title: Secretory phospholipase A₂ pathway during pediatric acute respiratory distress syndrome: a preliminary study.
abstract: OBJECTIVE
  To verify if secretory phospholipase A2 (sPLA2) is increased in pediatric acute respiratory distress syndrome (ARDS) triggered or not by respiratory syncytial virus infection and to clarify how the enzyme may influence the disease severity and the degree of ventilatory support.
  
  
  METHODS
  Prospective pilot study.
  
  
  METHODS
  Two academic pediatric intensive care units.
  
  
  METHODS
  All infants < 6 months old hospitalized for severe respiratory syncytial virus bronchiolitis, who developed ARDS (respiratory syncytial virus-ARDS group); all infants < 6 months old diagnosed with ARDS secondary to other causes (ARDS group); and infants < 6 months old who needed ventilation for reasons other than any lung disease (control group).
  
  
  METHODS
  None.
  
  
  RESULTS
  We enrolled six respiratory syncytial virus -ARDS babies, five ARDS babies, and six control infants. The sPLA2 activity and tumor necrosis factor (TNF)-α were significantly higher in the bronchoalveolar lavage of ARDS infants. Worst oxygenation, ventilation, and longer pediatric intensive care unit stay and ventilation time were present in ARDS babies. No differences were found in Clara cell secretory protein and in serum cytokines levels. Because there is no correlation between bronchoalveolar lavage protein content (a marker of permeability) and sPLA2, the enzyme seems mainly produced in the alveoli. TNF-α, the main inductor of sPLA2 expression, significantly correlates with the enzyme level in the bronchoalveolar lavage. Significant positive correlations exist between sPLA2, TNF-α and oxygen need, mean airway pressure, ventilatory index, and the Murray's lung injury score. Negative correlations were also found between sPLA2, TNF-α, and Pao2/Fio2 ratio.
  
  
  CONCLUSIONS
  The sPLA2 and TNF-α are increased in ARDS and seem correlated with clinical severity, higher oxygen requirement, and more aggressive ventilation. This correlation confirms findings from adult experience and should guide further investigations on pediatric ARDS pathophysiology.
authors.affiliation: Neonatal Intensive Care Unit, Institute of Mother And Child Sciences, Women's and Children Hospital G. Salesi, Polytechnical University of Marche, Ancona, Italy. dm.deluca@fastwebnet.it
authors.forename: Daniele
authors.initials: D
authors.lastname: De Luca
authors.forename: Angelo
authors.initials: A
authors.lastname: Minucci
authors.forename: Paola
authors.initials: P
authors.lastname: Cogo
authors.forename: Ettore D
authors.initials: ED
authors.lastname: Capoluongo
authors.forename: Giorgio
authors.initials: G
authors.lastname: Conti
authors.forename: Domenico
authors.initials: D
authors.lastname: Pietrini
authors.forename: Virgilio P
authors.initials: VP
authors.lastname: Carnielli
authors.forename: Marco
authors.initials: M
authors.lastname: Piastra
mesh_terms: D018893:Bronchoalveolar Lavage; D005260:Female; D006801:Humans; D007223:Infant; D015278:Intensive Care Units, Pediatric; D007558:Italy; D008297:Male; D054497:Phospholipases A2, Secretory / Q000378:metabolism*; D010865:Pilot Projects; D011446:Prospective Studies; D012128:Respiratory Distress Syndrome / Q000378:metabolism* / Q000821:virology*; D018357:Respiratory Syncytial Virus Infections / Q000150:complications* / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D014409:Tumor Necrosis Factor-alpha; D054497:Phospholipases A2, Secretory