Bronchopulmonary Dysplasia

Inflammatory response of fruit and maternal parts of placenta exerts protective effects on the development of bronchopulmonary dysplasia?

Intrauterine infection and identify an immune inflammatory response of the fetus (GPs) in the form of vasculitis umbilical vessels (CAP) and the inflammatory response of the mother (PTO) in the form of chorioamnionitis (CA) to reduce the risk of neonatal respiratory distress syndrome (RDS), but the role of fetal and neonatal infection the development of bronchopulmonary dysplasia (BPD) in infants remains controversial.

The purpose of this study was to determine the impact of CA, CP and neonatal sepsis (NS) on the development of BPD in preterm infants.
bronchopulmonary dysplasia treatment
Methods and progress in the study.
From 1 January 1992 to December 31, 2004, in University Center Level 3, the Sydney (Australia) study was conducted of all infants born at term gestation < 30 weeks admitted to the intensive care unit and neonatal intensive care (NICU) and surviving up to 36 weeks corrected age(CB). Patients with severe birth defects and children with no examination of the placenta were excluded from the study. Prenatal and perinatal data collected in databases the hospital, were compared within dependent central neonatal database and laboratory diagnostic messages. NA subdivided according to culture the blood of three groups: 1) caused by coagulase-negative staphylococci (KNU), 2) other bacteria (DB) and the species Candida (RK). Results. Total in this center during the study period there were 60,776 live births, and preterm birth ( <37 weeks' gestation) accounted for11%of all births. Among the premature infants were 798 infants born at gestational age(GA) <30 weeks admitted to NICU, and survived to 36 weeks of ST. 761 of 798 infants (95.4%) with an examination of the placenta were included in the study. 603 patients were from singleton pregnancies, 158 - from multiple pregnancy. Average HS infant in the cohort was 27.4 +1.5 weeks. Antenatal corticosteroids were 94.4% (718) of mothers, of whom 33.8% (257) - 1 dose and 60.6% (461) - 2 doses. When examining the placenta in 140 (18,4%) cases of 761 were identified only HA in 208(27,3%) - XA + EP. Full frame confirmed by histology of HA with or without the EPin, the cohort was 45.7% (348 of 761). The frequency of CA in relation to the gestation period was inversely proportional to the HSandranged from 67.9% in HS 24 weeks to 31.9% for hepatitis B 29 weeks. In 1 surviving child born at GW for 23 weeks, was HA+ CAP. VP without HA in the cohort study was not observed. Inflammation of the placenta was significantly lower in mothers who did not have contractions, pregnant women with hypertension and multiple pregnancy. There was no difference in the results of histological examination of the placenta, depending on the dose of antenatal steroids (0, 1 or two doses), sex, intrauterine growth, the presence of a functioning ductus arteriosus, NA or low Apgar evaluation at 1 or 5 minutes of life. In 236, patients were diagnosed with HC: at 6, 8% - with early-onset ( < 48 hours after birth) and 93, 2% - with late-onset (> 48 hours after birth). Histological HA with or without CP was not associated with early or late in the NA(P = 0, 46). In children without NA (n = 525 [69%])on at birth was significantly higher(27.7 + 1.3 weeks) than in patients with UA (26,7 + 1, 5; P < 0,001).BPD was diagnosed in 193 (25,4%) of 761 infants. Mean HBV at birth in infants with BPD was 26.5 + 1.5 weeks, where as the average HS children without BPD - 27,7 + 1,3 (P <0,001). In the first model of step wise logistic regression to identify risk factors and protective factors for BPD were taken into account: GW at birth (week), birth weight(BP) < 3rd percent, histological examination of the placenta(the absence of inflammation; XA EP) and HC (absence of sepsis, sepsis caused by CND, DB, or RK). Adjusted hazard ratio (SPA) for the EP showed a significant protective effect for BPD (SPA: 0.61,95% confidence interval [CI]: 0,39 - 0, 95), as well as an increase in HS (SPA: 0.58, 95% CI: 0,51 - 0, 67). There was a marked tendency for the protective effect of HA (SPA: 0.64, 95%CI: 0,39 - 1, 07). Significantly increased risk of BPD was diagnosed when BP <3rd percentile (SPA: 3.33, 95% CI: 1.29- 8.64) and NA: sepsis caused by the ANC (SPA: 3.17, 95% CI: 2, 08 - 4.83), sepsis caused by DB (SPA:2.46, 95%CI: 1.42- 4.27) and sepsis caused by RK (SPA:8.68, 95%CI: 1,65- 45, 63). The protective effect of the EP for the development of BPD remained in the model without the National Assembly. This suggested that the National Assembly - an independent risk factor for BPD.

In the second model to identify risk factors and protective factors for the development of BPD were taken into account histological examination of placenta and neonatal infections, which are classified into four groups:
1) the absence of placental inflammation and the absence of neonatal infection (n = 289),
2) HA ± VI and the absence of neonatal infection (n = 236), and
3) HA ± CP and neonatal infection (n = 112) and
4) the absence of HA ± CP and neonatal infection (n = 124).

The second step wise logistic regression model included: hepatitis B at birth (week), BP < 3rd percentile and the new combined variable. The results for HS and BP < 3rd percentile was essentially the same as the first model. Compared with the group with the absence of placental inflammation and neonatal infection in children with HA ± VI to the lack of infection was significantly less likely to have BPD (SPA: 0.58, 95% CI: 0,35 -0,96). In both groups, with neonatal infection risk of BPD was significantly increased, but children with HA ± CP had a lower risk of BPD (SPA: 1.98, 95% CI: 1.15 -3.39) than patients without inflammatory changes in the placenta (SPA: 2.71, 95% CI: 1.64 -4.51).

The study authors concluded that the presence of an inflammatory response of fruit and maternal part of placenta exerts a protective effect for the development of BPD. According to the authors, the National Assembly - an independent risk factor for BPD. The limitation of this study was a single center study.
The authors believe that sepsis caused by ANC, like sepsis caused by DSS, increases the risk of BPD; however, fungal sepsis leads toa very high risk of developing BPD.

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