Search PubMed⌕ Search

Biomedical subjects

N Paneth

Publications and source records attributed to N Paneth.

At least 55 records · Page 3Linked to original sources
PubMed1997

Correlates of low thyroxine values at newborn screening among infants born before 32 weeks gestation.

We assessed the relation of perinatal factors to severe hypothyroxinemia of prematurity, defined as thyroxine value more than 2.6 standard deviations below the mean for newborns. The 365 survivors of birth before 32 weeks gestation were enrolled in a population-based study of the correlates of neonatal brain injury. In this historical cohort study, mothers were interviewed; perinatal data were abstracted from medical records and neonatal data were collected prospectively. Neonatal thyroxine screening values were retrieved from the New Jersey State Department of Health. Associated with severe hypothyroxinemia were: gestational age 23-27 weeks vs. 31 weeks (OR = 5.1, 95% CI 1.7, 15.2), later age at thyroxine test (OR = 1.6 per day, 95% CI 1.2, 2.1), fraction inspired oxygen at age 24 h > 40% (OR = 3.2, 95% CI 1.1, 8.8), mechanical ventilation (OR = 5.1, 95% CI 1.3, 19.4), diastolic blood pressure < 20 mmHg (OR = 2.3, 95% CI 1.2, 4.3), and > 12 years of maternal education (OR = 0.4, 95% CI 0.22, 1.0). Infants with severe hypothyroxinemia had higher mortality, more days of oxygen supplementation, ventilation and hospitalization and were 11 times more likely to require oxygen supplementation at the postnatal age equivalent to 36 weeks gestational age (odds ratio 10.6, 95% CI 2.3, 48.8). In preterm infants, neonatal thyroxine levels obtained at newborn screening in the first week of life may convey important prognostic information about mortality, morbidity, and the risk for bronchopulmonary dysplasia.

Congenital Hypothyroidism↗
PubMed1997

Psychiatric outcomes in low-birth-weight children at age 6 years: relation to neonatal cranial ultrasound abnormalities.

BACKGROUND: This study examined the relation of neonatal cranial ultrasound abnormalities to psychiatric disorder at age 6 years in a regional birth cohort of low-birth-weight children. METHODS: Neonatal cranial ultrasound abnormalities were classified as (1) isolated germinal matrix and/or intraventricular hemorrhage (suggestive of injury to glial precursors) or (2) parenchymal lesions and/or ventricular enlargement (suggestive of white matter injury) with or without germinal matrix-intraventricular hemorrhage. Psychiatric disorders by DSM-III-R at age 6 years were assessed by means of a structured parent interview. Children with severe mental retardation were excluded. Analyses were conducted first in the entire sample and then in children with normal intelligence. RESULTS: Twenty-two percent of the cohort had at least 1 psychiatric disorder, the most common being attention deficit hyperactivity disorder (15.6%). In the entire sample, parenchymal lesions and/or ventricular enlargement increased risk relative to no abnormality, independently of other biological and social predictors, for any disorder (odds ratio [OR], 4.4; 95% confidence interval [CI], 1.8-10.3; P < .001), attention deficit hyperactivity disorder (OR, 3.4; CI, 1.3-8.7; P = .02), and tic disorders (OR, 8.7; CI, 1.3-57.7; P = .02). In children of normal intelligence, parenchymal lesions/ventricular enlargement independently increased risk for any disorder (OR, 4.8; CI, 1.6-12.0; P < .01), attention deficit hyperactivity disorder (OR, 4.5; CI, 1.3-16.0; P = .02), and separation anxiety (OR, 5.3; CI, 1.1-24.8; P = .03). These effects were not ameliorated by female sex or social advantage. Isolated germinal matrix/intraventricular hemorrhage was not related to psychiatric disorder at age 6 years. CONCLUSION: Neonatal cranial ultrasound abnormalities suggestive of white matter injury significantly increased risk for some psychiatric disorders at age 6 years in low-birth-weight children.

Age Factors↗
PubMed1997

Maternal receipt of magnesium sulfate does not seem to reduce the risk of neonatal white matter damage.

OBJECTIVE: To investigate whether in utero exposure to magnesium sulfate is associated with a lower incidence of cranial ultrasonographic abnormalities that predict cerebral palsy in infants who weigh less than 1501 g at birth. DESIGN: For a prospective study of the antecedents of cranial ultrasonographic abnormalities, we enrolled infants who weighed 500 to 1500 g when born at five institutions. Data were collected by interview of the mothers and review of medical records. Protocol cranial ultrasonograms were obtained as close as possible to postnatal days 1, 7, and 21. Abnormality on cranial ultrasound scans was determined by a consensus committee of three sonologists. RESULTS: Of the 1518 infants for whom we knew whether the mothers received magnesium sulfate, the first protocol cranial ultrasound scan was available for 1409 infants, the second for 1274 infants, and the third for 1050 infants. Forty-five percent of infants were exposed to magnesium sulfate before delivery. The major correlates of magnesium sulfate exposure were receipt of antenatal corticosteroids and a diagnosis of preeclampsia and/or pregnancy-induced hypertension. Maternal magnesium receipt was not associated with a reduced incidence of hypoechoic or hyperechoic images of white matter parenchyma, intraventricular hemorrhage, or ventriculomegaly, even when the sample was stratified by each of six potential confounders. When adjustment was made for gestational age, a measure of birth weight for gestational age, antenatal corticosteroid exposure, preeclampsia and pregnancy-induced hypertension, route of delivery, and the occurrence of any labor, the risk ratios for each cranial ultrasonographic abnormality associated with magnesium sulfate exposure hovered close to 1. CONCLUSION: Maternal receipt of magnesium sulfate does not seem to be associated with an appreciably reduced risk of cranial ultrasonographically defined neonatal white matter damage, intraventricular hemorrhage, or ventriculomegaly.

Adrenal Cortex Hormones↗
PubMed1997

Magnesium sulfate in labor and risk of neonatal brain lesions and cerebral palsy in low birth weight infants. The Neonatal Brain Hemorrhage Study Analysis Group.

OBJECTIVES: We tested the hypothesis that administration of magnesium sulfate in labor protects against the development of neonatal brain lesions and cerebral palsy (CP) in low birth weight infants. METHODS: Magnesium exposure was ascertained in a population-based cohort of 1105 infants weighing 2000 g or less through review of medical records of maternal magnesium sulfate administration and, where available, elevated maternal serum magnesium levels. Neonatal germinal matrix/intraventricular hemorrhage and parenchymal brain lesions were ascertained by a prospective, timed ultrasound scanning protocol in the first week of life. CP was ascertained at 2 years of age by clinical examination in 80% of survivors and by interview and medical record review in another 6% and was classified as disabling or nondisabling. RESULTS: No significant reduction in risk of nondisabling CP (adjusted odds ratio [OR], 1.00; 95% confidence interval [CI], 0.53 to 1.88) or disabling CP [DCP] (adjusted OR, 0.63; 95% CI, 0.32 to 1.24) CP with magnesium exposure was found in a logistic regression model that controlled for gestational age, fetal growth, gender, multiple birth status, mode of delivery, amnionitis, and hypertensive disorders. In a small subset of infants, those with onset of parenchymal lesions at 7 days of age or later (n = 29), magnesium exposure was associated with a significantly reduced risk of DCP (OR, 0.10; 95% CI, 0.02 to 0.65). Magnesium sulfate exposure was not associated with germinal matrix/intraventricular hemorrhage (adjusted OR, 0.89; 95% CI, 0.64 to 1.25) or with parenchymal brain lesions (adjusted OR, 0.83; 95% CI, 0.53 to 1.30). CONCLUSIONS: The hypothesis that magnesium sulfate use reduces the risk of neonatal brain lesions or CP in low birth weight infants was not statistically supported in this study, although a modest reduction in risk of DCP cannot be excluded. The data further suggest that magnesium exposure may be associated with reduction in risk of CP in low birth weight infants who have late-onset brain lesions, but this unpredicted observation requires confirmation in another data set.

Adult↗
PubMed1997

Thyroxine values from newborn screening of 919 infants born before 29 weeks' gestation.

OBJECTIVES: Severe transient hypothyroxinemia in premature infants is associated with cerebral palsy and mental retardation: this study assessed its prevalence in very premature infants. METHODS: Congenital hypothyroidism screening programs in three states provided thyroxine values for 919 newborn infants younger than 29 weeks who were enrolled in a multicenter study. RESULTS: Thyroxine values were lower than 4.0 micrograms/dL in 21% of survivors and increased each week by 0.6 microgram/dL (95% confidence interval [CI] = 0.4, 0.7). At tests done 1 to 2 days after birth, levels were 2.5 micrograms/dL higher (95% CI = 1.8, 3.3) than at tests done at 8 to 14 days. In New York, levels were 1.0 microgram/dL higher (95% CI = 0.3, 1.6) than elsewhere. The levels of infants who died were 1.3 micrograms/dL lower (95% CI = 0.6, 2.0) than those of survivors. CONCLUSIONS: Severe transient hypothyroxinemia is common in very premature infants and deserves further study.

Gestational Age↗
PubMed1996

The relation of transient hypothyroxinemia in preterm infants to neurologic development at two years of age.

BACKGROUND: Transient hypothyroxinemia, a common finding in premature infants, is not thought to have long-term sequelae or to require treatment. We investigated whether hypothyroxinemia in premature infants is a cause of subsequent motor and cognitive abnormalities. METHODS: In this historical cohort study, we retrieved blood thyroxine values, obtained on routine screening in the first week of life, from state screening records on children who weighted 2000 g or less at birth, who were born at 33 weeks' gestation or earlier, and who were enrolled in a population-based study of the late sequelae of neonatal brain hemorrhage. We investigated the relation of these values to the odds for disabling cerebral palsy among 463 subjects for whom data were available and to the mental-development score on the Bayley Scales of Infant Development or the Stanford-Binet Intelligence Scales for Children at the age of two years in 400 subjects. The effects of severe hypothyroxinemia, defined as a blood thyroxine value more than 2.6 SD below the mean for New Jersey newborns, were assessed before and after adjustment for gestational age and potentially confounding variables. RESULTS: In analyses adjusted for gestational age, infants with severe hypothyroxinemia had a risk of disabling cerebral palsy that was nearly 11 times that of infants without hypothyroxinemia (odds ratio, 10.8; 95 percent confidence interval, 3.0 to 39.3) and a mean mental-development score at the age of two that was 15.4 points lower (95 percent confidence interval, 8.1 to 22.6 points) than the mean score of children with normal neonatal blood thyroxine concentrations. After adjustment for gestational age and multiple prenatal, perinatal, and early and last neonatal variables, severe hypothyroxinemia was still associated with an increased risk of disabling cerebral palsy (odds ratio, 4.4; 95 percent confidence interval, 1.0 to 18.6) and a reduction of nearly 7 points (95 percent confidence interval, 0.3 to 13.2 points) in the mental-development score. CONCLUSIONS: Severe hypothyroxinemia in preterm infants may be an important cause of problems in neurologic and mental development detected at the age of two years.

Cerebral Palsy↗
PubMed1996

Blood pressure ranges in premature infants: II. The first week of life.

OBJECTIVE: To examine the arterial blood pressure in the first week of life in a healthy premature population. DESIGN: Population-based cohort study. SETTING: Three intensive care nurseries in central New Jersey. PATIENTS: Premature infants with birth weights less than 2000 g. MAIN OUTCOME MEASURES: We documented daily maximum and minimum systolic and maximum and minimun diastolic blood pressures during the first 7 days of life. To examine the effects on the ranges of blood pressure, we identified four groups of infants: (1) healthy infants without any of the major risk factors (n = 193); (2) infants who were mechanically ventilated but free of any of the other conditions (n = 225); (3) infants with histories of maternal hypertension or preeclampsia (n = 38) and (4) infants with low Apgar scores (less than 3 at 1 minute and less than 6 at 5 minutes) regardless of the presence of other conditions (n = 86). RESULTS: Blood pressure increased steadily in the first week of life in all four groups. There was no relationship between any of the four blood pressure variables, or trends in blood pressure over time, with birth weight, gender, or race. Regression equations (based on all infants with available data) for blood pressure ranges by day of life revealed that the maximum systolic blood pressure increased by 2.6 mm Hg/d, the minimum systolic blood pressure increased by 1.8 mm Hg/d,the maximum diastolic blood pressure increased by 2.0 mm HHg/d, and the minimum diastolic blood pressure increased by 1.3 Hg/d. CONCLUSIONS: Infants with birth asphyxia and ventilated infants had significantly lower systolic and diastolic blood pressures than healthy infants.

Age Factors↗
PubMed1996

Early nutritional origins of hypertension: a hypothesis still lacking support.

PURPOSE: It has been hypothesized that limitations in 'a baby's nourishment before birth', as reflected in reductions in birthweight and other newborn anthropometric measurements, are associated with subsequent elevations in blood pressure. We assess this hypothesis in light of four causal criteria commonly used by epidemiologists: specificity, consistency, strength and biological coherence. We also examine aspects of the methodology used in studies of this hypothesis. METHODOLOGIC PROBLEMS: Two major data sources for testing the hypothesis in Hertfordshire and Preston are flawed by very high attrition. The practice of testing this hypothesis by controlling for adult weight in the analysis overstates the benefit that might accrue from interventions to increase birthweight. CAUSAL CRITERIA: Studies used to support the hypothesis examine a wide variety of exposures and outcomes, without prespecification of which associations are expected. The inverse relationship of birthweight to blood pressure is found inconsistently and, when present, is not strong. Potential confounding variables, especially social class, have not generally been taken into account. Evidence from human nutrition studies, especially of famine exposure and pregnancy nutrition supplementation, are not supportive of the proposition that in industrialized countries variations in the birthweight of the population closely reflect pregnancy nutrition. CONCLUSION: When examined critically, the evidence thus far provided does not support the hypothesis that prenatal nutrition is a major determinant of adult blood pressure.

Fetus↗
PubMed1995

Plague in India.

Explore the source record for details and available documents.

Adolescent↗
PubMed1995

Efficiency of sampling: birthweight and gestational age distributions in two cohorts, < 31 weeks and 500-1499 grams.

We studied the efficiency of two common sampling strategies used to assemble cohorts to study the long-term problems of preterm infants: infants with birthweights of 500-1499 g, and infants with gestational ages (GA) of < 31 weeks. Birthweight, GA and 2-year outcome data from a population based study of infants < 2001 g, the Central New Jersey Brain Hemorrhage Study (NBH), were used to define the birthweight and GA distributions, at enrollment and at the age of 2 years, of overlapping subsets: infants 500-1499 g (n = 599) and infants < 31 weeks of age (n = 522). Using frequencies from the NBH study, we estimated that 1000 infants of 500-1499 g enrolled at birth would produce 712 infants at the age of 2 years, 498 below 31 weeks and 214 above. Enrolling 1000 infants < 31 weeks would produce a cohort of 697 infants at the age of 2, all of whom were < 31 weeks. Neither sampling strategy maximised the statistical power to investigate the pathophysiological determinants of long-term outcomes associated with short GA. Both methods oversampled older GAs. A stratified sampling technique based on GA, designed to produce equal numbers of subjects at each week of GA, would improve statistical power to study long-term outcomes. As we move from descriptive to analytical studies of preterm infants, we need to devise efficient, GA-based, sampling strategies that maximise statistical power to test pathophysiological hypotheses.

Birth Weight↗
PubMed1995

Perinatal brain injury in premature infants born to mothers using alcohol in pregnancy. Neonatal Brain Hemorrhage Study Team.

OBJECTIVE: Alcohol has been shown to have teratogenic effects on the fetal central nervous system. However, little research has been done to assess the impact of prenatal alcohol exposure on premature infants, a group particularly vulnerable to perinatal brain injury. METHODS: We examined the relation between maternal alcohol use and the most common forms of brain injury in premature infants--germinal matrix/intraventricular hemorrhage (GM/IVH) and white-matter damage--in a large population-based cohort of infants weighing 2000 g or less. The analyses included 349 infants younger than 31 weeks' gestation who received at least one cranial ultrasound scan and whose mothers were queried about prenatal alcohol use in a postpartum interview. RESULTS: Infants of mothers who reported "moderate" alcohol use (fewer than seven drinks per week and fewer than three drinks per occasion) to "high" use (seven or more drinks per week and/or three or more drinks per occasion) before recognized pregnancy, and moderate alcohol use during pregnancy, were not at increased risk for brain injury. However, after controlling for potentially confounding factors, infants of women reporting high alcohol use during pregnancy were at increased risk of developing isolated brain hemorrhage (odds ratio [OR] = 5.5, 95% confidence interval [CI] = 1.2, 24.7), any brain hemorrhage (OR = 6.7, 95% CI = 1.8, 26.4), and white-matter damage (OR = 9.5, 95% CI = 1.9, 46.4). CONCLUSION: Premature infants of women who report consuming seven or more drinks per week and/or three or more drinks per occasion during pregnancy have substantially elevated risks of both of the most common forms of brain injury in premature infants.

Alcohol Drinking↗
PubMed1995

Cranial ultrasound prediction of disabling and nondisabling cerebral palsy at age two in a low birth weight population.

OBJECTIVE: To employ multivariate analytic techniques to assess the association between neonatal cranial ultrasound (US) abnormalities and subsequent cerebral palsy (CP), defined as disabling CP (DCP) or nondisabling CP (NDCP) depending on the level of motor dysfunction. DESIGN: Prospective cohort study. SUBJECTS AND METHODS: The Neonatal Brain Hemorrhage Study enrolled a geographically representative sample of 1105 newborns 501 to 2000 g and obtained follow-up data on 777 (86%) of the 901 survivors at age two. One hundred thirteen children (14.6%) had motor findings severe enough to classify them as having CP. The 61 (7.9%) of these children who were disabled by their motor impairment we classified as having DCP. The remaining 52 (6.7%) who had definite neurologic findings (usually mild spastic diplegia) but without evidence of interference with daily living, we classified as having NDCP. RESULTS: In a multivariate logistic regression model of perinatal and postnatal variables, the following factors were found to be significant risk factors for DCP: parenchymal echodensities/lucencies or ventricular enlargement (PEL/VE) on cranial US (OR = 15.4; 7.6, 31.1), germinal matrix/intraventricular hemorrhage (GM/IVH) (OR = 3.5; 1.7, 6.9) and mechanical ventilation (OR = 2.9; 1.2, 7.1). Fully 93.4% of infants were correctly classified as to presence or absence of DCP on the basis of this model. Birth weight, gestational age, length of hospital stay, gender, race, plurality, presence of labor and Apgar score were not significant independent predictors of DCP. For NDCP, the only risk factor significant in the multivariate model was PEL/VE (OR = 5.3; 2.2, 12.6). CONCLUSIONS: Among perinatal and postnatal factors, cranial US abnormalities are by far the most powerful predictors of disabling CP in low birth weight infants. Although PEL/VE was the strongest predictor, GM/IVH also appeared to independently contribute to the risk of DCP. NDCP in low birth weight infants appears to have a different risk profile than DCP. In particular, it is less closely related to US evidence of perinatal brain injury.

Brain Diseases↗
PubMed1994

Blood pressure ranges in premature infants. I. The first hours of life.

We studied blood pressure in the first hours of life in a cohort of 1105 preterm infants weighing 501 to 2000 gm; these infants represented 83% of all births at these weights that resulted in admission to three intensive care nurseries during a 34-month period between 1984 and 1987. To assess the effects of specific risk factors, we identified 244 healthy infants, 164 infants who received mechanical ventilation but had no other conditions, 47 infants whose only risk factor was the presence of hypertension or preeclampsia in the mother, and 86 infants with depressed Apgar scores regardless of the presence of the other conditions. We documented each infant's minimum and maximum systolic (Smin, Smax) and diastolic (Dmin, Dmax) pressures during the first 3 to 6 hours of life. In the healthy group, Smin was 47 mmHg; Smax, 59 mmHg; Dmin, 24 mmHg; and Dmax, 35 mmHg. In the ventilation group, Smin was 41 mmHg; Smax, 57 mmHg; Dmin, 22 mmHg; and Dmax, 35 mmHg. The Smin and Dmin values were both significantly lower in infants who received mechanical ventilation than in healthy infants (p < 0.01). In the maternal hypertension group, Smin was 49 mmHg; Smax, 59 mmHg; Dmin, 25 mmHg; and Dmax, 34 mmHg. Only the Smin value was significantly higher than in healthy infants. In the group with low Apgar scores, Smin was 33 mmHg; Smax, 51 mmHg; Dmin, 19 Hg; and Dmax, 34 mmHg. Thus all these values were significantly lower than in all the other groups (p < 0.05). Of infants with low Apgar scores, 20% to 50% had values below the 5th percentile for healthy infants. Birth weight and gestational age correlated with blood pressure limits only in the infants with low Apgar scores. We conclude that in healthy premature infants the limits of systolic and diastolic blood pressure are independent of birth weight and gestational age. Infants with low Apgar scores tend to have lower pressures, and infants whose mothers have hypertension have higher pressures than infants in the healthy cohort.

Apgar Score↗