In vitro fertilisation and use of ovulation enhancers may both influence childhood height in very low birthweight infants.

CONTEXT: Term-born children conceived by in vitro fertilisation (IVF) are reportedly taller than naturally conceived (NC) children. High levels of growth promoting hormones and epigenetic imprinting have been suggested as pathogenetic mechanisms. HYPOTHESIS: Tall stature in prematurely born IVF-conceived (IVF-C) children suggests pre- or early implantation imprinting rather than a postnatal effect. METHODS: We studied 334 very low birthweight (VLBW: birth weight <1500 g) children born prematurely during 1995-1999 and obtained their anthropometric measures at 6-10 years of age. Perinatal and neonatal data were obtained from the Israeli VLBW database. We compared IVF-C, ovulating agents conceived (OA-C) and naturally conceived (NC) groups of children with respect to their and their parents' anthropometry and their perinatal/neonatal variables. RESULTS: Childhood height standard deviation scores (SDSs) were greatest in IVF-C (-0.12 (SD 1.25); p<0.022) and insignificantly greater in OA-C (-0.37 (SD 1.02)) as compared to NC (-0.58 (SD 1.36)) children. The IVF-C and NC groups were significantly different regarding 17 parental and perinatal variables; however, multiple regression analysis including these variables showed that, as compared with NC, IVF-C children had significantly older mothers at birth with earlier follow-up during pregnancy and more multi-fetal pregnancies. CONCLUSIONS: IVF-C and to a lesser extent OA-C prematurely born children are taller than otherwise NC children. After ruling out postnatal and parental causes, we speculate that pre- or early implantation factors might have contributed to the taller stature of IVF-C children.

Bhutani-based nomograms for the prediction of significant hyperbilirubinaemia using transcutaneous measurements of bilirubin.

AIM: Prospectively establish the relationship between transcutaneous bilirubin (TcB) and total serum bilirubin (TSB), and develop nomograms similar to Bhutani's nomograms, based on our TcB data. METHODS: Our study sample was from a total population of 1069 infants, near term and term healthy newborns, admitted during 2.5 month period of the study. TSB was performed on all infants who were felt to be clinically jaundiced. Before obtaining the TSB, a TcB was performed (Jaundice Meter Minolta/Draeger JM-103). Measurements were performed on two sites: forehead and mid-sternum, and the mean of both measurements was calculated. RESULTS: A total of 1091 paired measurements were obtained from 628 infants. Linear regression showed a significant relation between TSB and TcB (R(2) of 0.846). In multiple regression analysis, all independent variables studied, i.e. gestational age (or birthweight), age at sampling and ethnicity had a negligible influence on the relationship. We subsequently developed our local-nomograms of hour-specific mean TcB with 40, 75 and 95 percentile lines. CONCLUSIONS: In our local settings and population, we found a reliable correlation between laboratory measurements of TSB and TcB. We were able to develop our local-Bhutani-based TcB nomograms for screening babies during hospital stay and pre-discharge for assessing the risk of hyperbilirubinaemia.

Effect of maternal tocolysis on the incidence of severe periventricular/intraventricular haemorrhage in very low birthweight infants.

AIM: To examine the relation between grade III-IV periventricular/intraventricular haemorrhage (PVH/IVH) and antenatal exposure to tocolytic treatment in very low birthweight (VLBW) premature infants. STUDY DESIGN: The study population consisted of 2794 infants from the Israel National VLBW Infant Database, of gestational age 24-32 weeks, who had a cranial ultrasound examination during the first 28 days of life. Infants of mothers with pregnancy induced hypertension or those exposed to more than one tocolytic drug were excluded. Of the 2794 infants, 2013 (72%) had not been exposed to tocolysis and 781 (28%) had been exposed to a single tocolytic agent. To evaluate the effect of tocolysis and confounding variables on grade III-IV PVH/IVH, the chi(2) test, univariate analysis, and a logistic regression model were used. RESULTS: Of the 781 infants (28%) exposed to tocolysis, 341 (12.2%) were exposed to magnesium sulphate, 263 (9.4%) to ritodrine, and 177 (6.3%) to indomethacin. The overall incidence of grade III-IV PVH/IVH was 13.4%. In the multivariate logistic regression analysis, the following factors were related significantly and independently to grade III-IV PVH/IVH: no prenatal steroid treatment, low gestational age, one minute Apgar score 0-3, respiratory distress syndrome, patent ductus arteriosus, mechanical ventilation, and pneumothorax. Infants exposed to ritodrine tocolysis (but not to the other tocolytic drugs) were at significantly lower risk of grade III-IV PVH/IVH after adjustment for other variables (odds ratio = 0.3; 95% confidence interval 0.2 to 0.6). CONCLUSION: This study suggests that antenatal exposure of VLBW infants to ritodrine tocolysis, in contrast with tocolysis induced by magnesium sulphate or indomethacin, was associated with a lower incidence of grade III-IV PVH/IVH.

Neonatal withdrawal syndrome and behavioral effects produced by maternal drug use.

Over the last two decades, drug and alcohol abuse by pregnant women has spread to epidemic proportions. Maternal drug abuse has neurobehavioral and somatic effects which may be long-lasting and devastating to the offspring. Opiates, such as heroin and pain killers that contain a narcotic component, are widely abused today. A prominent manifestation of fetal exposure to these drugs is the neonatal withdrawal syndrome, which typically includes wakefulness, jitteriness and other symptoms of cerebral irritability. These, in turn, may interrupt early mother-infant interaction, affecting the infant's long-term emotional and cognitive development. Fetal cocaine exposure may cause neonatal cerebral irritability, changes in habituation responses, reduced head circumference, poor mental development and long-lasting impairment of the brain. Benzodiazepines can cause fetal dysmorphism (including microcephaly), neurological and behavioral impairments and neonatal withdrawal symptoms. Maternal use of amphetamines may cause neonatal dysphoria and agitation, as well as long-term lassitude and drowsiness that may result in poor feeding. Fetal exposure to alcohol may cause neonatal withdrawal symptoms, maladaptive behavior in childhood and the fetal alcohol syndrome (including microcephaly). Maternal alcohol consumption is also a common cause of mental retardation. Fetal exposure to marijuana may delay maturation of the visual system and impair memory and verbal performance at 2 years of age. The inevitable conclusion is that society must seek ways not only to treat, but also to prevent this epidemic. To this end, a key factor would be to identify potential drug abusing mothers before they reach the stage of prenatal care and educate them regarding the fatal consequences of drug abuse.