Maternal obesity: significance on the preterm neonate.

BACKGROUND: What is known of neonatal outcomes associated with maternal obesity is limited. The impact on the preterm neonate, delivery room (DR) course and need for neonatal intensive care unit (NICU) admission has not been well established. METHODS: A review was done of our 17 county perinatal regions from the New York State Perinatal Data System database over the 3-year period of 1 January 2010-31 December 2012 for mother/baby dyad information for all live births 34-36 6/7 weeks' gestation. The National Institutes of Health body mass index (BMI) classification was used for maternal BMI with the category definitions of underweight, normal, overweight, obese Level I, obese Level II, and obese Level III. RESULTS: Information was obtained on 2155 women. In this group, 29% had obese BMIs. The incidence of pre-pregnancy diabetes mellitus (DM), DM during gestation and cesarean delivery (CD) in obese mothers was significantly different from normal weight mothers, P<0.001. More infants of Level III mothers required DR resuscitation when compared with infants of normal BMI mothers, 36 vs 16%, P <0.001. The need for assisted ventilation beyond 6 h of age and need for NICU admission was more likely in infants of Level III mothers, P<0.001. Women in all of the obese subgroups had preterm infants with increased birth weights (BWs) compared with preterm infants of normal weight mothers, P<0.001. DISCUSSION: Late preterm infants born to obese mothers are more likely to be delivered by cesarean section and have larger BWs. We found that infants born to obese Level III mothers are much more likely to require assisted ventilation in the DR and NICU admission.

Antagonistic effects of pyrrolidine dithiocarbamate and N-acetyl-L-cysteine on surfactant protein A and B mRNAs.

Pulmonary surfactant, a mixture of phospholipids and specific associated proteins, reduces surface tension at the air-liquid interface of the lung and protects the large epithelial surface of the lung from infectious organisms. Surfactant proteins, SP-A and SP-B, are required for normal surfactant function. In the current work, increased levels of oxidized glutathione (GSSG) are demonstrated at doses of pyrrolidine dithiocarbamate (PDTC) which decrease SP-A and SP-B mRNAs, suggesting that cellular oxidation reduces surfactant protein expression. Similarly, reduction of SP-A and SP-B mRNA levels following accumulation of GSSG induced by glutathione reductase inhibitor 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU), supports the hypothesis that surfactant protein synthesis is reduced in response to oxidation of pulmonary epithelial glutathione. Concurrent induction of apolipoprotein J (apoJ) mRNA by PDTC demonstrates the selectivity of pulmonary gene regulation by the dithiocarbamate. In contrast, the glutathione precursor N-acetyl-l-cysteine (NAC) prevented PDTC-dependent increase in GSSG/GSH ratio, inhibition of SP-A and -B mRNAs, and induction of apoJ. Insufficiency of SP-A and -B, which occurs in inflammatory lung diseases, may result from the exposure of the pulmonary epithelium to oxidant stress and may be reversed by the antioxidant NAC.

Fulminant necrotizing enterocolitis in a premature neonate treated for supraventricular tachycardia.

A premature neonate with supraventricular tachycardia was treated prenatally and postnatally, without significant signs of congestive heart failure. Enteral feeding was initiated after 48 hours of age. The infant developed fatal, fulminant necrotizing enterocolitis 28 hours after starting feeds.

Three-year follow-up of vaccine response in extremely preterm infants.

OBJECTIVE: To assess whether the adequate antibody response observed in former extremely premature infants after the primary series of immunizations is sustained after the first booster vaccines. SUBJECTS AND METHODS: Sixteen former extremely premature (<29 weeks, <1000 g at birth) and 17 former full-term (>37 weeks) infants had sera obtained for antibody titer measurement at 3 to 4 years of age. All had received the primary series and first booster vaccines for diphtheria, pertussis, tetanus, polio, and Haemophilus influenzae type b. Twelve preterm and 14 full-term children had completed the hepatitis B vaccine series. RESULTS: At 3 to 4 years of age, former preterm and full-term children had similar geometric mean titer (GMT) values of antibodies to tetanus, diphtheria, and pertussis. Preterm children had a lower GMT value of Haemophilus polyribosylribitol phosphate (PRP) antibody than did full-term children (0.99 vs 3.06 microg/mL). Fifty percent of preterm and 88% of full-term children had PRP antibody >1.0 microg/mL; 100% of preterm and 94% of full-term children had anti-PRP titers >0.15 microg/mL. GMT values of neutralizing antibodies to polio serotypes 1 and 2 were similar, with 94% to 100% of both groups above protective levels (>/=1:8). The difference in GMT values of polio serotype 3 approached significance (29 vs 73); fewer preterm children had protective titer values (75% vs 100%). Among children vaccinated against hepatitis B, 75% of preterm and 71% of full-term children were protected (10 mIU/mL). CONCLUSIONS: Preterm children immunized at the recommended chronological ages displayed antibody responses similar to those for full-term children for most immunizing antigens. Responses to PRP and polio serotype 3 were less robust than those of full-term children.

Regulation of surfactant proteins A and B by TNF-alpha and phorbol ester independent of NF-kappa B.

Acute lung inflammation is complicated by altered pulmonary surfactant phospholipid and protein composition. The proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and the phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (TPA) inhibit expression of surfactant-associated proteins A and B (SP-A and SP-B), both important for normal surfactant function. The transcription factor nuclear factor-kappa B (NF-kappa B) frequently mediates regulation of gene expression by TPA and TNF-alpha. In the present study, electrophoretic mobility shift assays (EM-SAs) and pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-kappa B activation, were utilized to determine the role of NF-kappa B activation in TPA and TNF-alpha inhibition of the surfactant proteins in NCI-H441 cells. Pentoxifylline (PTX), which inhibits TNF-alpha cellular effects without preventing NF-kappa B activation, was also tested. By EMSA, TPA and TNF-alpha increased nuclear NF-kappa B binding activity in temporally distinct patterns. PDTC decreased TPA- and TNF-alpha-induced NF-kappa B binding activity but did not limit their inhibition of SP-A and SP-B mRNAs. PDTC independently decreased both SP-A and SP-B mRNAs. PTX partially reversed TNF-alpha-but not TPA-mediated inhibition of SP-A and SP-B mRNAs without altering NF-kappa B binding. The effects of PDTC and PTX on NF-kappa B and the surfactant proteins suggest that NF-kappa B activation does not mediate TPA or TNF-alpha inhibition of SP-A and SP-B mRNA accumulation.