Serial changes in levels of IL-6 and IL-1beta in premature infants at risk for bronchopulmonary dysplasia.

The aim of this study was to define the inflammatory changes occurring in the lungs of infants at risk for bronchopulmonary dysplasia (BPD) over the first 28 days of life, and to define an optimal strategy for steroids therapy in the prevention of BPD. We measured levels of interleukin-6 (IL-6) and interleukin-1 beta (IL-1beta) in tracheal aspirate (TA) samples and blood of premature infants with severe respiratory distress syndrome RDS (n = 45) on the first day of life prior to initiation of surfactant therapy and on days 5-7, 12-14, 19-21, and 26-28. Levels of IL-6 and IL-1beta were determined with a commercially available enzyme-linked immunoassay. Logistic regression analyses were performed in order to examine differences in trends in levels of IL-6 and IL-1beta between groups of infants. Infants were divided into group I (n = 30, FiO(2) < or = 0.35 at 28 days) and group II (n = 15, FiO(2) > 0.35 based on their likelihood of developing BPD at 36 weeks postconceptional age (PCA). The infants were comparable with respect to mean ( +/- SEM) birth weight (895 +/- 33 g vs. 900 +/- 40 g), gestational age (27 +/- 0.38 weeks vs. 27 +/- 0.54 weeks), and severity of respiratory illness at entry into the study (mean airway pressure: 12 +/- 1 cmH(2)O vs. 12 +/- 1 cmH(2)O, and oxygen index: 15 +/- 2 vs. 19 +/- 4) (group I vs. group II, respectively). Logistic regression analyses failed to reveal any significant differences in linear trends of levels of IL-6 and IL-1beta in TA samples between both groups of infants. No particular pattern of change in levels of IL-6 or IL-1beta could be identified among groups of infants. Levels of IL-6 and IL-1beta in TA samples on the first day of life failed to predict the need for FiO(2) > 0.35 at 28 days of age. We could not identify an increasing trend or a specific pattern of changes in postnatal levels of IL-6 or IL-1beta in TA samples of infants who were at greater risk of developing BPD at 36 weeks PCA compared to infants who were not.

Surfactant phospholipids and surface activity among preterm infants with respiratory distress syndrome who develop bronchopulmonary dysplasia.

Our objective was to determine if preterm infants with respiratory distress syndrome who develop bronchopulmonary dysplasia have abnormalities in surfactant phospholipids and/or function. Tracheal aspirate samples obtained from preterm infants with respiratory distress syndrome on days 1, 3-5, 7-10, 14-17, 21-24 and 27-30 were analyzed for total phospholipids and phospholipids fractions by determination of total phospholipid phosphorus and thin layer chromatography, respectively. Surfactant properties were assessed with captive bubble surfactometer. Sixteen out of 56 (29%) infants died during the first 30 d of life. Infants who died were more immature, required more ventilatory support and had a surfactant with lower surface-tension-reducing properties than infants who survived (p < 0.05). Surviving infants were divided into group I (no bronchopulmonary dysplasia at 27-30 d, n = 25) and group II (with bronchopulmonary dysplasia at 27-30 d, n = 15). No significant differences in concentrations of surfactant phospholipids nor measurements of surface tension were noted among groups of infants. Surfactant therapy after birth was associated with a significant increase in concentrations of total phospholipids, lecithin, phosphatidylinositol and lower surface-tension measurements at 3-5 d of age among surviving infants (p < 0.01). Abnormalities in concentrations of surfactant phospholipids or surfactant function could not be demonstrated during the first month of life among preterm infants with respiratory distress syndrome who develop bronchopulmonary dysplasia.

Yield and costs of screening growth-retarded infants for torch infections.

Many infants with intrauterine growth retardation (IUGR) are screened for TORCH infections. The yield and costs of such a practice may not be justifiable. Medical charts of infants with IUGR who had a workup for toxoplasmosis, other (infections), rubella, cytomegalovirus (infection), and herpes (simplex) (titer) (TORCH) infections were reviewed for the presence of clinical findings, laboratory and head ultrasound abnormalities associated with intrauterine infections. Maternal charts and reports of placental pathology were reviewed for identifying maternal illnesses and placental causes associated with IUGR. Seventy-five out of 182 infants (41%) with IUGR had a workup for TORCH infection. Maternal conditions associated with IUGR included: pregnancy-induced hypertension (19%), tobacco use (43%), alcohol abuse (21%), illicit drug use (24%), chronic hypertension, diabetic vasculopathy or collagen vascular disease (12%), and multiple gestation (3%). Placental pathology was available in 53/75 cases. Thirty-six of fifty-three (67%) placentae had abnormalities associated with IUGR: placental infarcts (22 of 36), vasculitis/villitis (15 of 36), placenta previa (1 of 36), abruptio placenta (2 of 36), and velamentous insertion of umbilical cord (1 of 36). Clinical findings among infants included hepatosplenomegaly, cataract or rash (1 of 75), thrombocytopenia and/or neutropenia and/or direct hyperbilirubinemia (11 of 75). Seven out of 75 infants had dysmorphic features. None of the infants (0 of 75) had positive IgM titers for toxoplasma, rubella, cytomegalovirus (CMV), or herpes simplex virus (HSV). No infants (0 of 43) had elevated total IgM titers; one infant (1 of 57) had a positive urine culture for CMV. One infant had evidence of calcifications on head ultrasound and a second infant had hydrocephalus (2 of 43). The costs associated with workup for TORCH infections among 75 infants included: TORCH titers determination: $17,816, total IgM titers: $1318, urine culture for CMV: $5734, and head ultrasound: $28,165. The yield of workup for TORCH infection among infants with IUGR is poor and does not justify the incurred costs.

Antenatal phenobarbital therapy and neonatal outcome. I: Effect on intracranial hemorrhage.

OBJECTIVE: To evaluate the effect of antenatal phenobarbital (PB) therapy on neonatal intracranial hemorrhage (ICH) in preterm infants. DESIGN: Prospective, randomized, controlled trial. SETTING: Single institution study. SUBJECTS AND INTERVENTIONS: Women in preterm labor ( < 35 weeks' gestation) were assigned to control and treatment groups. The treatment group received 10 mg/kg (maximum, 1000 mg) PB intravenously, followed by 100 mg orally daily, until delivery. Neonates did not receive PB after birth. Head sonograms were performed on days 3, 7, and 14 and at discharge. Hemorrhage was classified as mild, moderate, or severe by a single reader. OUTCOME MEASURES: Incidence of neonatal ICH in all infants, infants weighing less than 1250 g, and infants of multiple gestations. RESULTS: The study population comprised 110 women, 60 in the control group and 50 in the PB group. Neonates in the control group (n = 74, including 10 pairs of twins and 2 sets of triplets) were comparable to those in the treatment group (n = 62, including 7 pairs of twins, 1 set of triplets, and 1 set of quadruplets) regarding birth weight, gestational age, and other clinical risk factors for ICH. There was a trend for the incidence of any grade of hemorrhage to be lower in the PB group (22% [14 of 62]) compared with the control group (35% [26 of 74]). Moderate and severe hemorrhages were significantly lower in the PB group (1.6% [1 of 62]) compared with the control group (9.4% [7 of 74]). Among infants weighing less than 1250 g, overall ICH was lower in the PB group (23% [6 of 26]) compared with the control group (51% [18 of 35]). Among multiple-gestation infants, overall ICH was 4.7% (1 of 21) in the PB group, compared with 31% (8 of 26) in the control group. CONCLUSIONS: Antenatal PB therapy results in a significant decrease in moderate and severe ICH in infants born at less than 35 weeks' gestation. Antenatal PB therapy also resulted in a decrease in the incidence of all grades of ICH in infants weighing less than 1250 g and infants born of multiple gestations.

Noninvasive prediction of hyaline membrane disease: an optimized classification of sonographic placental maturation.

Accurate prediction of fetal pulmonary maturity by means of a less invasive procedure than amniocentesis would be desirable. Sonographic diagnosis of a Grade III placenta has been reported to be an excellent predictor of fetal lung maturity. The standard classification of placental grading assigns grade according to the most advanced portion of the placenta. Using this classification, we studied 230 patients. In 80 pregnancies with Grade III placenta, three of the neonates developed respiratory distress syndrome. With reclassification of the placentas as immature, (no Grade III areas), intermediate, (only a portion of the placenta being Grade III), or mature, (Grade III placenta throughout), it was found that no neonatal hyaline membrane disease occurred in the 41 pregnancies with mature placentas, whereas 12% of the neonates in the immature group and 8% in the intermediate group developed hyaline membrane disease. These findings suggest that when sonographic examination of the placenta shows both Grade III and non-Grade III sections, there is still a risk for an immature amniotic fluid lecithin/sphingomyelin ratio and neonatal hyaline membrane disease. The placentas should be considered mature only when Grade III changes are present in all sections examined by ultrasound.