Premature infants receiving delayed cord clamping with and without cord milking: a randomized control trial.

BACKGROUND: Preterm infants often have long hospital stays and frequent blood tests; they often develop anemia requiring multiple blood transfusions. Placental transfusion via delayed cord clamping (DCC) or umbilical cord milking (UCM) helps increase blood volume. We hypothesized umbilical cord milking (UCM), together with DCC, would be superior in reducing blood transfusions. OBJECTIVES: To compare the effects of DCC and DCC combined with UCM on hematologic outcomes among preterm infants. METHODS: One hundred twenty singleton preterm infants born at 280/7- 336/7 weeks of gestation at Thammasat University Hospital were enrolled in an open-label, randomized, controlled trial. They were placed into three groups (1:1:1) by a block-of-three randomization: DCC for 45 s, DCC with UCM performed before clamping (DCM-B), and DCC with UCM performed after clamping (DCM-A). The primary outcomes were hematocrit levels and number of infants receiving blood transfusions during the first 28 days of life. Intraventricular hemorrhage (IVH) and necrotizing enterocolitis (NEC) were secondary outcomes. Analyses were performed with an intent-to-treat approach. RESULTS: One hundred twenty preterm infants were randomized. There was no statistically significant difference in neonatal outcomes; hematocrit on admission 54.0 ± 5.5, 53.3 ± 6.0, and 54.3 ± 5.8 (p = 0.88), receiving blood transfusions 25%, 20%, and 12.5% (p = 0.24), incidence of NEC 7.5, 0 and 10% (p = 0.78) in the DCC, DCM-B and DCM-A groups, respectively. There were no preterm infants with severe IVH, polycythemia, maternal or neonatal death. CONCLUSION: The placental transfusion techniques utilized, DCC and DCC combined with UCM, provided the same benefits for preterm infants born at GA 28 and 33 weeks in terms of reducing the need for RBC transfusions, severities of IVH and incidence of NEC without increasing comorbidity. TRIAL REGISTRATION: TCTR20190131002 . Registered 31 January 2019-Retrospectively registered.

Necrotizing fasciitis: a rare manifestation of late-onset neonatal group B streptococcal infection.

Preterm infants have a risk factor of developing late-onset group B streptococcal (GBS) infection. A 62-day-old infant who was a former 25-week male infant presented with fever and an erythematous, warm and tender, soft tissue swelling in the right submandibular region. He was diagnosed with cellulitis. Within 72 hours, his lesion had rapidly progressed to necrotizing fasciitis. His blood culture grew penicillin-sensitive GBS. This reported case illustrates necrotizing fasciitis as a rare manifestation of late-onset neonatal GBS infection.

Association between UGT 1A1 Gly71Arg (G71R) polymorphism and neonatal hyperbilirubinemia.

BACKGROUND: Neonatal hyperbilirubinemia is a common problem in neonates and affects 60% of Asian newborn babies which is twice that found in Caucasians. These findings suggest that a genetic factor might be involved. Recently, a relationship between polymorphisms of the bilirubin uridine 5-diphosphate-glucuronosyltransferase (UGTA1) gene and neonatal hyperbilirubinemia has been reported. It was demonstrated that the genetic variations cause a decrease in UGT1A1 activity in neonates, leading to an accumulation of unconjugated bilirubin in serum. However in Asians the G to A missense mutations in the UGTA1 at nucleotide 211 (known as G71R), were the predominant findings. Therefore, the impact of this polymorphism on serum bilirubin in healthy Thai neonates is of interest. OBJECTIVE: The aim of the present study was to investigate the frequency of UGT1A1 allele in healthy Thai neonates and to determine its role in neonatal hyperbilirubinemia. MATERIAL AND METHOD: A cross sectional study was conducted to investigate an association between the UGT1A1 G71R polymorphism and neonatal hyperbilirubinemia. Cord blood of 291 neonates was obtained to determine the gene frequency of UGT1A1 G71R by PCR-restriction fragment length polymorphism method. During the first 48 to 72 hours of the infants' life, the infants' blood was collected to measure their microbilirubin. RESULTS: PCR-RFLP analysis revealed the UGT1A1 G71R polymorphism in 42 infants (14.4%). In addition, six of this group (14.3%) had a microbilirubin level more than 95th percentile which was approximately 2.5 times more than those with the wild type allele (5.6%). The maximum microbilirubin level of infants in the R71 allele group was significantly higher than those in the G71 allele group, (11.79 +/- 3.34 mg/dL and 9.53 +/- 2.34 mg/dL, respectively p < 0.01). CONCLUSION: In the present study, the UGT1A1 G71R allele was found to be one of the risk factors for neonatal hyperbilirubinemia in Thai neonates.

Perinatal lethal osteogenesis imperfecta in a Thai newborn: the autopsy and histopathogical findings.

Osteogenesis imperfecta (OI) is an inherited disorder of type I collagen synthesis with an estimate incidence of I in 100,000 live births. Among all types, OI type II is the most severe type with perinatal death. The authors describes a male neonate with characteristic features of osteogenesis imperfect type II, including short crumpling limbs, beaded ribs, poorly bony ossification and blue sclera. Autopsy with histological study revealed not only multiple fractures, but pulmonary hypoplasia and intracerebral hemorrhages were also present. Both are the leading causes of death in the lethal type OI patients.

Genetic polymorphisms in Thai neonates with hyperbilirubinemia.

AIM: Polymorphisms of the UGT1A1 gene, SLCO1B1 gene and GST gene have been associated with significant hyperbilirubinemia. We would like to determine whether the variation of UGT1A1 gene, SLCO1B1 gene and GST gene may play a significant role in neonatal hyperbilirubinemia in Thai infants. METHODS: Ninety-one study subjects (hyperbilirubinemic group) and 86 control subjects were studied. RESULTS: The cause of neonatal hyperbilirubinemia could not be identified in 64 infants (70.3%), ABO blood group incompatibility in 14.3% and Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency in 8.8%. In the hyperbilirubinemic group, 23 of 91 (25.3%) infants demonstrated variant of UGT1A1 at nucleotides (nt) 211 as compared to 6 of 86 (7%) in the control group (p = 0.001). There were no significant differences between groups in the variants UGT1A1 at nt 686, SLCO1B1 gene at nt 388, 463 and the GST gene. Male infants with G-6-PD deficiency were associated with hyperbilirubinemia (21.2% vs. 4.8% in the control group) with an odds ratio (OR) of 5.37 (p = 0.02). The relationship between G-6-PD and variant in UGT1A1 gene at nt 211 could not be determined. CONCLUSION: Thai infants with variant in the UGT1A1 at nt 211 or with G-6-PD deficiency are at higher risk for developing neonatal hyperbilirubinemia.