The Combined Effect of Phototherapy and Phenobarbital on Serum Bilirubin Levels of Premature Infants

PEDIATRICS ◽  
1972 ◽  
Vol 49 (1) ◽  
pp. 110-112
Author(s):  
Michael G. Blackburn ◽  
Marcello M. Orzalesi ◽  
Penelope Pigram
Keyword(s):  
Premature Infants ◽  
Serum Bilirubin ◽  
Combined Therapy ◽  
Newborn Infants ◽  
Neonatal Hyperbilirubinemia ◽  
Combined Effect ◽  
Sufficient Evidence ◽  
Monochorionic Twins ◽  
Photo Oxidation ◽  
Prevention And Treatment

The effectiveness of phototherapy in the prevention and treatment of neonatal hyperbilirubinemia is well established. There is also sufficient evidence to indicate that phenobarbital is effective in decreasing serum bilirubin levels in newborn infants. Since light is thought to break down bilirubin in the skin by photo-oxidation, and phenobarbital is known to induce bilirubin conjugating activity in the liver, the possibility of an additive effect in combined therapy was investigated in the present study. Materials and Methods Six sets of premature identical (monochorionic) twins (33 to 35 weeks' gestation) were studied after obtaining parental permission. Each set of twins was admitted to the study at 12 hours of life if both infants were considered normal with the exception of prematurity.

scholarly journals Correlation between Neonatal Hyperbilirubinemia and Serum Magnesium and Copper Levels in Dhaka City

2020 ◽  
pp. 125-131
Author(s):  
Mohammad Anwar Hossain ◽  
Md. Ekramul Islam ◽  
Ashik Mosaddik ◽  
Md. Saiful Islam ◽  
Md. Nazmul Huda ◽  
...  
Keyword(s):  
Serum Bilirubin ◽  
Serum Magnesium ◽  
Colorimetric Method ◽  
Newborn Infants ◽  
Sulfanilic Acid ◽  
Neonatal Hyperbilirubinemia ◽  
P Value ◽  
Control Groups ◽  
Automated Method ◽  
Acid Reaction

Background: Neonatal hyperbilirubinemia is a condition when a newborn has an excessive amount of bilirubin in the blood and is one of the most prevalent problems in   neonates. Many studies reported that copper and magnesium play an important role in the pathogenesis and development of neonatal hyperbilirubinemia. Objectives: The aim of this study is to find out the correlation between the level of magnesium and copper with hyperbilirubinemia. Methodology: Serum bilirubin was assayed with colorimetric method by the use of diazotized sulfanilic acid reaction. A photometric automated method was used to determine the levels of magnesium and copper in the serum of neonates in both controls group (162) and cases group (220). Results: In the present study a significantly higher levels of Mg was found in hyperbilirubinemia of newborn infants when compared with control groups (23.67 ±2.33 mg/L versus 19.74 ±2.18 mg/L respectively and p value <0.001 which was significant) and correlation between hyperbilirubinemia and magnesium also significant (p value <0.001). Copper levels was significantly higher in hyperbilirubinemia of newborn infants (0.74 ±0.08 mg/L) compared with control groups (0.41 ±0.12 mg/L), where p value was <0.001, which was significant and correlation between hyperbilirubinemia and copper also significant (p value <0.001). Conclusion: It can be concluded that current study showed the concentrations of magnesium and copper levels were found to be significantly greater than control groups and may have a correlation with neonatal jaundice.

scholarly journals A Nanoceutical Agent for Chemoprevention of Bilirubin Encephalopathy

2021 ◽  
Author(s):  
Aniruddha Adhikari ◽  
Vinod K Bhutani ◽  
Susmita Mondal ◽  
Monojit Das ◽  
Soumendra Darbar ◽  
...  
Keyword(s):  
Serum Bilirubin ◽  
Mixed Valence ◽  
Newborn Infants ◽  
Neonatal Hyperbilirubinemia ◽  
Pharmacokinetic Data ◽  
List Type ◽  
Valence Transition ◽  
Bilirubin Encephalopathy ◽  
Sustainable Action

ABSTRACTBackgroundTargeted degradation of bilirubin in vivo may enable safer and more effective approach to manage incipient bilirubin encephalopathy consequent to severe neonatal hyperbilirubinemia (SNH). This report builds on the use of a spinel structured mixed-valence transition metal oxide (trimanganese tetroxide) nanoparticle duly functionalized with biocompatible ligand citrate (C-Mn3O4 NP) having the ability to degrade bilirubin without photo-activation.MethodThe efficiency of C-Mn3O4 NP in in vivo degradation of serum bilirubin and amelioration of severe bilirubin encephalopathy and associated neurobehavioral changes was evaluated in C57BL/6j animal model of SNH.ResultsOral single dose (0.25 mg kg-1 body weight) of the NPs efficiently reduced serum bilirubin levels (both conjugated and unconjugated) in study mice. It prevents bilirubin-induced neurotoxicity with reduction of SNH as observed by neurobehavioral and movement studies of SNH-mice. Pharmacokinetic data suggests intestinal reabsorption of the NPs and explain sustainable action. Biodistribution, pharmacokinetics, and biocompatibility of the NPs were tested during sub-chronic exposure.ConclusionThus, we report preliminary studies that explore an affordable chemoprevention mechanism to acutely prevent or minimize bilirubin neurotoxicity in newborn infants.IMPACT STATEMENTDespite several attempts, no pharmaco-therapeutics are available for the treatment of severe neonatal hyperbilirubinemia (SNH) and associated neurotoxicity.Our newly developed nanodrug, citrate functionalized Mn3O4 nanoparticles (C-Mn3O4 NPs), can efficiently ameliorate SNH and associated neurotoxicity as investigated in preclinical rodent model.Chemoprevention effect of the nanodrug is found to be safe and sustainable.If successfully translated into clinical trials, C-Mn3O4 NPs could become the first drug to treat SNH.

PREVENTION OF HYPERBILIRUBINEMIA OF PREMATURITY BY PHOTOTHERAPY

PEDIATRICS ◽  
1968 ◽  
Vol 41 (6) ◽  
pp. 1047-1054 ◽  
Author(s):  
Jerold Lucey ◽  
Mario Ferreiro ◽  
Jean Hewitt
Keyword(s):  
Premature Infants ◽  
Fluid Intake ◽  
Serum Bilirubin ◽  
Newborn Infants ◽  
Controlled Clinical Trial ◽  
Simple Method ◽  
Decomposition Products ◽  
Significant Difference ◽  
Photochemical Decomposition ◽  
The Ideal

The ideal treatment for hyperbilirubinemia of prematurity would be a safe and simple method for preventing its occurrence. In 1958 it was first demonstrated that serum bilirubin concentrations of newborn infants can be reduced by exposure to light. This treatment has not been widely used because of doubts as to its effectiveness and concern for the possible toxicity of the photochemical decomposition products of bilirubin. Recent experimental evidence indicates that these products are non-toxic. A controlled clinical trial has been carried out among 111 premature infants to test the effectiveness of artificial blue light in preventing hyperbilirubinemia of prematurity. Treated infants were placed in light from 12 to 144 hours of age and serial bilirubin determinations were carried out. The control (58 infants) and treated (53 infants) groups were comparable with respect to birth weight, gestational age, fluid intake, and weight loss. The results indicate a statistically significant difference between the groups. By taking advantage of this alternate route of elimination of bilirubin in the newborn infant, it should be possible to greatly reduce the need for exchange transfusion for hyperbilirubinemia of prematurity.

Neonatal hyperbilirubinemia prediction by cord blood and 24-hour serum bilirubin analysis

2020 ◽  
Vol 13 (3) ◽  
pp. 47-50
Author(s):  
Gurajala Chandra Sekhar ◽  
◽  
Radha Lavanya Kodali ◽  
Ramisetty Uma Mahesh ◽  
R Kedarnath ◽  
...  
Keyword(s):  
Cord Blood ◽  
Serum Bilirubin ◽  
Neonatal Hyperbilirubinemia

Oral Vitamin E Supplementation for the Prevention of Anemia in Premature Infants: A Controlled Trial

PEDIATRICS ◽  
1987 ◽  
Vol 79 (1) ◽  
pp. 61-68 ◽  
Author(s):  
A. Zipursky ◽  
E. J. Brown ◽  
J. Watts ◽  
R. Milner ◽  
C. Rand ◽  
...  
Keyword(s):  
Vitamin E ◽  
Premature Infants ◽  
Controlled Trial ◽  
Newborn Infants ◽  
Serum Vitamin ◽  
Hemoglobin Concentration ◽  
Erythrocyte Morphology ◽  
Significant Difference ◽  
Vehicle Treatment ◽  
Vitamin E Supplementation

Serum vitamin E levels are reduced in newborn infants. It has been reported that this deficiency is responsible, in part, for the development of anemia in premature infants during the first 6 weeks of life. The efficacy of vitamin E supplementation for the prevention of anemia in premature infants has been studied in a randomized, controlled, and blinded trial. Premature infants whose birth weights were less than 1,500 g were given, by gavage, 25 IU of dl-α-tocopherol or a similar volume of the drug vehicle. Treatment was continued for the first 6 weeks of life. A total of 178 infants were studied. Vitamin E levels were significantly higher in a supplemented group by day 3 and for the remainder of the 6-week period. At 6 weeks of age, there was no significant difference between the supplemented and unsupplemented groups in hemoglobin concentration, reticulocyte and platelet counts, or erythrocyte morphology. It is concluded that there is no evidence to support a policy of administering vitamin E to premature infants to prevent the anemia of prematurity.

Growth Hormone Response to Insulin–Induced Hypoglycemia in Newborn Infants

PEDIATRICS ◽  
1971 ◽  
Vol 48 (6) ◽  
pp. 998-999
Author(s):  
S. H. Reisner ◽  
M. Cornblath ◽  
Ronald W. Gotlin
Keyword(s):  
Growth Hormone ◽  
Premature Infants ◽  
Newborn Infants ◽  
Full Term ◽  
Growth Hormone Response ◽  
Hormone Response ◽  
Marked Rise ◽  
Hormone Levels

In the article by J. R. Humbert and R. W. Gotlin,1 the authors state that previous reports in which hypoglycemia was induced artificially with insulin demonstrated a variable growth hormone response. They then refer to the paper by Cornblath, et al.2 as reporting a failure to obtain a rise in growth hormone levels. This is incorrect as we found that insulin-induced hypoglycemia actually resulted in a very marked rise in growth hormone levels in both the full-term and premature infants tested.

Neonatal Hyperbilirubinemia and Physical and Cognitive Performance at 17 Years of Age

PEDIATRICS ◽  
1991 ◽  
Vol 88 (4) ◽  
pp. 828-833
Author(s):  
Daniel S. Seidman ◽  
Ido Paz ◽  
David K. Stevenson ◽  
Arie Laor ◽  
Yehuda L. Danon ◽  
...  
Keyword(s):  
Test Scores ◽  
Serum Bilirubin ◽  
School Achievement ◽  
Ethnic Origin ◽  
Full Term ◽  
Neonatal Hyperbilirubinemia ◽  
Intelligence Test ◽  
Coombs Test ◽  
Intelligence Test Scores ◽  
The Military

To estimate the effect of neonatal hyperbilirubinemia on long-term cognitive ability in full-term newborns with a negative Coombs test, we performed a 17-year historical prospective study of 1948 subjects. Intelligence tests and medical examinations performed at the military draft board were stratified according to serum bilirubin concentration. A logistic regression analysis was used to adjust for the confounding effects of gestational age, birth weight, Apgar score, ethnic origin, socioeconomic class, paternal education, birth order, and the administration of phototherapy and exchange transfusion. No direct linear association was shown between neonatal bilirubin levels and intelligence test scores or school achievement at 17 years of age. However, the risk for low intelligence test scores (IQ score &lt;85) was found to be significantly higher (P = .014) among full-term male subjects with serum bilirubin levels above 342 µmol/L (20 mg/dL) (odds ratio, 2.96; 95% confidence interval, 1.29-6.79). This association was not observed among female subjects. We conclude that severe neonatal hyperbilirubinemia, among full-term male newborns with a negative Coombs test, could be associated with lower IQ scores at 17 years of age.

Breast-Feeding and Hyperbilirubinemia in Full-Term Newborn Infants

PEDIATRICS ◽  
1985 ◽  
Vol 75 (3) ◽  
pp. 617-618
Author(s):  
CARLO CORCHIA ◽  
MARIA RUIU ◽  
MARCELLO ORZALESI
Keyword(s):  
Breast Feeding ◽  
Newborn Infants ◽  
Positive Association ◽  
Full Term ◽  
Neonatal Hyperbilirubinemia ◽  
Term Infants ◽  
Term Newborn ◽  
School Of Medicine

To the Editor.— Osborn et al1 have reported a positive association between breast-feeding and neonatal hyperbilirubinemia in full-term infants. To give further support to the findings of Osborn et al, we wish to report the results of two similar studies that have been completed in two different hospitals. The first study was carried out in the nursery of the Second School of Medicine of Naples.2 Rooming-in was practiced from 9 am to 12 pm, and during the day, breastfed babies were only offered a supplement of 5% dextrose in water when appropriate.

scholarly journals Intestinal NCoR1, a regulator of epithelial cell maturation, controls neonatal hyperbilirubinemia

2017 ◽  
Vol 114 (8) ◽  
pp. E1432-E1440 ◽  
Author(s):  
Shujuan Chen ◽  
Wenqi Lu ◽  
Mei-Fei Yueh ◽  
Eva Rettenmeier ◽  
Miao Liu ◽  
...  
Keyword(s):  
Acid Metabolism ◽  
Serum Bilirubin ◽  
Neonatal Hyperbilirubinemia ◽  
Intestinal Epithelial ◽  
Targeted Deletion ◽  
Bilirubin Encephalopathy ◽  
Intestinal Maturation ◽  
Immunohistochemistry Analysis ◽  
Developmental Maturation ◽  
Target Activation

Severe neonatal hyperbilirubinemia (SNH) and the onset of bilirubin encephalopathy and kernicterus result in part from delayed expression of UDP-glucuronosyltransferase 1A1 (UGT1A1) and the inability to metabolize bilirubin. Although there is a good understanding of the early events after birth that lead to the rapid increase in serum bilirubin, the events that control delayed expression of UGT1A1 during development remain a mystery. HumanizedUGT1(hUGT1) mice develop SNH spontaneously, which is linked to repression of both liver and intestinal UGT1A1. In this study, we report that deletion of intestinal nuclear receptor corepressor 1 (NCoR1) completely diminishes hyperbilirubinemia inhUGT1neonates because of intestinalUGT1A1gene derepression. Transcriptomic studies and immunohistochemistry analysis demonstrate that NCoR1 plays a major role in repressing developmental maturation of the intestines. Derepression is marked by accelerated metabolic and oxidative phosphorylation, drug metabolism, fatty acid metabolism, and intestinal maturation, events that are controlled predominantly by H3K27 acetylation. The control of NCoR1 function and derepression is linked to IKKβ function, as validated inhUGT1mice with targeted deletion of intestinal IKKβ. Physiological events during neonatal development that target activation of an IKKβ/NCoR1 loop in intestinal epithelial cells lead to derepression of genes involved in intestinal maturation and bilirubin detoxification. These findings provide a mechanism of NCoR1 in intestinal homeostasis during development and provide a key link to those events that control developmental repression of UGT1A1 and hyperbilirubinemia.

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