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Biomedical subjects

L M Gartner

Publications and source records attributed to L M Gartner.

At least 37 records · Page 2Linked to original sources

Breastfeeding and human milk: their association with jaundice in the neonate.

As demonstrated by this discussion, jaundice in breastfeeding infants appears to be related both to feeding-related issues and to an as-yet unidentified factor in the human milk of a small minority of women. In the case of feeding-related factors, how a mother breastfeeds; that is, how often she offers the breast and how well the baby suckles, as well as how often and how much the baby is offered complementary or supplementary feedings of water, glucose solutions, or a nonhuman mammal milk, influence serum bilirubin concentrations in the first week of postnatal life. We call this breastfeeding-related jaundice, recognizing that the feeding process is a key element in the condition. We urge that management recommendations focus on the feeding process to reduce the level of serum bilirubin concentration in the first week of life. It is appropriate to note at this juncture that hyperbilirubinemia also occurs in bottlefed infants; the frequency of feeding of these infants also may play a role in the severity of jaundice. If research findings bear out such a relationship, we may see a corollary label of "feeding-related" jaundice also applied to bottlefed babies. In a very small percentage of breastfeeding infants, a second form of jaundice occurs. Its onset appears somewhat later in the postnatal period, and it is characterized by a higher peak and a slower decline in the level of serum bilirubin concentration. We call this breast milk jaundice, recognizing that it appears to stem from the milk the baby receives rather than the manner in which he or she is fed. Eliminating other causes of jaundice prior to considering even a brief interruption of breastfeeding is appropriate when caring for the infant with this syndrome. In the breastfeeding infant, both early- and late-onset jaundice appear to be related. We suggest this because the baby with breast-feeding jaundice may be more responsive to the factor in abnormal milk, which produces breast milk jaundice. The infant with breast-feeding jaundice has a larger bilirubin load at the time the abnormal milk is being ingested. The recycling of this increased load, because of exaggerated enterohepatic circulation, results in a further late rise in serum bilirubin. If the initial bilirubin pool is smaller, the effect of the abnormal milk might well be insignificant or at least markedly diminished.(ABSTRACT TRUNCATED AT 400 WORDS)

Bilirubin↗

Effect of milk feeding on intestinal bilirubin absorption in the rat.

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.

Animals↗

Thyroid hormone and hepatic UDP-glucuronosyl transferase activity: contrary effects in rat and mouse.

The administration of tri-iodothyronine (T3) to female Sprague-Dawley (SD) rats lowered the basal activity of uridine diphosphoglucuronate glucuronosyl transferase (UDPGT:EC 2.4.1.17) for bilirubin (Bili) by 75 percent, but dramatically increased the level of UDP-glucuronosyl transferase for p-nitrophenol (UDPGT-PNP) by more than 100 percent. Similar experiments performed in four strains of female mice produced results contrary to those observed in the rat. T3 administered to C57BL/6J, DBA/2J, Swiss-Webster (SW) and CD-1 mice significantly increased hepatic UDPGT-Bili by 28, 69, 79 and 94%, respectively. The increase of UDPGT-Bili in the selected strains was observed to be inversely and linearly proportional to the basal level of enzyme measured in each strain (r = -0.99215; p less than 0.001). Only in the DBA/2J strain was UDPGT-PNP significantly diminished to 66% of control levels, producing a result exactly opposite to that observed in the SD rat; in the other three strains, UDPGT-PNP was not significantly altered.

Animals↗

Recent trends in neonatal mortality: the Canadian experience.

In Canada between 1958 and 1977 the neonatal mortality dropped by more than 50%. the decline was most prominent from 1963 and was almost entirely due to an improvement in neonatal birthweight-specific mortality, which suggests an improvement in perinatal medical care. The timing and pattern of the decline are similar to those reported for the United States. There was a transient increase in the incidence of low and very low birthweight in both countries in the late 1960s. The cause of this increase remains unexplained.

Adult↗

Determinants of neurobehavioral outcome in low-birth-weights infants.

The relative importance of (1) birth weight, gestational age, and head circumference at birth, and (2) appropriateness of birth weight and head circumference to gestational age in the predictability of neurobehavioral outcome was evaluated in 127 low-birth-weight infants at 7 months of age. Lower absolute birth weights, shorter gestational ages, and smaller head circumferences at birth correlated with poorer outcome (Bayley Scales of Infant Development and abnormal neurologic examination) at the corrected chronologic age of 7 months (r = .28 to .42, all P less than .005). The incidence of low scores on the Mental Development Index and of severe neurologic deficit was significantly higher in small head circumference for gestational age infants than in appropriate head circumference for gestational age infants (both, P less than .05). In the absence of small head circumference, small for gestational age infants had similar incidences of low Bayley scores and abnormal neurologic examinations as did appropriate for gestational age infants. These observations suggest that head circumference at birth may be the single most important variable for subsequent neurobehavioral outcome, and that both birth weight and gestational age may simply be markers of fetal head growth in their relationship to later outcome.

Birth Weight↗

Comparative measurements of phototherapy: a practical guide.

Increasing the dose of administered phototherapy has been shown to increase the rate of bilirubin decrement up to a saturation point beyond which no further increases in bilirubin degradation are observed. This study provides irradiance measurements which can be used to interpret phototherapy dose-response and saturation data clinically and to determine an optimal phototherapy lamp combination for maximal bilirubin degradation.

Bilirubin↗

The very low-birth-weight rate: Principal predictor of neonatal mortality in industrialized populations.

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.

Austria↗

Neonatal mortality: an analysis of the recent improvement in the United States.

To test the hypothesis that the recent substantial decline in the United States neonatal mortality rate (20.0/1000 in 1950 to 11.6/1000 in 1975) is associated with improvements in perinatal medical care, we examined this change in relation to the two primary components which determine neonatal mortality: birthweight distribution and birthweight-specific mortality. No improvement in the weight distribution of U.S. live births has occurred during this 25-year period, indicating that the change in neonatal mortality is attributable to improved survival for one or more birthweight groups. Decline in the mortality rate in the first 15 years was slow; three-fourths of the decline in the entire 25-year period occurred since 1965. With the exception of perinatal medical care, factors known to affect survival at a given birthweight have not changed in prevalence in the 25-year period. It is a plausible hypothesis that improved perinatal medical care is a major factor in declining neonatal mortality in the U.S.

Birth Weight↗

The association of kernicterus with bacterial infection in the newborn.

A total population of 29,395 neonates cared for in the six-year period from 1971 to 1976 was reviewed for evidence of autopsy-proven kernicterus. A total of 327 neonates died and 232 were autopsied. The only cases of kernicterus occurred in four near-term infants with antemortem proven sepsis. All four of these infants weighed more than 2,200 gm and were delivered after gestations of either 36 or 37 weeks. These cases of kernicterus occurred during a period when more aggressive management of hyperbilirubinemia in low-birth-weight infants had apparently eliminated immaturity as a predisposing factor in the development of kernicterus, uncovering bacterial infection as the major remaining etiologic co-factor.

Bacterial Infections↗

Comparative studies of biliary atresia in the human newborn and reovirus-induced cholangitis in weanling mice.

The hepatobiliary histologic lesions of human newborns with biliary atresia have been compared to those induced in weanling mice by reovirus type III. Although the obliterative fibrotic lesions, the hallmark of human disease, are only transient or segmental in the mouse and therefore do not result in permanent or complete obstruction of bile flow, many of the inflammatory stages of the disease are identical in humans and in the mouse. Prompted by these similarities, antibodies to reovirus type III were sought in sera of human newborns with biliary atresia. Two of 12 babies had elevated and rising neutralizing titers to reovirus type III during the course of their illness. Using recobinant reoviruses which contain some genes from a nonpathogenic reovirus type I and other genes from the pathogenic parental reovirus type III, we have shown that hepatobiliary murine pathology is not the property of a single viral gene.

Animals↗