Summarybe denied on the basis that such effects have not been observedThe effect of 100 mg of phenobarbital (PB) at bedtime for the last few wk of pregnancy on the incidence and severity of neonatal hyperbiirubinemia was studied. No effect was observed in the newborns of mothers who took less than ten tablets. In the 1310 newborns of adequately treated mothers (PB 1 1.0 g), the incidence of marked jaundice (bilirubin > 16.0 mg/dl) and the need to perform an exchange transfusion were reduced by a factor of six in relation to the incidence in 1553 control infants.A randomly selected group of 415 children (182 control, 233 PB) were reexamined at 61 to 82 months of age. There was no difference in the overall morbidity and mortality between the control and treatment group. A detailed neurologic assessment failed to reveal any differences between the two groups. In the VisuoMotor Integration test, the PB group scored significantly better than the control group. In the Draw-A-Woman and the Verbal Intelligence Test, the difference was in the same direction but was not statistically significant. The degree of jaundice was not found to significantly influence the performance in the neurological examination and the intelligence tests. Sensorineural hearing defect was significantly more common in the children with moderate or marked jaundice (bilirubin > 12 mg/dl) than in those with lesser degrees of jaundice.Prenatal PB is a practical, effective, and safe method for decreasing the incidence of neonatal hyperbilirubinemia.

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Background. Studies in vitro, in animal models, and in adult and newborn humans have demonstrated that certain tin(Sn)-porphyrins that competitively inhibit the activity of heme oxygenase, the rate-limiting enzyme in heme catabolism, reduce production of bilirubin and can thereby substantially diminish plasma levels of the bile pigment. Objectives. To assess the effectiveness of increasing doses of the heme oxygenase inhibitor, Sn-mesoporphyrin (SnMP), in moderating the development of significant hyperbilirubinemia and thus the requirements for phototherapy in preterm newborns. Methods. In five randomized, blinded, placebo-controlled trials, SnMP in increasing doses from 1 µmol to 6 µmol/kg body weight was administered intramuscularly in the first 24 hours of life in preterm newborns of 210 to 251 days gestational age. "Special blue" lamps (Phillips F20T12/BB) were used for phototherapy in newborns exceeding a predetermined plasma bilirubin concentration, irrespective of study group. Results. A total of 517 newborns were randomized in the five trials carried out sequentially over a 4-year period. SnMP in a dose-related manner significantly ameliorated the course of hyperbilirubinemia in the treated newborns Of all gestational ages. With a SnMP dose of 6 µmol/kg body weight, the mean peak incremental plasma bilirubin concentration was reduced by 41% and the phototherapy requirements were decreased by 76% compared to control subjects. Erythema observed in a few SnMP-treated newborns who required phototherapy was mild, transient, and without sequelae. No other untoward effects were observed during hospitalization or at a follow-up at post-term age of 3 and 18 months. Conclusions. SnMP, by inhibiting the production of bilirubin, substantially moderates the development of hyperbilirubinemia in preterm newborns. This compound and similarly acting enzyme inhibitors merit further clinical study as agents for controlling neonatal hyperbilirubinemia, particularly in neonatal populations for whom other treatment modalities are not available.

α-Fetoprotein (α-FP) was measured in dried blood spots from normal, congenital hypothyroid (CH) and transient hyperthyrotropinemic (TH) newborns as well as in serum from CH and TH babies together with thyroxine, triiodothyronine and thyrotropin. The half-life of α-FP had a median value of 12 days in the CH cases and 4.9 days in the TH cases. α-FP was significantly higher in the CH group before treatment and showed a significant rise after discontinuation of thyroxine therapy. It would appear that thyroid hormones influence α-FP metabolism and that a hypothyroid environment results in increased α-FP levels.

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