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Certain factors in infants of HIV-positive mothers appear to associate with increased likelihood of HIV infection and early death. Among 351 infants born to HIV-positive mothers, 24% were eventually found to be infected. Among these, researchers collected data and compared outcomes for 248 uninfected and 84 infected infants. Fifty-eight percent of mothers of infected infants had CD4 counts less than 500 and 21% had AIDS whereas 39% of noninfecting mothers had CD4 counts that low and 11% had AIDS. Three percent of mothers taking zidovudine infected their infants versus 11% of mothers not taking zidovudine. Infected infants were twice as likely to be born before 37 weeks gestation and almost four times as likely to be born before 34 weeks. Infected infants were twice as likely to be low birth weight, low birth weight at full term, or small for gestational age. Ten percent of infected newborns had generalized infections versus 3% of uninfected infants., ABSTRACT. Background and Methods. Differences in newborn outcome measures for human immunodeficiency virus (HIV-1-infected and HIV-1-exposed but uninfected infants have been found in several studies, but not in others. Eighty-four infected and 248 uninfected children born to HIV-1-seropositive mothers followed prospectively in a multicenter, perinatal HIV-1 transmission cohort study were compared for differences in maternal demographics, health status, and newborn outcome measures, including delivery complications, physical examination findings, neonatal complications, and laboratory results. Results. Mothers of HIV-1-infected infants were more likely than those of uninfected infants to have acquired immunodeficiency syndrome (AIDS) diagnosed through 2 weeks postpartum (21% vs 11%, P = .04); the transmission rate for the 38 women with AIDS was 37% compared with 22% for the 245 women without AIDS. Two of 27 (7%) women receiving zidovudine during pregnancy had infected infants compared with 73 (27%) of 275 women who did not receive zidovudine (P = .033). Mean gestational age was significantly lower among HIV-1-infected (37 weeks) than among uninfected infants (38 weeks; P < .001). Infected infants had significantly higher rates of prematurity (gestational age less than 37 weeks) (33% vs 19%, P = .01) and extreme prematurity (gestational age less than 34 weeks) (18% vs 6%, P = .001) than uninfected infants. Infection was associated with lower birth weight (2533 g vs 2862 & P < .001) and smaller head circumference (32.0 cm vs 33.1 cm, P = .001). HIV-1-infected infants were significantly more likely to be small for gestational age (26% vs 16%, P = .04) and low birth weight (less than 2500 g) (45% vs 29%, P = .006) than infants who were uninfected. Twenty-two (26%) HIV-1-infected children died during a median follow-up of 27.6 months (range 1.9 to 98.3 months). Prematurity was predictive of survival: by Kaplan-Meier, an estimated 55% (95% confidence interval, 31% to 72%) of preterm infected children survived to 24 months compared with 84% (95% confidence interval, 70% to 92%) of full-term infected children (P = .005). Conclusion. Infants born to women with AIDS are at higher risk for HIV-1 infection than are infants born to HIV-1-infected women with AIDS not yet diagnosed. Women receiving zidovudine appear less likely to transmit HIV-1 to their infants. Significantly higher rates of prematurity and intrauterine growth retardation were found among HIV-1-infected infants than among those in the uninfected, HIV-1-exposed control group. Prematurity was associated with shortened survival in HIV-1-infected infants. Measures of intrauterine growth and gestation appear to be important predictors of HIV-1 infection status for seropositive infants and of prognosis for the infected infant. Pediatrics 1995;96:451-458; neonatal predictors of HIV-1 infection, pediatric HIV-1, prematurity., ABBREVIATIONS. AIDS, acquired immunodeficiency syndrome; HIV, human immunodeficiency virus; CDC, Centers for Disease Control and Prevention; ZDV, zidovudine; SGA, small for gestational age; LBW, low birth weight; PCP, Pneumocystis carinii; [...]

Objective. To evaluate the relationship between head circumference, birth weight, and cocaine dose in healthy term and near-term newborns exposed to cocaine in utero. Methods. We used radioimmune assay (RIAH) of cocaine metabolite in maternal hair to quantify third trimester cocaine exposure in 240 healthy newborn infants (gestational age: >36 weeks). Cocaine exposure was categorized into 3 levels: no exposure (n = 136), low cocaine exposure (n = 52; RIAH: 2-66 ng/10 mg hair), and high cocaine exposure (n = 52; RIAH: 81-4457 ng/10 mg hair). We collected information on maternal demographic characteristics, the pregnancy, and the use of substances through a structured interview and from the medical record. Results. Means of birth weight, length, and head circumference of infants with high cocaine exposure differed significantly from those with low exposure and no exposure, but were similar between low exposure and no exposure. We used a multiple linear regression model to assess the association between newborn head circumference and cocaine level, adjusting for the effects of birth weight; gestational age; infant sex; and several maternal factors, including height, weight gain during pregnancy, syphilis during pregnancy, and the use of alcohol, cigarettes, marijuana, and opiates during pregnancy. Only birth weight, sex, and high cocaine exposure were significantly associated with newborn head circumference. The predicted head circumference deficit associated with high cocaine exposure (.44 cm) represents 34% of the unadjusted difference (1.28 cm) between mean head circumferences of infants in the high cocaine exposure and no exposure groups. Conclusion. Newborns exposed to a high level of cocaine in utero (RIAH: [is greater than] 81 ng/10 mg hair) exhibit asymmetric intrauterine growth retardation in which the head circumference is disproportionately smaller than would be predicted from the birth weight (head wasting). The deficit in head size associated with cocaine exposure may reflect the effects of a specific central nervous system insult that interferes with prenatal brain growth. Pediatrics 2000;106(3). URL: http://www.pediatrics.org/ cgi/content/full/106/3/e33; cocaine, infant, newborn, fetal development, head.

Background. Ureaplasma urealyticum and its association with chronic lung disease (CLD) of prematurity has remained a controversial topic. To readdress this question, we performed a longitudinal study using culture and polymerase chain reaction to detect U urealyticum in the respiratory tract of very low birthweight infants throughout their neonatal intensive care unit hospitalizations. Methods. We screened 125 infants weighing Results. Forty infants (32%) had 1 or more positive specimens by culture or polymerase chain reaction. We identified 3 patterns of U urealyticum colonization: persistently positive (n = 18), early transient (n = 14), and late acquisition (n = 8). We compared the rates of CLD in each of the 3 colonized groups with the rate of CLD in the noncolonized group. We found a significantly higher rate of CLD at 28 days of age (odds ratio: 8.7; 95% confidence interval: 3.3, 23) and at 36 weeks&apos; postconception (odds ratio: 38.5, 95% confidence interval: 4.0, 374) only for infants with persistently positive colonization. Conclusions. This study demonstrates that the risk of developing CLD varies with the pattern of U urealyticum colonization. Only the persistently positive colonization pattern, which accounted for 45% of the U urealyticum-positive infants, was associated with a significantly increased risk of development of CLD. Pediatrics 2002; 110(4). URL: http://www.pediatrics.org/cgi/content/full/ 110/4/e45; bronchopulmonary dysplasia, chronic lung disease, premature infant, polymerase chain reaction, Ureaplasma urealyticum, very low birth weight infant.

Newborn infants exposed to cocaine in the uterus are at risk of developmental abnormalities. Researchers gave 240 newborn infants extensive tests to determine if the 104 infants who were exposed to cocaine prenatally would be more likely to have developmental defects. Compared to infants not exposed, those exposed were more likely to have retarded growth, small heads, neurologic abnormalities, and postural abnormalities. Analysis of cocaine in maternal hair samples indicated the risk was greatest in infants exposed to the most cocaine., Background. Studies of fetal cocaine exposure and newborn neurologic function have obtained conflicting results. Although some studies identify abnormalities, others find no differences between cocaine-exposed and cocaine-unexposed infants. To determine the effects of prenatal cocaine exposure on intrauterine growth and neurologic function in infants, we prospectively evaluated 253 infants shortly after birth. Methods. Women who delivered a live singleton [is greater than] 36 weeks by dates were eligible for enrollment. Maternal exclusionary criteria were known parenteral drug use, alcoholism, and acquired immunodeficiency syndrome; infant exclusionary criteria were Apgar scores [is less than or equal to] 4 at 5 minutes, obvious congenital malformations, seizures, or strokes. A total of 98% of infants were evaluated between 1 to 7 days of age. Newborns were assessed with the Neurological Examination for Children (NEC) by a pediatric neurologist (C.A.C.) who was blinded to exposure status. Gestational age was determined by Ballard&apos;s examination. Cocaine exposure was determined for the last trimester by radioimmunoassay of maternal hair (RIAH). Exposure values ranged from 2 to 4457 ng/10 mg hair. Infants were excluded if a maternal hair sample was missing (N = 13). The sample comprises 240 woman and infant pairs--104 cocaine-exposed and 136 cocaine-unexposed. Results. Compared with unexposed controls, cocaine-exposed infants exhibited higher rates of intrauterine growth retardation (24% vs 8%), small head circumference ([HC] [is less than] 10th% percentile) (20% vs 5%) and neurologic abnormalities: global hypertonia (32% vs 11%), coarse tremor (40% vs 15%), and extensor leg posture (20% vs 4%). We found increasing odds (odds ratio) of growth and neurologic impairment with increasing level of cocaine exposure in stratified analyses. The odds ratio associated with three levels of cocaine exposure (no exposure, low exposure = RIAH 2-66 ng/mg; and high exposure = RIAH 81-4457 ng/mg) respectively are: 1.0, 3.3, and 6.1 for small head size ([chi square] for trend); 1.0, 3.3, and 4.3 for global hypertonia ([chi square] for trend); 1.0, 3.4, and 7.4 for extensor leg posturing ([chi square] for trend); and 1.0, 3.8, and 3.8 for coarse tremor ([chi square] for trend). Significant associations between cocaine exposure and neurologic signs were found in logistic regression equations that controlled for 20 or more variables. Conclusion. We conclude that adverse neonatal effects associated with fetal cocaine exposure follow a dose-response relationship: newborns with higher levels of prenatal cocaine exposure show higher rates of impairments in fetal head growth and abnormalities of muscle tone, movements, and posture. Significant relationships between cocaine exposure and these outcomes remain in controlled analyses. Pediatrics 1999;103:79-85; neurologic, in utero, cocaine exposure, neonates, hypertonia, central nervous system, movement disorder., ABBREVIATIONS. AIDS, acquired immunodeficiency syndrome; HIV, human immunodeficiency virus; PCP, phencyclidine; BW, birth weight; HC, head circumference; IUGR, intrauterine growth retardation; SGA, small for gestational age; NEC, Neurological Examination for [...]