Incidence and risk factors of post-phototherapy neonatal rebound hyperbilirubinemia.

BACKGROUND: To determine the incidence and risk factors of post-phototherapy rebound hyperbilirubinemia because data about bilirubin rebound in neonates are lacking and few studies have concerned this condition. METHODS: A prospective observational study was conducted on 500 neonates with indirect hyperbilirubinemia who were treated according to standard guidelines. Total serum bilirubin (TSB) was measured at 24-36 h after phototherapy; significant bilirubin rebound (SBR) is considered as increasing TSB that needs reinstitution of phototherapy. RESULTS: A total of 124 (24.9%) neonates developed SBR with TSB increased by 3.4 (2.4-11.2) mg/dL after stopping phototherapy. Multiple logistic regression model revealed the following significant risk factors for rebound: low birth weight (B = 1.3, P <  0.001, OR 3.5), suspected sepsis (B = 2.5, P <  0.001, OR 12.6), exposure to intensive phototherapy (B =  0.83, P =  0.03, OR 2.3), hemolysis (B =  1.2, P <  0.001, OR 3.1), high discharge bilirubin level (B =  0.3, P =  0.001, OR 1.3), and short duration of conventional phototherapy (B =  - 1.2, P <  0.001, OR 0.3). CONCLUSIONS: SBR should be considered in neonates with hemolysis, low birth weight, suspected sepsis, short duration of conventional phototherapy, exposure to intensive phototherapy, and relatively high discharge TSB. These risk factors should be taken into account when planning post-phototherapy follow-up.

Anti-oxidant profiles and markers of oxidative stress in preterm neonates.

BACKGROUND: Preterm birth is associated with an increased oxidant burden which places these infants at a higher risk of injury. AIMS: This prospective study aimed to assess levels of antioxidants and a marker of oxidative stress in preterm neonates. OBJECTIVES: (i) To compare levels of anti-oxidants [vitamin A, vitamin E, catalase, total anti-oxidant status (TAS)] as well as malondialdehyde level (MDA) (a marker of lipid peroxidation) between preterm and full-term neonates; (ii) to determine changes in the values of measured vitamins at birth and at discharge among preterm neonates; and (iii) to compare levels of anti-oxidants with MDA levels in relation to complications of prematurity and outcome. METHODS: The study was undertaken in 100 preterm neonates and 100 full-term neonates as a control group. MDA was estimated by a thiobarbituric acid-reactive technique; TAS was determined using a Randox assay kit; catalase activity was measured spectrophotometrically and vitamin A and E levels were estimated by high performance liquid chromatography. RESULTS: The plasma levels of vitamin A, vitamin E, TAS and catalase were significantly lower in the preterm than in the full-term group (P < 0.01), and the plasma level of MDA was significantly higher in preterm than full-term neonates (P < 0.01). Vitamin A and E levels in preterm neonates were significantly higher at discharge than at birth (P < 0.01). Vitamin A, vitamin E and catalase levels at birth were significantly lower in patients who developed necrotizing enterocolitis or bronchopulmonary dysplasia than in those who did not. CONCLUSION: Preterm neonates are exposed to increased oxidant stress at birth and are susceptible to anti-oxidant deficiencies. A higher dose of enteral vitamin A supplementation in preterm neonates might reduce morbidity and improve outcome. Further studies are warranted to evaluate the appropriate dose of oral vitamin E supplementation for preterm neonates.

Relationship between angiotensin-converting enzyme gene polymorphism and respiratory distress syndrome in premature neonates.

OBJECTIVE: The aim of this study was to investigate the possible relationship between angiotensin-converting enzyme (ACE) gene polymorphism (D/D and I/D genotypes) and respiratory distress syndrome (RDS) in preterm neonates. STUDY DESIGN: Our study included 120 preterm neonates (<37 weeks of gestation) with RDS (the patient group) and 120 preterm neonates without RDS (the control group). Blood samples were obtained from patients and control groups, and ACE gene polymorphism was analysed using the polymerase chain reaction method. RESULTS: D/D genotype was highly significant in the patient group compared with the control group (48.3% of RDS group vs 20% of the control group, P < 0.001). Meanwhile, I/D and I/I genotypes were significantly higher in the control group (75% and 5% of the control group vs 50% and 1.7% of the patient group, P < 0.001). D/D genotype was highly significant in neonates with bronchopulmonary dysplasia (BPD) compared with I/D genotype (P = 0.001). CONCLUSION: Our results may suggest that D/D genotype is associated with increased risk of RDS and BPD development in preterm neonates.

Glutathione S-transferase gene polymorphisms in neonatal hyperbilirubinemia.

BACKGROUND: Glutathione S-transferases (GSTs) are a polymorphic superfamily of multifunctional enzymes known to play an important role in the detoxification of several substances. GSTM1 and GSTT1 are present in the liver in relatively high levels. Polymorphisms of the GSTM1 and GSTT1 genes may affect ligandin functions that are important in bilirubin transportation. OBJECTIVE: The aim of this study was to investigate the role of GSTM1 and GSTT1 gene polymorphisms as risk factors for neonatal jaundice. METHODS: This study was conducted on 72 neonates with pathologic hyperbilirubinemia (bilirubin >15 mg/dL) and 112 neonates with bilirubin level less than 15 mg/dL as a control group. GSTM1 and GSTT1 genotypes were assessed by multiplex polymerase chain reaction. RESULTS: GSTM1 null genotype was significantly higher in the patient compared with control groups (P = 0.005; odds ratio = 2.43; 95% confidence interval, 1.29-4.55) and was significantly associated with higher bilirubin levels compared with the wild genotype (P < 0.001). There was no statistically significant difference in the GSTT1 genotypes between the patient and the control groups. In the patient group, total bilirubin levels did not vary significantly among the null and wild GSTT1 genotypes (P = 0.108). CONCLUSIONS: Neonates with the GSTM1 null genotype are at high risk to develop pathologic hyperbilirubinemia and may have higher bilirubin levels.