Article Text

IMBALANCE BETWEEN METALLOPROTEASES AND INHIBITORS IN PRETERM NEWBORNS WITH RESPIRATORY DISTRESS SYNDROME IN RELATION TO BRONCHOPULMONARY DYSPLASIA
  1. P G Matassa1,
  2. M R Colnaghi1,
  3. G Vento2,
  4. E Capoluongo3,
  5. V Vendettuoli2,
  6. M Pierro1,
  7. V Condo’1,
  8. C Tirone2,
  9. F Ameglio3,
  10. M Tana2,
  11. F Ciralli1,
  12. F Mosca1
  1. 1Institute of Pediatrics and Neonatology, Fondazione IRCCS Mangiagalli, Milan, Italy
  2. 2Division of Neonatology, Pol A Gemelli, Rome, Italy
  3. 3Department of Biochemistry and Clinical Biochemistry, Pol A Gemelli, Rome, Italy

Abstract

Objective To evaluate metalloproteinases and their inhibitor levels in preterm infants with respiratory distress syndrome (RDS), and to correlate them with the development of bronchopulmonary dysplasia (BPD).

Methods In infants born with gestational age <30 weeks and/or birth weight <1250 g, ventilated for RDS within 24 h of life, we collected bronchoalveolar lavage fluid (BAL) on the third day of life in order to determine levels of matrix metalloprotease (MMP)-1, MMP-2, MMP-8, MMP-9, MMP-10, tissue inhibitor of metalloproteases (TIMP)-1, TIMP-2 (ng/ml), and MMP-9/TIMP-1 and MMP-2/TIMP-2 ratio.

Results We studied 69 infants (birth weight 880.220 g, gestational age 27.2 weeks; mean SD) divided into two groups according to the definition of new BPD: group 1 not developing BPD (n  =  30) and group 2 (n  =  39) developing BPD. Group 2 showed significantly increased levels of MMP-9/TIMP-1 ratio (0.27 vs 0.11, p = 0.03), and significantly reduced levels of TIMP-1 (median value 182 949.00 vs 370 058.85, p<0.001), in comparison with group 1. No significant difference was found for MMP-1, MMP-2, MMP-8, MMP-9, MMP-10, TIMP-2 and MMP-2/TIMP-2 ratio. The data were analysed using non-parametric median score test, Brown Mood test, statistical software SAS STATA.

Conclusions Our results show a significant and early imbalance between some MMP and their inhibitors in infants developing BPD. Such imbalance may lead to an important extracellular matrix (ECM) damage, and a reduced capacity for ECM remodelling involved in BPD development.

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