Abstract
The study aimed to explore the prevalence of glucose-6-phosphate dehydrogenase (G-6-PD) deficiency among male newborn infants in northeastern Thailand and its relationship with neonatal jaundice (NJ). This prospective cohort study included male newborn infants with gestational age (GA) ≥35 weeks born between July 1, 2019, and March 1, 2021. Cord blood was sent for G-6-PD fluorescent spot test (FST) and results were reported as normal, partial, or complete deficiency. Infants with NJ would have blood tested for total serum bilirubin (TSB) level and other possible causes of NJ. Duration of phototherapy, length of hospital stays, and complications were documented. There were 922 male infants included in this study with 854 (93.1%) term and 63 (6.9%) preterm infants. FST showed 132 infants (14.4%) had G-6-PD deficiency. Incidence of NJ was significantly higher among infants with G-6-PD deficiency compared with infants with normal G-6-PD level (47.7 vs. 25.8%; relative risk [RR]: 2.62, 95% confidence interval [CI]: 1.79-3.82; p < 0.001). Regardless of G-6-PD level, preterm infants had significantly higher incidence of NJ than term infants (52.4 vs. 27.3%; RR: 2.93, 95% CI: 1.75-4.92; p < 0.001). Duration of phototherapy was significantly longer in infants with G-6-PD deficiency with NJ but hospital stays were similar. Infants with combined G-6-PD deficiency and other causes of hemolysis did not have higher TSB level than infants with isolated G-6-PD deficiency. Risk factors associated with NJ were G-6-PD deficiency and preterm infants, whereas more advance GA was associated with reduced risk for NJ. G-6-PD deficiency and preterm infants were important risk factors for NJ. Routine G-6-PD screening, close monitoring for signs of NJ in infant with risks, and appropriate parental counseling should be implemented. · G-6-PD deficiency increases risk of neonatal jaundice.. · Preterm infants have higher risk for neonatal jaundice.. · G-6-PD deficiency does not link with severe jaundice..
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