Risk Of Neonatal Hyperbilirubinemia Research Articles

The correlation between serum total bile acid and alanine aminotransferase of pregnant women and the disorders of neonatal hyperbilirubinemia-related amino acid metabolism

BackgroundTo explore the association between liver metabolism-related indicators in maternal serum and neonatal hyperbilirubinemia (NHB), and further investigate the predictive value of these indicators in NHB-related amino acid metabolism disorders.Methods51 NHB and 182 No-NHB newborns and their mothers who treated in the Fourth Hospital of Shijiazhuang from 2018 to 2022 were participated in the study. The differences in clinical data were compared by the Mann-Whitney U test and Chi-square test. Multivariate logistic regression was used to analyze the relationship between maternal serum indicators and the occurrence of NHB. The correlation analysis and risk factor assessment of maternal serum indicators with NHB-related amino acid metabolic disorders were performed using Spearman correlation analysis and multivariate logistic regression.ResultsCompared to the non NHB group, the NHB group had higher maternal serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), ALT/AST, and total bile acid (TBA), while lower levels of serum albumin (ALB), total cholesterol (TC) and high-density lipoprotein (HDL). The levels of alanine (ALA), valine (VAL), ornithine (ORN), and proline (PRO) in the newborns were reduced in NHB group, while arginine (ARG) showed a tendency to be elevated. Multiple logistic regression analysis showed that maternal ALT, AST, ALT/AST, and TBA levels were all at higher risk with the development of NHB, whereas ALB, TC, and HDL levels were negatively associated with NHB development. Increasing maternal TBA level was associated with lower ALA (r=-0.167, p = 0.011), VAL (r=-0.214, p = 0.001), ORN (r=-0.196, p = 0.003), and PRO in the newborns (r=-0.131, p = 0.045). Maternal ALT level was negatively associated with ALA (r=-0.135, p = 0.039), VAL (r=-0.177, p = 0.007), ORN (r=-0.257, p < 0.001), while ALT/AST was positively correlated with ARG (r = 0.133, p = 0.013). After adjustment for confounding factors, maternal serum TBA and ALT were the independent risk factor for neonatal ORN metabolic disorders [(adjusted odds ratio (AOR) = 0.379, 95%CI = 0.188–0.762, p = 0.006), (AOR = 0.441, 95%CI = 0.211–0.922, p = 0.030)]. Maternal ALT level was an independent risk factor for neonatal VAL metabolic disorders (AOR = 0.454, 95%CI = 0.218–0.949, p = 0.036).ConclusionsThe levels of high TBA, ALT, AST, and low HDL, TC of maternal were associated with the risk of NHB. Maternal TBA and ALT levels were independent risk factors for NHB-related amino acid disturbances which have value as predictive makers.

Genetic Association of UGT1A1 Promoter Variants (c.-3279T>G and c.-3156G>A) with Neonatal Hyperbili-rubinemia in an Iranian Population

Background: Several studies have reported that two promoter variants (c.-3279T>G and c.-3156G>A) in UDP-glucuronosyltransferase (UGT1A1) gene may contribute to neonatal hyperbilirubinemia. However, these variants have not been investigated in Iranian neonates. This cross-sectional study aimed to determine if the UGT1A1 promoter variants are significant risk factors associated with neonatal hyperbilirubinemia. Methods: A total of 178 unrelated neonates, including newborns with neonatal jaundice (n=95) and healthy controls (n=83), were included in this study. Each individual was genotyped by the PCR-RFLP and COP-PCR at nucleotides -3279 and -3156, respectively, using fresh blood DNA. Logistic regression analyses were performed to assess the association of UGT1A1 promoter variants with the presence of significant hyperbilirubinemia. Anthropometric indices and clinical variables were also compared between the different genotype groups. Results: Allele and genotype analysis of the c.-3279T>G and c.-3156G>A variants showed no significant association with the risk of neonatal hyperbilirubinemia neither in the crude nor after adjustment for gestational age, gender, and birth weight in different genetic models (P>0.05). However, in haplotype-association analysis, only one haplotype (A-T) was found to be associated with the risk of neonatal hyperbilirubinemia (OR=0.19, 95% CI; [0.18–0.20], P=0.001). Conclusion: This study failed to demonstrate that c.-3279T>G and c.-3156G>A variants alone might contribute to the risk of neonatal hyperbilirubinemia in Iranian neonates. However, the A-T haplotype may play a significant role in increasing the risk of hyperbilirubinemia.

Effect of delayed cord clamping on jaundice and hypoglycemia in the neonates of mothers with gestational diabetes mellitus

AbstractObjectiveTo study the effect of delayed cord clamping (DCC) on the bilirubin levels and hypoglycemia in neonates with diabetic mothers (NDMs).MethodsThis is a comparison between a prospective cohort and a historical control cohort. Women with gestational diabetes mellitus who performed DCC were enrolled into the prospective cohort (n = 156), and those who performed early cord clamping (ECC) were enrolled into the historical control cohort (n = 161).ResultsNDMs who received DCC had higher transcutaneous bilirubin than those in the ECC group whether maternal glycemic control was good or poor. DCC increased the rate of neonatal hyperbilirubinemia and phototherapy when maternal blood glucose was well controlled but not when it was poorly controlled. No differences were found in initial blood glucose levels on days 1 to 3 of life between the two groups.ConclusionDelayed cord clamping increased bilirubin levels, the risk of neonatal hyperbilirubinemia, and phototherapy in IDMs without improved initial blood glucose levels. Therefore, DCC was not recommended in NDMs.

Relation of Uridine Diphosphate Glucuronosyltransferase 1A1 Promoter Gene Polymorphism (211G>A) With Risk of Hyperbilirubinemia in Neonates

Background: The gene 211G>A variants, that underlie complex disorders, are characteristically common in the neonatal hyperbilirubinemia. However, it is the contribution of multiple different co-expressed susceptibility genes that individually confer a small increase in risk coupled with environmental factors that generate complex disorder phenotypes. Objective: This study aimed to understand the relation of 211G>A promoter polymorphism in UGT1A1 gene and the risk of hyperbilirubinemia in newborns. Patients and Methods: The study included 50 newborns with hyperbilirubinemia with gestation age of ≥ 37weeks and postnatal age of ≤ 2 weeks with normal birth weight. 34 were males and 16 were females. They were divided into two groups; case group consisting of 30 neonates with the peak of total serum bilirubin (TSB) levels ≥ 16 mg /dl and control group consisting of 20 neonates with the peak total serum bilirubin (TSB) levels A genotype can be used as a novel method to detect susceptibility to indirect hyperbilirubinemia in neonates. Conclusion: Our findings added to the understanding of the significance of UGT1A1 in association with neonatal hyperbilirubinemia in East Delta of Egyptian population. Additionally we are in need for other studies to investigate the protective mechanisms.

Relation of Uridine Diphosphate Glucuronosyltransferase 1A1 Promoter Gene Polymorphism (211G&gt;A) With Risk of Hyperbilirubinemia in Neonates

Background: The gene 211G>A variants, that underlie complex disorders, are characteristically common in the neonatal hyperbilirubinemia. However, it is the contribution of multiple different co-expressed susceptibility genes that individually confer a small increase in risk coupled with environmental factors that generate complex disorder phenotypes. Objective: This study aimed to understand the relation of 211G>A promoter polymorphism in UGT1A1 gene and the risk of hyperbilirubinemia in newborns. Patients and Methods: The study included 50 newborns with hyperbilirubinemia with gestation age of ≥ 37weeks and postnatal age of ≤ 2 weeks with normal birth weight. 34 were males and 16 were females. They were divided into two groups; case group consisting of 30 neonates with the peak of total serum bilirubin (TSB) levels ≥ 16 mg /dl and control group consisting of 20 neonates with the peak total serum bilirubin (TSB) levels A genotype can be used as a novel method to detect susceptibility to indirect hyperbilirubinemia in neonates. Conclusion: Our findings added to the understanding of the significance of UGT1A1 in association with neonatal hyperbilirubinemia in East Delta of Egyptian population. Additionally we are in need for other studies to investigate the protective mechanisms.

UGT1A1*28 gene polymorphism was not associated with the risk of neonatal hyperbilirubinemia: a meta-analysis

Background This study aimed to evaluate the relationship between UGT1A1*28 gene polymorphism and the risk of neonatal hyperbilirubinemia (NHBI). Methods The studies meet certain selection condition which was obtained from databases such as PubMed, Embase, and Cochrane Library. Newcastle-Ottawa Scale (NOS) was used to evaluate the quality of included studies. Meta-analysis was performed according to criteria such as country. Hardy–Weinberg’s equilibrium (HWE) tests were performed on the control group using chi-square test, while the evaluation index was represented by odds ratio (OR) and 95% confidence interval (CI). Egger’s test and sensitivity analysis were used to evaluate the publication bias and reliability, repetitively. Results Totally, four studies with high overall quality were enrolled in this study. No association was observed between UGT1A1*28 gene polymorphisms and NHBI in allele model (TA7 versus TA6, OR (95% CI) = 2.13 (0.81–5.62), p = .13), codominance models (TA7/6 versus TA6/6, OR (95% CI) = 2.94 (0.90–9.57), p = .07; TA7/7 versus TA6/6, OR (95% CI) = 2.08 (0.37–11.52), p = .40), recessive model (TA7/7 versus TA6/6 + TA7/6, OR (95% CI) = 1.44 (0.41–5.14), p = .57), and dominant model (TA7/7 + TA7/6 versus TA6/6, OR (95% CI) = 2.92 (0.84–10.12), p = .09). Furthermore, there was no publication bias found in current meta-analysis. Conclusions Gene polymorphism of UGT1A1*28 might not be associated with the risk of NHBI.

Neonatal morbidity in late preterm small for gestational age neonates

Introduction To compare neonatal respiratory morbidity among small for gestational age (SGA; birth weight less than 10th percentile for gestational age) versus appropriate for gestational age (AGA; BW at 10–90th percentile) neonates born in the late preterm period. Methods A secondary analysis of a multicenter randomized trial of antenatal corticosteroids for women at risk for late preterm birth. Singleton, nonanomalous, AGA or SGA births that delivered at 34–36 weeks were included. Women were excluded if they delivered after 37 weeks or had a large for gestational age baby (LGA; weight over 90th for gestational age). The primary outcome was a composite of any of the following: respiratory support by 72 h (continuous positive airway pressure or high flow nasal cannula ≥2 h, oxygen with a fraction of inspired oxygen of ≥30% for ≥4 h, extra corporeal membrane oxygenation or mechanical ventilation) or neonatal death. The secondary outcomes included several neonatal and maternal morbidities. Multivariable Poisson regression models were used to examine the association between neonatal weight and outcomes (using adjusted relative risk [aRR] and 95% confidence intervals [CI]). Results Of the 2831 women in the parent trial, 2315 (82%) women met inclusion criteria; among them, 426 (18%) of the neonates were SGA. There was no significant difference in the risk of the primary outcome between SGA and AGA (13.1 versus 15.1%, aRR 0.85, 95% CI 0.66–1.10). SGA, however, was associated with an increased risk for neonatal intensive care unit admission (68 versus 45%, aRR 1.60, 95% CI 1.47–1.74), hypothermia (12.2 versus 8.8%, aRR 1.36, 95% CI 1.01–1.83), feeding problems (47.2 versus 36.9%, aRR 1.24, 95% CI 1.07–1.45) and a decreased risk of neonatal hyperbilirubinemia (7.5 versus 12.7%, aRR 0.59, 95% CI 0.41–0.84), when compared to AGA. Conclusion In this cohort of late preterm birth, there was no significant difference in the rate of composite respiratory morbidity between SGA and AGA newborns.

Association between genetic polymorphism of heme oxygenase 1 promoter and neonatal hyperbilirubinemia: a meta-analysis

Objective: The association between a (GT)n dinucleotide length polymorphism in the promoter region of heme oxygenase 1 (HMOX1) and the risk of neonatal hyperbilirubinemia remains controversial. This meta-analysis was, therefore, performed with aims to examine the correlation between the HMOX1 (GT)n repeat length polymorphism and neonatal hyperbilirubinemia susceptibility.Materials and methods: We searched the databases including PubMed, Embase, Cochrane Library, China national knowledge infrastructure (CNKI), and Wanfang Data, with all reviewed studies published before 28 June 2018. After the evaluation of quality, we used RevMan to perform the meta-analyses. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to assess the effect of HMOX1 gene promoter polymorphisms on the risk of neonatal hyperbilirubinemia.Results: Seven studies, involving 584 patients with neonatal hyperbilirubinemia and 1655 controls, were included. A statistically significant association was found between the HMOX1 (GT)n repeat length polymorphism and risk of neonatal hyperbilirubinemia under the allele (allele S vs. allele L: OR = 1.81, 95% CI = 1.22–2.67, p = .003), recessive (genotype SS vs. genotypes LS + LL: OR = 1.38, 95% CI = 1.02–1.86, p = .04), dominant (genotypes SS + LS vs. LL: OR = 1.37, 95% CI = 1.01–1.76, p = .01), and homozygous genetic models (genotype SS vs. genotype LL: OR = 1.47, 95% CI = 1.02–2.11, p = .003), but not under the heterozygous genetic model. Interestingly, subgroup analysis revealed that the cutoffs of the S allele < 25 showed significant associations in any of the five genetic models (allele S vs. allele L: OR = 2.26, 95% CI = 1.68–3.05, p < .00001; genotype SS vs. genotypes LS + LL: OR = 2.56, 95% CI = 1.41–4.65, p = .002; genotypes SS + LS vs. genotype LL: OR = 1.82, 95% CI = 1.28–2.59, p = .0009; genotype SS vs. genotype LL: OR = 3.09, 95% CI = 1.50–6.36, p = .002; genotype LS vs. genotype LL: OR = 1.64, 95% CI = 1.11–2.42, p = .01); however, this association was not observed in the cutoffs of the S allele ≥25.Conclusion: The results of this study indicate that there is a significant association between the HMOX1 (GT)n repeat length polymorphism and susceptibility to neonatal hyperbilirubinemia. Newborns carrying shorter (GT)n repeats in the HMOX1 gene promoter may have a higher risk of neonatal hyperbilirubinemia.

Analysis of short-term clinical outcomes in 98 newborns with severe hyperbilirubinemia treated by peripheral arteriovenous synchronous exchange transfusion

Objective To study the type of disease, the optimal time and clinical effect of peripheral arteriovenous synchronous exchange transfusion in the treatment of newborns with hyperbilirubinemia. Methods The clinical data of admitted neonates with severe hyperbilirubinemia who received peripheral arteriovenous synchronous exchange transfusion were retrospectively analyzed from January 2015 to December 2016. Results Ninety-eight neonates were enrolled and the mean gestational age was(38.7±1.2)weeks, the mean birth weight was(3 275.1±483.7) grams, 76 cases were term infants, 20 cases were preterm infants and 2 cases were post term infants.The causes of hyperbilirubinemia included 39 cases of ABO incompatibility(39.8%), 16 cases of Rh incompatibility(16.3%), 3 cases of C3d incompatibility(3.1%), 2 cases of infection(2.0%), 2 cases of cranial hematoma(2.0%), 2 cases of adrenal hematoma(2.0%) and 34 cases of unknown hyperbilirubinemia(34.7%). The mean age of exchange transfusion was(5.8±4.4)days.Exchange transfusion removed 45.0% of total body bilirubin.After exchange transfusion, the total serum bilirubin, platelet level decreased as compared with those of pre-exchange levels, the differences were statistically significant(t=15.85, P<0.05; t=13.75, P<0.05). The white blood cell counts and hemoglobin increased, the differences were statistically significant(t=4.06, P<0.05; t=4.41, P<0.05). A total of 44 cases who had bilirubin encephalopathy were compared to other 54 cases who didn′t have bilirubin encephalopathy, there were no significant differences in fetal age, age of onset, bilirubin before and after blood exchange.There were significantly differences at time of exchange transfusion and the grade of hospital which the patient admitted at first time(t=2.46, P<0.05; t=6.15, P<0.05). Conclusion Hemorrhagic disease is the most important cause of neonatal severe hyperbilirubinemia.Clinical effect of peripheral arteriovenous synchronous exchange transfusion in the treatment of newborns with hyperbilirubinemia is obvious.Timely exchange transfusion can reduce the occurrence of bilirubinencephalopathy.For basic-level hospitals, it is still necessary to strengthen the implementation of hour-specific bilirubin to predict the risk of neonatal hyperbilirubinemia. Key words: Peripheral arteriovenous synchronous exchange transfusion; Hyperbilirubinemia; Bilirubin encephalopathy; Newborn

Association between rooming-in policy and neonatal hyperbilirubinemia

The practices promoted by the Baby-friendly Hospital Initiative have become a part of current mainstream postpartum infant care. Rooming-in to facilitate skin-to-skin contact and breastfeeding is a major component of this initiative. However, whether rooming-in is associated with admission for neonatal hyperbilirubinemia has seldom been reported. The aim of this study was to evaluate the association between rooming-in and neonatal hyperbilirubinemia. This was a retrospective cohort study. Term neonates were consecutively enrolled from the nursery of a medical center from January 2011 to December 2013. During the study period, rooming-in care was strongly encouraged according to the World Health Organization guidelines, if the parents agreed. The endpoint was defined as admission for phototherapy. Risk of neonatal hyperbilirubinemia in rooming-in neonates was calculated. Potential confounding factors, including exclusive breastfeeding, potential ABO incompatibility, Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency, and body weight loss (BWL), were adjusted by multiple logistic regression models. Totally, 3341 infants were enrolled in this study after excluding 40 infants admitted for other reasons. The rooming-in rate increased yearly during the study period. However, the rate of neonatal hyperbilirubinemia also increased simultaneously. The odds ratio (OR) of neonatal hyperbilirubinemia in the rooming-in group was 7.04 (95% CI, 4.41∼11.24). The rooming-in group demonstrated a higher percentage of exclusive breastfeeding and BWL >10% at 3 days of age. After adjusting for potential confounding factors, rooming-in was still a significant risk factor for neonatal hyperbilirubinemia (OR: 8.48; 95% CI: 5.04∼14.25). The practice of rooming-in is now part of the mainstream postpartum newborn care. However, the increased incidence of neonatal hyperbilirubinemia is a potential side effect of which healthcare providers should be aware. Further research is needed to confirm the role of rooming-in in neonatal hyperbilirubinemia.

Association of biliverdin reductase A gene polymorphisms with neonatal hyperbilirubinemia from Fujian area

Objective To assess the association of single nucleotide polymorphisms(SNPs)of biliverdin reductase A (BLVRA) with neonatal hyperbilirubinemia from Fujian area. Methods A total of 286 patients with neonatal hyperbilirubinemia and 250 healthy controls were enrolled.Genotypes of 5 SNPs within BLVRA gene including rs699512, rs1802846, rs7738, rs1637530 and rs2302032 were determined with matrix-assisted laser desorption ionization/time of flight mass spectrometer.The frequencies of genotype, allele, haplotype and their differentiations were analyzed. Results All 5 SNPs had conformed to Hardy-Weinberg equilibrium (all P>0.05). rs699512 and rs1637530 showed a significant difference between the 2 groups in both allelic and genotypic frequencies(all P 0.05). In recessive model, the frequency of rs699512 GG genotype of patients was significantly lower than that of the healthy control group(OR=0.494, 95%CI: 0.276-0.886, P=0.018), while in dominant model, the frequencies of rs699512 GG+ AG and rs1637530 TT+ CT genotype of patients were significantly lower than that of the healthy control group(OR=0.678, 0.627; 95%CI: 0.482-0.954, 0.444-0.885; P=0.026, 0.008). Based on linkage disequilibrium analysis and haplotype construction, rs1637530, rs2302032, rs699512 and rs1802846 locus in the same area.Based on haplotype CGAT, TGGT, CTAT and CGGT had significant differences between the 2 groups(all P<0.05), and could reduce the risk of high blood bilirubin(OR=0.588, 0.687, 0.501; 95%CI: 0.434-0.797, 0.496-0.952, 0.250-1.004). Conclusions rs699512 and rs1637530 may be associated with neonatal hyperbilirubinemia, A allele in rs699512 and C allele in rs1637530 may be associated with significantly increased risk of neonatal hyperbilirubinemia. Key words: Hyperbilirubinemia; Infant, newborn; Biliverdin reductase A gene; Single nucleotide polymorphism

Do triple test results predict risk for neonatal hyperbilirubinemia?

Objective:Neonatal jaundice is the most common condition that requires hospital admission and outpatient follow-up after discharge in neonates. The values of more than 17 mg/dL in term infants are accepted as neonatal significant hyperbilirubinemia. We aimed to define if there is any relationship between second trimester serum markers and neonatal severe hyperbilirubinemia to protect the neonates from its neurological damage.Methods:Total 1372 pregnant women were enrolled who had done triple test between April 2014 and 2015 and then given birth at our hospital. Our primary outcome was neonatal significant hyperbilirubinemia.Results:The mean age of our study population was 27.9±5.6. A total of 59 patients had babies with neonatal hyperbilirubinemia after exclusion of Rh incompatibility. We detected that the presence of in vitro pregnancy, maternal health problems or poor obstetric history had no effect on the risk for neonatal hyperbilirubinemia. Neonatal hyperbilirubinemia was related with low E3 levels. The ratios of AFP/E3 and hCG/E3 were the most helpful to predict the neonatal hyperbilirubinemia.Conclusions:According to our results, low E3 levels in the triple test result can be helpful to predict the development of the neonatal hyperbilirubinemia. However, this is a bit expensive and many developing countries may not afford it.

Prediction of neonatal hyperbilirubinemia by transcutaneous bilirubin nomograms

Objective To predict the risk of neonatal hyperbilirubinemia by transcutaneous bilirubin (TcB) nomograms and clinical risk factors. Methods Healthy term and late-preterm newborns (≥ 35 gestational weeks, and birth weight ≥ 2 000 g) born in Guizhou Maternal and Child Care Hospital between January 1, 2013 and December 31, 2013, were included. TcB levels were continuously recorded within 168 hours after birth. The value of hour-specific TcB nomogram combined with receiver operating characteristic (ROC) curves and Logistic regression model for predicting risk of hyperbilirubinemia was evaluated. Pearson's Chi-square test was also used for statistical analysis. Results A total of 5 250 cases were enrolled. TcB increased rapidly in the first 40 hours after birth, slowly increased between 40 to 96 hours, and reached a high level after 96 hours. Among them, the 95th percentile TcB stablized at 96 hours after birth. The 40th, 75th and 95th percentile TcB peak levels were 173, 217 and 248 μmol/L. Among the 5 250 neonates, there were 277 cases (5.3%) in the high-risk zone within 72 hours. The positive predictive value (PPV) was 22.02%; 1 087 cases (20.7%) and 1 854 cases (35.3%) were in the medium-high risk and medium-low risk zones along with the PPV of 10.58% and 3.72%, respectively. There were 2 032 cases (38.7%) in the low-risk zone with the PPV of 1.38%. Multivariate analysis showed that the TcB high-risk zone after 72 hours was associated with gestational age, delivery mode, feeding mode and TcB level of risk zones within 72 hours. Compared to those born at ≥40 gestational weeks, those born at ≥37-<40 gestational weeks were more likely in the TcB high-risk zone after 72 hours (OR=1.80, 95%CI: 1.29-2.51). The likelihood was reduced by 42% among neonates born with cesarean section compared to those delivered vaginally in term of the TcB high-risk zone after 72 hours. Infants who received mixed feeding were less likely to be in the TcB high-risk zone after 72 hours when compared to breast-fed infants (OR=0.51, 95%CI: 0.29-0.88). With the reduction of the high-risk zone level within 72 hours, the likelihood in the TcB high-risk zone after 72 hours was also decreased. ROC curve showed that the area under the curve (AUC) for predicting hyperbilirubinemia was 0.75 and its 95%CI was 0.72-0.78, with a sensitivity of 90.00% and specificity of 40.00%. The AUC of a combination of predictive results obtained by the Logistic regression model with significant variables in univariate analysis and high-risk zone after 72 hours was 0.66, and its 95%CI was 0.62-0.69. AUC estimated by Logistic regression model according to the TcB levels of risk zones within 72 hours combining with clinical risk factors was 0.79, and its 95%CI was 0.76-0.82 (P<0.01). Conclusions Hour-specific TcB nomograms of newborns in our hospital have been obtained, which facilitates the prediction and early intervention of neonatal hyperbilirubinemia. Key words: Hyperbilirubinemia, neonatal; Bilirubin; Risk factors; Forecasting

Early Neonatal Bilirubin, Hematocrit, and Glucose-6-Phosphate Dehydrogenase Status

To document the patterns of bilirubin and hematocrit values among glucose-6-phosphate dehydrogenase (G6PD)-deficient and G6PD-normal Nigerian neonates in the first week of life, in the absence of exposure to known icterogenic agents. The G6PD status of consecutive term and near-term neonates was determined, and their bilirubin levels and hematocrits were monitored during the first week of life. Infants were stratified into G6PD deficient, intermediate, and normal on the basis of the modified Beutler's fluorescent spot test. Means of total serum bilirubin (TSB) and hematocrits of the 3 groups of infants were compared. The 644 neonates studied comprised 353 (54.8%) boys and 291 (45.2%) girls and 540 (83.9%) term and 104 (16.1%) near-term infants. They consisted of 129 (20.0%) G6PD-deficient, 69 (10.7%) G6PD-intermediate, and 446 (69.3%) G6PD-normal neonates. The G6PD-deficient and G6PD-intermediate infants had higher mean TSB than their G6PD-normal counterparts at birth and throughout the first week of life (P < .001). Mean peak TSB levels were 14.1 (9.48), 10.2 (3.8), and 6.9 (3.3) mg/dL for G6PD-deficient, G6PD-intermediate, and G6PD-normal neonates, respectively. Peak TSB was attained on approximately day 4 in all 3 groups, and trends in TSB were similar. Mean hematocrits at birth were similar in the 3 G6PD groups. However, G6PD-deficient and -intermediate infants had higher declines in hematocrit, bilirubin levels, and need for phototherapy than G6PD-normal infants (P < .001). The G6PD-deficient and G6PD-intermediate neonates had a higher risk of neonatal hyperbilirubinemia and would therefore need greater monitoring in the first week of life, even without exposure to known icterogenic agents.

Relationship between the antigenic titer of anti-A(B) IgG in pregnant women and the incidence of hyperbilirubinemia in newborns

Objective To study the relationship between the antigenic titer of anti-A(B) IgG in pregnant women with blood-type O and the incidence of hyperbilirubinemia in newborns with blood-type A or B.Methods The antigenic titer of anti-A(B) IgG were determined in pregnant women with blood-type O whose blood type were incompatible with their mates'.Serological tests for the umbilical blood were analyzed in the neonates with blood-type A or B.The incidence and the pathogenic time of hyperbilirubinemia in newborns were studied by gravidity and test results.Results (1) There was no significant difference in the antigenic titer of anti-A(B) IgG,test results of umbilical blood and the incidence of hyperbilirubinemia between the first and the second pregnancy (P>0.05).(2) With the antigenic titer of anti-A(B) IgG increased,there was significant difference in the positive rate of antibody releasing test to newborns,positive rate of free antibody and the incidence of hyperbilirubinemia (P 0.05).Conclusion The gravidity is not correlative with the antigenic titer of anti-A(B) IgG and the incidence of hyperbilirubinemia in neonates.The risk of hyperbilirubinemia in neonates increases as the antigenic titer of anti-A(B) IgG in gravida ≥1∶32.The incidence of hyperbilirubinemia in neonates become higher as the antigenic titer of anti-A(B) IgG in their mother increasing,however,it has no influence on the onset time of hyperbilirubinemia in newborns. Key words: Gravidity; Newborns; Hyperbilirubinemia; ABO blood type

Breast-feeding, neonatal jaundice and kernicterus

Despite the many advantages of breast-feeding, there is ample documentation of the strong association between breast-feeding and an increase in the risk of neonatal hyperbilirubinaemia. Breast-fed infants have higher bilirubin levels than formula-fed infants. Suggested mechanisms for these findings include poor fluid and caloric intake, inhibition of hepatic excretion of bilirubin, and intestinal absorption of bilirubin (enterohepatic circulation). On rare occasions, breast-fed infants without evidence of haemolysis have developed extreme hyperbilirubinaemia and kernicterus. Because almost all of the cases of kernicterus reported in the last 15 years have occurred in fully or partially breast-fed newborns, it is important that these infants be followed closely. Appropriate support and advice must be provided to the lactating mother so that successful breast-feeding can be established and the risk of severe hyperbilirubinaemia reduced.

Risk of neonatal hyperbilirubinemia in babies born to ‘O’ positive mothers: A prospective cohort study

Hyperbilirubinemia in a neonate is one of the most common problems that may occur in 60-70 % of term and 80% of preterm babies. It is known to be associated with significant morbidity like neonatal bilirubin encephalopathy and even death. Clinically, and almost exclusively ABO incompatibility occur in 'A' and 'B' blood group babies of O '+ve' mothers. These babies are reported to be at high risk of severe hyperbilirubinemia (serum bilirubin level more than 16 mg/dl). To find out the incidence of hyperbilirubinemia in babies born to 'O' positive mothers. To estimate the risk of ABO incompatibility in babies born to 'O' positive mothers. A prospective cohort study conducted in B. P. Koirala institute of Health Science (Department of Pediatrics and Dept. of Gynae and Obstetric) from July 2002 to June 2003. A total of 199 women having 'O' positive blood group admitted to the Department of Gynae and Obstetric were included in the study. A piloted proforma was used to collect information. The blood group of neonates was tested by tile and slide method and serum bilirubin was estimated by diazo method in the Central Laboratory Services and Emergency laboratory of BPKIHS. The data was observed and analysis was carried out using statistical software SPSS-10. Total 37 (18.5%) babies had developed hyperbilirubinemia and among them 14 (38%) were from group of babies having 'O' Positive blood group and 23 (62%) were from group of babies having other than 'O' Positive blood group. There was 2.6 times higher chance of having hyperbilirubinemia in the babies with ABO incompatibility than 'O' Positive babies after adjusting other significant variables. Among different significantly associated variables, ABO incompatibility was found to be a major risk factor for neonatal hyperbilirubinemia.It was seen that neonate with ABO incompatibility had two times higher chances of having hyperbilirubinemia than those babies with O '+ve' blood group. This finding in BPKIHS suggests that there is a need of screening cord blood bilirubin and continuous monitoring of bilirubin level in the hospital especially among ABO incompatible neonates.