Article Text

ACUTE RESPIRATORY DISTRESS SYNDROME SECONDARY TO RESPIRATORY SYNCYTIAL VIRUS BRONCHIOLITIS: AN IN-VIVO MODEL TO STUDY THE ROLE OF SECRETORY PHOSPHOLIPASE A2
  1. D De Luca1,
  2. A Minucci2,
  3. E Capoluongo2,
  4. M Piastra1,
  5. D Pietrini1,
  6. E Zecca3,
  7. G Conti1
  1. 1Pediatric Intensive Care Unit, Department of Anaesthesiology and Intensive Care, University Hospital “A Gemelli”, Catholic University of The Sacred Heart, Rome, Italy
  2. 2Laboratory of Clinical Molecular Biology, Institute of Biochemistry and Clinical Biochemistry, University Hospital “A Gemelli”, Catholic University of The Sacred Heart, Rome, Italy
  3. 3Division of Neonatology, Department of Pediatrics, University Hospital “A Gemelli”, Catholic University of The Sacred Heart, Rome, Italy

Abstract

Objectives Respiratory syncytial virus (RSV) is a major cause of viral respiratory infections. Bronchiolitis is its main manifestation and acute respiratory distress syndrome (ARDS) has been rarely described as the worst complication. Secretory phospholipase A2 (PLA2) is a key enzyme in ARDS pathophysiology and the cause of airways hyperresponsiveness and increased mucous production. RSV has been proved to cause direct induction of PLA2. No data are available about it in paediatric ARDS. We aimed to study the model of RSV-related ARDS to investigate the role of PLA2, just after the viral stimulus.

Methods During the RSV season two bronchiolitis evolving in ARDS were observed. Patients were enrolled according to American-European criteria for ARDS. We enrolled six age-matched controls, ventilated for non-pulmonary reasons. Static respiratory mechanics, Murrey’s score and ventilation parameters were considered. Bronchoalveolar lavage fluid (BALF) and serum were assayed for PLA2, every 24 h, using an ultrasensitive enzyme immunoassay method. Data were corrected using serum/supernatant urea ratio.

Results Lung PLA2 is higher in patients than in controls (p = 0.039). ARDS babies have a lower static compliance (p = 0.035). Enzyme is more elevated in serum, although this is insignificant. Lung PLA2 activity decreases during ARDS recovery, whereas respiration and mechanics parameters improve. PLA2 is higher in serum than in BALF and remains high, despite the patients’ improvement.

Conclusions PLA2 is elevated in patients and is associated with lung stiffness. Findings confirm the adult data: lung PLA2 is produced by alveolar macrophages and circulating enzyme is unrelated to ARDS pathogenesis. RSV-induced ARDS is a promising model to study the lung injury pathophysiology.

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