Gastroschisis, the most common type of abdominal wall defect, has seen a steady increase in its prevalence over the past several decades. It is identified, both prenatally and postnatally, by the location of the defect, most often to the right of a normally-inserted umbilical cord. It disproportionately affects young mothers, and appears to be associated with environmental factors. However, the contribution of genetic factors to the overall risk remains unknown. While approximately 10% of infants with gastroschisis have intestinal atresia, extraintestinal anomalies are rare. Prenatal ultrasound scans are useful for early diagnosis and identification of features that predict a high likelihood of associated bowel atresia. The timing and mode of delivery for mothers with fetuses with gastroschisis have been somewhat controversial, but there is no convincing evidence to support routine preterm delivery or elective cesarean section in the absence of obstetric indications. Postnatal surgical management is dictated by the condition of the bowel and the abdominal domain. The surgical options include either primary reduction and closure or staged reduction with placement of a silo followed by delayed closure. The overall prognosis for infants with gastroschisis, in terms of both survival as well as long-term outcomes, is excellent. However, the management and outcomes of a subset of infants with complex gastroschisis, especially those who develop short bowel syndrome (SBS), remains challenging. Future research should be directed towards identification of epidemiological factors contributing to its rising incidence, improvement in the management of SBS, and obstetric/fetal interventions to minimize intestinal damage.

Objective: High-mobility group box-1 (HMGB1) is a potent inflammatory mediator and contributes to acute lung injury in adults. The role of HMGB1 in neonatal lung injury and the development of bronchopulmonary dysplasia (BPD) is unknown. We studied the association between HMGB1 levels in tracheal aspirates (TAs) and adverse outcomes (BPD/death) in ventilated premature infants (VPIs) and modulation of HMGB1 levels with dexamethasone (Dex) use.Study Design: Infants born before 32 weeks gestation and requiring mechanical ventilation were enrolled. Serial TA samples were collected on days 1, 3, 5 and 7 and HMGB1 levels were measured. HMGB1 levels in TA samples were compared between infants with no BPD and infants who developed BPD or died. HMGB1 TA levels were also compared before and after using Dex.Result: In all, 24 infants (gestational age 26.4±1.9 weeks, birth weight 859 ± 200 g) had no BPD, 60 infants (gestational age 25.4 ± 1.8 weeks, birth weight 749±156 g) developed BPD or died before 36 weeks postmenstrual age. Mean HMGB1 level in first week of life was significantly lower in infants with no BPD (27.3±16.5 ng mg -1 ) compared with those who developed BPD or died (45.1 ± 30.9 ng mg -1 , P ¼ 0.004). In total, 29 VPIs received Dex. There was no significant change in HMGB1 levels with steroid therapy (before 47.0 ± 43.9, after 60.1.5 ± 58.8, P ¼ 0.3).Conclusion: Our data suggest that higher HMGB1 levels in TA are associated with the development of BPD or death in VPI. Dex use had no effect on HMGB1 levels.

BackgroundInterferon‐gamma (IFN‐γ) and interferon‐inducible protein of 10 kDa (IP‐10) are potent inflammatory mediators and contribute to acute lung injury in adults. Recently, a potential role for IFN‐γ and IP‐10 in the pathogenesis of bronchopulmonary dysplasia (BPD) has been reported in animal models.ObjectiveTo study the association between IFN‐γ and IP‐10 in tracheal aspirate (TA) and the development of BPD in premature infants.Design/MethodsTA samples collected within 48 hr after birth from 79 mechanically ventilated premature neonates [gestational age (GA) <30 weeks (w), birth weight (BW) <1,250 g (g)] were analyzed. IFN‐γ was measured in a subgroup of 38 infants by using a biochip multi‐analyte immunoassay. The level of IP‐10 was determined using a commercially available ELISA kit. Total protein in TA was measured by Bradford assay to correct for sampling related dilution. BPD was defined as the need of supplemental oxygen at 36 weeks postmenstrual age (PMA).ResultsTwenty infants (GA 26.4 ± 1.9w, BW 860 ± 201 g) survived without BPD at 36 weeks PMA and 59 infants (GA 25.5 ± 1.5w, BW 751 ± 163 g) died before 36 weeks PMA or developed BPD. The mean IFN‐γ level was higher in infants who died or developed BPD (9.7 ± 2.8 vs. 3.1 ± 1.1 pg/ml, P = 0.03). Similarly, the mean IP‐10 level was higher in infants who died or developed BPD (63.4 ± 17.5 pg/ml) compared to those who survived without BPD (18.5 ± 7.5 pg/ml, P = 0.02).ConclusionsHigher IFN‐γ and IP‐10 levels in TA samples are associated with the development of BPD or death in premature infants. Pediatr Pulmonol. 2013; 48:8–13. © 2012 Wiley Periodicals, Inc.