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.

Use of lung ultrasound in detection of complications of respiratory distress syndrome.

Repeated chest radiography is required for the diagnosis and follow-up of neonates with respiratory distress syndrome (RDS) and carries the risk of radiation hazards. Lung ultrasound (LUS) is a non-invasive bedside diagnostic tool that has proven to be effective in the diagnosis of RDS. Our aim was to assess the role of LUS with respect to the standard chest X-ray (CXR) in the detection of complications of RDS in neonates. Ninety premature newborns of both genders with RDS (mean gestational age = 29.91 ± 1.33 wk) and 40 premature babies as a control group were involved in this study. All patients underwent initial clinical assessment as well as CXR and LUS. Those who presented with respiratory distress and/or exhibited deterioration of oxygenation parameters were followed by CXR and, within 4 h, by LUS. Alveolo-interstitial syndrome and pleural line abnormalities were detected in all cases (100%) in the initial assessment, patchy consolidation was detected in 34 cases and white lung was detected in 80 cases. Alveolo-interstitial syndrome was detected in 19 controls. In follow-up of the patients, LUS was superior to CXR in detection of consolidation and sub-pleural atelectasis, but not in detection of pneumothorax. We concluded that bedside LUS is a good non-hazardous alternative tool in the early detection and follow-up of RDS in the neonatal intensive care unit; it could be of value in reducing exposure to unnecessary radiation.

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.

Empirical antibiotic treatment and the risk of necrotizing enterocolitis and death in very low birth weight neonates.

BACKGROUND AND OBJECTIVES: Antibiotics are one of the most overused drugs in the neonatal unit. Our objective was to assess associations between the duration of the initial antibiotic course and subsequent necrotizing enterocolitis (NEC) and/or death in very low birth weight (VLBW) neonates with sterile initial postnatal culture results. DESIGN AND SETTING: A retrospective cohort analysis of VLBW neonates admitted to a tertiary center during the period from 1 January 2008 to 31 december 2009. PATIENTS AND METHODS: The study included VLBW neonates who had been inborn and admitted to the neonatal intensive care unit within the first 24 hours after birth. We used descriptive statistics to characterize the study population, and multivariate analyses to evaluate associations between therapy duration, prolonged empirical therapy, and subsequent NEC and/or death. RESULTS: Of 328 VLBW neonates admitted to our center, 207 (63%) survived >5 days and received initial empirical antibiotic treatment for ≥5 days. The median duration of initial empirical antibiotic therapy was 7 days (range 5-10 days). those neonates were more likely to be of younger gestational age, lower birth weight, and to have lower Apgar scores (P<.001, .001 and .017, respectively). each empirical treatment day was associated with increased odds of death (or 1.45, CI 1.24-1.69), NEC (or 1.32, CI 1.05-1.65), and the composite measure of NEC or death (or 2.13, CI 1.55-2.93). CONCLUSION: The use of prolonged initial empirical antibiotic therapy in VLBW neonates with initial sterile culture results may be associated with an increased risk of NEC or death and should be used with caution.

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.

The role of PTPN22 gene polymorphism in childhood immune thrombocytopenic purpura.

Immune thrombocytopenia is an autoimmune disorder characterized by antibody-mediated platelet destruction. A protein tyrosine phosphatase (PTPN22) present in lymphocytes is an important negative regulator of signal transduction for the T-cell receptor-MHC complex and has been associated with autoimmune disorders that produce autoantibodies. The present study investigated the frequency of the 1858C>T single-nucleotide polymorphism (SNP) in the PTPN22 gene in idiopathic thrombocytopenic purpura (ITP) patients. This case series study included 50 children with ITP, 24 acute and 26 chronic cases, and 50 normal children as a control group. All were subjected to clinical history and laboratory investigations including complete blood count, genotyping of PTPN22 1858C/T SNP by polymerase chain reaction-restriction fragment length polymorphism and platelet antibodies using platelets suspension immunofluorescence test for the cases. Thirteen patients (26%) were positive for the PTPN22 1858C>T SNP. Three patients were homozygous for the mutation and 10 were heterozygous. Comparison of the 26% of the ITP patients who were positive for the PTPN22 1858C>T mutation with the 6% positive in the control group yielded a P value of 0.006. Antiplatelet antibodies were detected in five patients (20.8%) with acute ITP and in three patients (11.5%) with chronic ITP; no significant association between the presence of PTPN22 1858C>T mutation and the presence of antiplatelet antibodies was detected. The prevalence of PTPN22 gene mutation was higher in ITP patients, thus it may be considered as a genetic risk factor in the development of ITP in Egyptian children.

Glucose-6-phosphate dehydrogenase and red cell pyruvate kinase deficiency in neonatal jaundice cases in egypt.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency can lead to acute hemolytic anemia, chronic nonspherocytic hemolytic anemia, and neonatal jaundice. Neonatal red cell pyruvate kinase (PK) deficiency may cause clinical patterns, ranging from extremely severe hemolytic anemia to moderate jaundice. The authors aimed at studying the prevalence of G6PD and PK deficiency among Egyptian neonates with pathological indirect hyperbilirubinemia in Cairo. This case-series study included 69 newborns with unconjugated hyperbilirubinemia. All were subjected to clinical history, laboratory investigations, e.g., complete blood counts, reticulocytic counts, direct and indirect serum bilirubin levels, Coombs tests, qualitative assay of G6PD activity by methemoglobin reduction test, and measurement of erythrocytic PK levels. The study detected 10 neonates with G6PD deficiency, which means that the prevalence of G6PD deficiency among Egyptian neonates with hyperbilirubinemia is 14.4% (21.2% of males). G6PD deficiency was significantly higher in males than females (P = .01). The authors detected 2 cases with PK deficiency, making the prevalence of its deficiency 2.8%. These data demonstrate that G6PD deficiency is an important cause for neonatal jaundice in Egyptians. Neonatal screening for its deficiency is recommended. PK deficiency is not a common cause of neonatal jaundice. However, this needs further investigation on a larger scale.