for identification of those with G6PD deficiency, a major cause of
hyperbilirubinaemia in neonates in Jos. This will help to reduce morbidity and mortality
associated with severe hyperbilirubinaemia from this deficiency. In addition, it will assist in
policy making towards health education and increase public awareness on prevention of
haemolytic crisis and hyperbilirubinaemia from this disorder

GLUCOSE-6-PHOSPHATE DEHYDROGENASE LEVELS IN ICTERIC NEONATES IN JOS

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