Background Oral zinc has been shown to reduce serum unconjugated bilirubin in animals, adolescents and low birth weight neonates. However, studies in healthy tenn neonates given oral zinc showed no reduction in hyperbilirubinemia based on time measurement in days. In order to improve accuracy, hyperbilirubinemia may be determined based on time measurements in hours.Objective To determine the effect of oral zinc on hyperbiliru-binemia in full term neonates, based on time measurement in hours, rather than days.Methods We conducted a randomized, double-blind clinical trial on healthy term neonates born spontaneously or through elective caesarean section in Hasan Sadikin Hospital from June to July 2010. Subjects were randomized into two groups: those receiving 5 mg of zinc sulphate and those receiving a placebo, sucrose, each twice daily. Serum total bilirubin level was examined at discharge and upon followup at day 5 of life. Factors which may be related to hyperbilirubinemia such as maternal age, infants' gender, umbilical cord bilirubin levels and type of feeding, were analyzed by Chi-square test. Hyperbilirubinemia persistence and comparison of survival distributions were analyzed by Kaplan-Meier survival analysis and Logrank test.Results Out of 60 subjects, 26 had hyperbilirubinemia. The mean duration of hyperbilirubinemia in the 15 subjects in the zinc group and 11 in the placebo group were 116.5 hours and 117.3 hours, respectively. There was no significant difference in hyperbilirubinemia duration between the two groups ( P=0.496, 95% CI 111.5 to 122.7). In addition, Chi-square analysis of factors which may be related to hyperbilirubinemia showed no significant difference between the two groups (P > 0.05).Conclusions Oral zinc 5 mg tMce daily made no significant difference in hyperbilirubinemia duration in full tenn neonates despite measuring in hours.
Probiotic bacteria will improve of immune deviation in infants born by cesarean delivery. A new effector T Cell subset that produces IL-17 has been identified. IL-23 promotes the expansion of antigen primed Th17 cells. The aim of this study is to find out the difference of IL-23 in breastfed infants born by cesarean delivery given probiotic formula and non probiotic Formula. Randomized open label clinical trial was performed on 96 healthy breastfed infants, birthweight ≥ 2500 g, born by cesarean delivery in Hasan Sadikin General Hospital Bandung. Fourty eight infants were breastfed combined with probiotic formula and 48 infants as control group. Daily notes were taken on duration of breastfeeding, the amount of milk formula given and any diseases up to fourth weeks. Plasma Il-23, determined by enzyme immunoassay technique at the fourth weeks of life. The duration of daily breastfeeding was not significantly different in both groups (p>0,05). None of the infants got ill during follow-up. The mean of IL-23 in group breasfeeding with probiotic and non probiotic formula were 1.59 (0,23) and 1.50 (0.29). It was significantly different (p< 0,05). Conclusion of this study: Il-23 was significantly different between infants receiving breastmilk with probiotic formula and non probiotic formula.
Neonatal hyperbilirubinemia (NH) is a common finding in newborn babies in Indonesia. Common and rare variants of UGT1A1 have been known to contribute to NH etiology. This study aims to identify UGT1A1 genetic variation and haplotype associated with NH in Indonesian population. DNA was isolated from 116 cases and 115 controls and a targeted-deep sequencing approach was performed on the promoter, UTRs, and exonic regions of UGT1A1. Determining association of common variants and haplotype analysis were performed using PLINK and Haploview. Ten and 4 rare variants were identified in cases and controls, respectively. The UGT1A1 rare variants frequency in cases (5.17%) was higher than that in controls (1.7%). Four of those rare variants in cases (p.Ala61Thr, p.His300Arg, p.Lys407Asn, and p.Tyr514Asn) and three in controls (p.Tyr79X, p.Ala346Val, and p.Thr412Ser) are novel variants. The frequencies of p.Gly71Arg, p.Pro229Gln, and TA7 common variants were not significantly different between cases and controls. A haplotype, consisting of 3 major alleles of 3′ UTRs common variants (rs8330C>G, rs10929303C>T, and rs1042640C>G), was associated with NH incidence (p = 0.025) in this population. Using targeted-deep sequencing and haplotype analysis, we identified novel UGT1A1 rare variants and disease-associated haplotype in NH in Indonesian population.
BackgroundNeonatal jaundice is a common finding in newborns in Asia, including Indonesia. In some cases, the serum total bilirubin levels exceeds the 95th percentile for hours of life (neonatal hyperbilirubinemia). Severe neonatal hyperbilirubinemia (NH) could lead to kernicterus and neonatal death. Glucose-6-Phosphage Dehydrogenase (G6PD) genetic variations and deficiency have been reported in several studies to be associated with NH. This study aimed to analyze the G6PD genetic variations and its activity in neonates with and without hyperbilirubinemia in the Deutromalay Indonesian population.MethodsDeoxyribose Nucleic Acid (DNA) was isolated from peripheral blood of 116 and 115 healthy term neonates with and without hyperbilirubinemia. All infants underwent the following laboratory examinations: routine hematologic evaluation, Coombs test, G6PD activity measurement using the Randox kit method, and serum total bilirubin level. All exons of the G6PD gene were targeted for deep sequencing using MiSeq (Illumina). An association study of G6PD polymorphisms with NH was performed using PLINK.ResultsThe prevalence of G6PD deficiency in neonates with and without hyperbilirubinemia in Indonesian Deutromalay population were 1.72% (95% Confidence Interval (CI): 0.6–4.1%) and 1.74% (95% CI: 0.7–4.1%), respectively. The most common G6PD polymorphisms, i.e. rs1050757/c.* + 357A > G, rs2230037/c.1311C > T, and rs2071429/c.1365-13 T/IVS11, were identified. However, none of those polymorphisms and their haplotype were associated with NH (p > 0.05, Odds Ratio (OR) ~1.00). The prevalence of G6PD mutations in neonates with and without hyperbilirubinemia were 6.8% (95% CI: 2.3–11.5%) and 6.9% (95% CI: 2.3–11.6%), respectively. The most frequently identified G6PD mutation was the Viangchan variant (p.V291 M), which was followed by the Canton (p.R459L) and Vanua Lava (p.L128P) variants. Two novel mutations were identified both in case (p.V369A, p.I167F) and control (p.L474=, p.I36T) groups.ConclusionThe prevalence of G6PD deficiency is low in neonates with or without hyperbilirubinemia in Deutromalay Indonesian population. The majority of G6PD mutations identified among Indonesian Deutromalay population in this study are Viangchan, Canton and Vanua Lava variants.
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