RESUMO
The hypothesis that the etiologic mechanism of the late-onset, prolonged, unconjugated hyperbilirubinemia of the breast-fed infant, known as the breast milk jaundice syndrome, results from exaggeration of intestinal bilirubin absorption has been investigated in an adult rat model, which permits quantitative measurement of the enterohepatic circulation of bilirubin. After instillation of unconjugated bilirubin in buffer into the duodenum, 25% of the dose was absorbed and appeared in bile. Administration of bilirubin in human milk or cow milk formula resulted in a marked reduction in absorption to 2%. Administration of bilirubin in milk from mothers of infants with breast milk jaundice syndrome not only failed entirely to prevent the absorption of bilirubin, but enhanced late absorption, to produce a total absorption of 60% of the bilirubin dose. Thus, although normal milk significantly retarded intestinal bilirubin absorption and diminished the bilirubin load to the liver, milk from mothers of infants with breast milk jaundice syndrome appeared to enhance the enterohepatic circulation of bilirubin and to increase the total hepatic bilirubin load. This exaggeration of the enterohepatic circulation of bilirubin may be related to the increased concentrations in these milks of long-chain nonesterified fatty acids.
Assuntos
Bilirrubina/metabolismo , Circulação Êntero-Hepática , Absorção Intestinal , Leite Humano/metabolismo , Animais , Bile/análise , Bilirrubina/análise , Feminino , Humanos , Recém-Nascido , Icterícia Neonatal/etiologia , Gravidez , Ratos , Ratos EndogâmicosAssuntos
Mortalidade Infantil , Análise de Regressão , Humanos , Recém-Nascido de Baixo Peso , Recém-Nascido , MétodosRESUMO
We have examined the relationship between the rate of very low-birth-weight deliveries in a population and the neonatal mortality of that population on three ecologic levels: in one hospital over a 12-year span; among the 50 states and the District of Columbia; and among 13 industrialized nations. In each of the three sets of populations the VLBW rate is an excellent predictor of neonatal mortality, accounting for about three-quarters of the variance in the outcome in all of the populations studied. The relatively high neonatal mortality of the United States as compared to that in some other industrialized nations is primarily attributable to its disadvantageous birth-weight distribution. Holding the adverse birth-weight distribution constant, the United States appears to do better than most of these nations in neonatal mortality. The weight distribution of live births in any population is closely linked to indices of social class. Survival of infants at a given birth weight, however, might well be a function of perinatal care. Since weight-specific mortality rates for populations are not widely available, examination of the variance in neonatal mortality rates once the VLBW rate is held constant might be a first step in comparing the quality of medical care for newborn infants among different populations.
PIP: The authors examine the relationship between the rate of very low-birth-weight deliveries in a population and neonatal mortality, using data for one New York hospital over a 12-year period, U.S. data by state, and data for 18 industrialized countries. The results show that the very low-birth-weight rate is an excellent predictor of neonatal mortality, accounting for about three-quarters of the variance in the populations studied. The reasons for variations in neonatal mortality between the United States and other countries and within the United States are discussed
Assuntos
Mortalidade Infantil , Recém-Nascido de Baixo Peso , Áustria , Canadá , Europa Oriental , Alemanha , Humanos , Recém-Nascido , Israel , Japão , Nova Zelândia , Países Escandinavos e Nórdicos , Estados UnidosAssuntos
Resina de Colestiramina/efeitos adversos , Hipernatremia/induzido quimicamente , Ductos Biliares Intra-Hepáticos/anormalidades , Resina de Colestiramina/uso terapêutico , Feminino , Hepatite/tratamento farmacológico , Humanos , Lactente , Recém-Nascido , Doenças do Recém-Nascido/tratamento farmacológico , MasculinoRESUMO
Hepatic transport and metabolism of bilirubin have been examined in term, premature, and postmature newborn Macaca mulatta (rhesus) monkeys with and without prior phenobarbital treatment of pregnant mother and neonate. In untreated neonates a biphasic pattern of physiologic unconjugated hyperbilirubinemia has been observed. Phase I was characterized by a rapid increase in serum bilirubin concentration to 4.5 mg/dl by 19 hours and an equally rapid decline to 1.0 mg/dl by 48 hours of age. Phase II was characterized by a stable elevation at 1.0 mg/dl (four times greater than in the adult) from 48 to 96 hourse of age, followed by a decline to normal adult concentrations thereafter. An identical pattern was observed in 29 normal, term human neonates, but the duration of each phase was approximately three times as long as that in the monkey. Phase I hyperbilirubinemia appears to result from a sixfold increase in bilirubin load presented to the liver in the neonatal period, combined with marked deficieny in hepatic bilirubin conjugation, the rate-limiting step during Phase I. Hepatic uptake of bilirubin is not rate limiting during Phase I but may contribute to Phase II hyperbilirubinemia. An increased bilirubin load persists throughout the first 19 days of life in the monkey. Phase I physiologic jaundice in the monkey neonate was completely eliminated by prenatal maternal and neonatal administration of phenobarbital. A threefold enhancement of hepatic conjugation of bilirubin (glucuronyl transferase activity) during Phase I entirely accounted for the prevention of hyperbilirubinemia. The bilirubin load was unaffected by administration of phenobarbital. Whereas in control neonates the bilirubin load slightly exceeded hepatic bilirubin conjugating capacity and resulted in retention of bilirubin, in phenobarbital-treated neonates, hepatic conjugating capacity slightly exceeded that required for the bilirubin load. Administration of phenobarbital failed to alter Phase II hyperbilirubinemia and did not enhance either maximal hepatic uptake or excretion of bilirubin. Hepatic glucuronly transferase activity was increased threefold during Phase II and during the remainder of the neonatal period. Premature birth retarded maturation of hepatic glucuronyl transferase activity. In one phenobarbital-treated premature monkey neonate, there was no apparent response to treatment. Accelerated maturation of bilirubin uptake, conjugation, and excretion of bilirubin was observed in one postmature monkey neonate.
Assuntos
Animais Recém-Nascidos/metabolismo , Bilirrubina/metabolismo , Animais , Transporte Biológico , Feminino , Glucuronosiltransferase/metabolismo , Haplorrinos , Humanos , Recém-Nascido , Icterícia Neonatal/metabolismo , Fígado/anatomia & histologia , Fígado/metabolismo , Macaca mulatta , Tamanho do Órgão/efeitos dos fármacos , Fenobarbital/administração & dosagem , Fenobarbital/farmacologia , Gravidez , Proteínas/metabolismoRESUMO
The effect of the administration of promethazine in the treatment of erythroblastosis fetalis was studied in four maternal-fetal pairs. The three infants exposed for a prolonged period of time had decreased neonatal number and function of T cells, and abnormal specific humoral immune responses. The possible role of promethazine in the induction of fetal immunoincompetence is discussed.