Executive Summary

PEDIATRICS ◽  
1985 ◽  
Vol 75 (2) ◽  
pp. 385-386

A randomized, controlled study of phototherapy for neonatal hyperbilirubinemia was supported by the National Institute of Child Health and Human Development between 1974 to 1976. The study included 672 infants receiving phototherapy and 667 control infants. Phototherapy was effective in preventing hyperbilirubinemia in low-birth-weight infants (<2,000 g) who were placed under daylight fluorescent lights at 24 ± 12 hours of life for 96 hours. In this weight group, the number of exchange transfusions that were required due to hyperbilirubinemia was significantly lower in infants receiving phototherapy (4.1%) than in control infants (24.4%, P < .001). This was true even in infants with hemolysis and may be related to the fact that light treatment was initiated well before the development of hyperbilirubinemia. Phototherapy was effective in controlling hyperbilirubinemia in infants of birth weight 2,000 to 2,499 g when initiated after serum bilirubin concentration had risen above 10 mg/dL (mean 12.3 ± 1.9 mg/dL), as well as in infants with birth weight greater than 2,500 g whose serum bilirubin level had risen above 13 mg/dL (mean 15.7 ± 2.5 mg/dL) and in whom there was no hemolytic disorder. Light therapy instituted at these high levels of serum bilirubin did not effectively control hyperbilirubinemia in these two groups if hemolysis was present. Black infants responded to phototherapy as well as the nonblack infants. Phototherapy was most effective in the first 24 to 48 hours of its use. The pattern of declining efficacy after 48 hours is consistent with the thesis that unstable bilirubin isomers (photobilirubin) formed during the light treatment revert to natural bilirubin in the intestine following hepatic excretion and are reabsorbed via the enterohepatic circulation and contribute again to the bilirubin load to be cleared by the liver.

PEDIATRICS ◽  
1972 ◽  
Vol 50 (1) ◽  
pp. 165-165
Author(s):  
Orestes S. Valdes ◽  
Harold M. Maurer ◽  
Clare N. Shumway

The study by Blackburn and associates, showing the lack of additive effect of phenobarbital when used in combination with phototherapy in lowering the serum bilirubin concentration in one identical twin in each of six sets, eliminates the possible interference of genetic background on bilirubin metabolism. As part of a larger study, we have previously presented and reported similar results in a controlled study of 75 low birth weight infants of a predominantly Negro population. Members of each of our therapy groups (phenobarbital, light, phenobarbital and light, no therapy) were comparable with respect to birth weights and initial serum bilirubin concentrations, and were kept in similar environments, although their genetic backgrounds were dissimilar.


PEDIATRICS ◽  
1985 ◽  
Vol 76 (3) ◽  
pp. 351-354
Author(s):  
L. S. de Vries ◽  
S. Lary ◽  
L. M.S. Dubowitz

During a 4-year period, 12 premature infants, all less than 34 weeks of gestation and all with a bilirubin level above 240 µmol/L (14 mg/dL) were determined to have bilateral sensorineural deafness. In order to investigate how far the hyperbilirubinemia or any associated factor might have been a causative factor, all infants of 34 weeks of gestation or less who had a serum bilirubin level above 240 µmol/L were investigated. For a period of 4 years, 99 infants meeting these criteria were classified as high risk or low risk on the basis of perinatal risk factors. Eight of the 22 high-risk infants with birth weight less than 1,500 g, but only two of 43 high-risk infants with birth weight greater than 1,500 g were deaf (P < .05). The deaf infants were also matched with infants of normal hearing who had similar bilirubin levels and the same number of adverse perinatal factors. The mean duration of hyperbilirubinemia was significantly longer in the deaf infants (P < .02), and they appeared to have a greater number of acidotic episodes while they were hyperbilirubinemic. These findings suggest that in healthy preterm infants with birth weight greater than 1,500 g, high bilirubin levels carry little risk, whereas a serum bilirubin level greater than 240 µmol/L in highrisk preterm infants with birth weight of 1,500 g or less is associated with a high risk of deafness.


PEDIATRICS ◽  
1978 ◽  
Vol 62 (4) ◽  
pp. 460-464 ◽  
Author(s):  
Mark A. Pearlman ◽  
Lawrence M. Gartner ◽  
Kwang-sun Lee ◽  
Rachel Morecki ◽  
Dikran S. Horoupian

A review of 34 autopsied infants weighing 2,250 gm or less who died on the third to seventh days of life during the six-year period from 1971 through 1976 failed to reveal any cases of kernicterus. This contrasts with an incidence of 64% in low-birth-weight infants selected in the same manner from the same neonatal intensive care unit-premature center during the period 1966 and 1967. The 34 infants in the 1971-1976 series were not significantly different with regard to their birth weights, Apgar scores, perinatal complications, or pathologic findings, other than their lack of kernicterus, from the 14 infants in the 1966-1967 series. The only significant difference between these two groups of infants was a lower mean peak serum bilirubin concentration in the 1971-1976 series, corresponding with the establishment in 1970 of a more aggressive policy of exchange transfusion and phototherapy. The prevention of excessive hyperbilirubinemia along with the development of more sophisticated intensive care of the neonate in recent years may be responsible for the elimination of kernicterus in the 1971-1976 series of infants.


2017 ◽  
Vol 19 (3-4) ◽  
pp. 63
Author(s):  
H.E. Monintja ◽  
B. Wirastari ◽  
N. Kadri ◽  
A. Aminullah ◽  
S. Muslichan

This study revealed the incidence of neonatal jaundice in the Dr. Cipto Mangunkusumo Hospital Jakarta to be 32.1%, i.e 42.97% in low birth weight infants and 29.70% in fulllerm infants. No pathological basis was proven in many cases. The factors which may cause pathological jaundice according to the frequency are as follows: infections, anoxia and hypoxia, hemolysis due to G6PD deficiency, multiple factors and hypoglycemia etc. This study also revealed that 69.5% of jaundiced infants had bilirubin concentration of more than 10 mg%. Analysis of the factors showed that most of them were preventable.


PEDIATRICS ◽  
1967 ◽  
Vol 40 (6) ◽  
pp. 1062-1062
Author(s):  
JEROLD F. LUCEY ◽  
JEAN HEWITT ◽  
MARIO FERREIRO

Many factors are known to influence physiologic jaundice in premature infants. However no studies have been reported of the effect intra-uterine growth retardation or malnutrition has upon the average serum bilirubin concentrations in "small for dates" infants. It has been a policy in the nurseries of the University of Vermont Hospitals to do serum bilirubins on all low birth weight infants (2,500 gm or less) on the fourth to sixth day of life. Any infant with a positive Coomb's test or clinical evidence of A.B.O. incompatibility was excluded from this review.


2019 ◽  
Vol 37 (06) ◽  
pp. 652-658
Author(s):  
Yingfang Yu ◽  
Lizhong Du ◽  
An Chen ◽  
Lihua Chen

Abstract Objective This study aimed to assess the probable relationship between icter in neonates with ABO incompatibility hemolysis and UGT1A1 gene polymorphism. Study Design There were 65 ABO hemolytic disease of the newborn (HDN) neonates of full term in the study group and 82 non-ABO HDN neonates of full term in the compared group. We tested the UGT1A1 gene mutation of neonates of ABO HDN and non-ABO HDN. We compared the incidence of hyperbilirubinemia between neonates with and without UGT1A1 mutations in the ABO HDN and non-ABO HDN, to determine the relationship between icter in neonates with ABO HDN and UGT1A1 gene polymorphism. SPSS 13.0 were used to analyze those two groups' data. Results There was statistically significant difference of the serum bilirubin level between the Gly71Arg homozygous and no mutation group in the ABO HDN patients (p < 0.05). When hyperbilirubinemia was defined as serum bilirubin concentration >342 μmol/L, the incidence of hyperbilirubinemia between patients of UGT1A1 and non-UGT1A1 mutations in the ABO HDN group was significantly different (p < 0.05). But in the non-ABO HDN group, no significant difference was found. Conclusion Individuals with Gly71Arg homozygous contributed to their hyperbilirubinemia in ABO HDN patients.


2017 ◽  
Vol 4 (5) ◽  
pp. 1827
Author(s):  
Vikram R. ◽  
C. S. Balachandran

Background: To study non-obstructive causes and laboratory profile of neonatal hyperbilirubinemia. Design: prospective study.Methods: Selection of cases were done from routine cases reporting to newborn unit in the department of paediatrics, with clinical evidence of jaundice in neonates. Blood group of the mother and baby, Serum bilirubin estimation, Complete blood count with peripheral smear examination, Reticulocyte count, Direct coomb’s test and C-reactive protein of the baby were done.Results: Study includes 89 cases of newborn admitted in our tertiary care institute. Out of 89 neonates, 52 (58.42%) were male while 37 (41.57%) were females. Total number of Pre-term babies was 35 (39.32%). Neonates having low birth weight were 30 (33.7%) and very low birth were 10 (11.23%). Physiological jaundice constituted majority cases. Septicemia was the commonest cause of pathological jaundice and ABO incompatibility is second commonest cause of pathological jaundice. Pre-term and low birth weight babies were having higher levels of serum total bilirubin but the difference was not significant (P >0.05). The rise in serum bilirubin level was found to be more in pathological jaundice as compare to physiological jaundice. Difference was significant statistically with p value of <0.05.Conclusions: Most of the cases were having physiological jaundice although septicemia and ABO-Rh incompatibility were not exceptional. Peak serum bilirubin levels were found to be more among the pathological jaundice. Also, prematurity and low birth weight were having higher levels of serum bilirubin. Special care must be given to them in order to avoid future complications of hyperbilirubinemia.


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