Abstract
There is little data on the association between Human Leucocyte Antigen (HLA) alleles and Bronchopulmonary Dysplasia (BPD) of the preterm newborn. Our aim was to assess associations between HLA alleles and BPD susceptibility. We studied 156 preterm neonates (82 M/74 F) < 32 weeks gestational age, alive at 36 weeks gestational age. Detailed clinical data were collected. HLA typing was performed by PCR-SSO. HLA allele frequencies where determined by direct counting for BPD and no-BPD groups. Comparison between BPD and no BPD groups was performed usingt-test, χ2test or Fisher exact test and logistic regression as appropriate. Relative risks (RR) and their 95% confidence intervals (95% CI) were also calculated as association measures. We diagnosed 56 (35.9%) neonates with mild BPD and 27 (17%) with moderate/severe BPD. We found a significant association between HLA-DRB1*01 and mild BPD (OR=3.48[1.23–10.2]). The alleles HLA-A*24, -A*68, -B*51,-Cw*07, -Cw*14, -Cw*15 and -DRB1*01 presented a significant association with moderate/severe BPD. When adjusted to gestational age and birth weight HLA-A*68 (OR=5.41[1.46; 20.05]), -B*51 (OR=3.09[1.11; 8.63]) and -Cw*14 (OR=4.94[1.15; 21.25]) were significantly associated with moderate/severe BPD. Conclusion – Our findings suggest an association between HLA-A*68, -B*51 and -C*14 and BPD susceptibility, and that an autoimmune mechanism may be implicated in the pathogenesis of the disease.
Highlights
Chronic lung damage of the preterm newborn is the consequence of disturbed lung development and inflammation due to prematurity and perinatal triggering factors
Four hundred caucasian preterm neonates less than 32 weeks gestational age (31 weeks and 6 days, inclusive), born between January 2000 and June 2009 at two tertiary neonatal intensive care units (NICU) in the north of Portugal, and alive at 36 weeks postmenstrual age were selected for major histocompatibility complex (MHC) study
Preterm neonates affected by a TORCH infection, a chromosomal or a major congenital anomaly, twin-twin transfusion syndrome, asphyxia, any inborn error of metabolism detected during the neonatal period, as well as those transferred to another institution or deceased before 36 weeks corrected age, were excluded
Summary
Chronic lung damage of the preterm newborn is the consequence of disturbed lung development and inflammation due to prematurity and perinatal triggering factors. This condition, generally termed as bronchopulmonary dysplasia (BPD) affects about 20–30% of very low birth weight infants (birthweight < 1500 g) and is a major cause of morbidity and mortality in this vulnerable population [6,8]. In addition to the infant‘s clinical status their genetic predisposition may contribute to BPD as supported by recent twin studies [1,9,12]. Disturbed intrauterine lung development and vascularization may contribute to BPD; these processes may be impaired in the presence of some rare genetic mutations. There is a genetic component in the susceptibility to other perina-
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