Platelet-activating factor acetylhydrolase and haemophagocytosis in the sepsis syndrome

Citation
F. Trimoreau et al., Platelet-activating factor acetylhydrolase and haemophagocytosis in the sepsis syndrome, MEDIAT INFL, 9(3-4), 2000, pp. 197-200
Citations number
15
Categorie Soggetti
Immunology
Journal title
MEDIATORS OF INFLAMMATION
ISSN journal
09629351 → ACNP
Volume
9
Issue
3-4
Year of publication
2000
Pages
197 - 200
Database
ISI
SICI code
0962-9351(2000)9:3-4<197:PFAAHI>2.0.ZU;2-#
Abstract
SEPSIS syndrome (SS) is associated with depressed PAF acetylhydrolase, the enzyme responsible for the de gradation of plate let activating factor. PAF acetylhydrolase is in a large part produced by macrophages, whose inadequa te activation with haemophagocytosis is frequent in patients with SS. The aim of this study was to test the hypothesis that PAF acetylhydrolase l evels could be affected in these critically ill patients, be cause of the l arge amounts produced by activated macrophages in vitro and in vivo in anim al models. The levels of serum PAF acetylhydrolase were assessed in 90 SS patients, wh o were divided into thr ee groups : patients with (n = 34) or without haemo phagocytos is (n = 31), and patients without thrombocytopenia (n = 25) who were used as a control group. The number of organ dysfunctions was matched between patients with haemophagocytosis and controls. Normal reference valu es were obtained in 59 randomly selected blood donors. Circulating levels of PAF acetylhydrolase were significantly (p = 0.0001) d ecreased in patients with SS (57 +/- 3 nnol/ml/min, n = 90) when compared w ith healthy subjects (69 +/- 3 nmol/ml/min, n = 59). PAF acetylhydrolase le vels were greater in the presence of a haemophagocytos is but without stati stical significance (64.2 +/- 6.5 vs 50.1 +/- 2.8: p = 0.25). Despite the fact that macrophagic activation stimulates the in vitro releas e of PAF acetylhydrolase, no difference was found between patients with or without haemophagocytosis. The mechanism and the role of the PAF acetylhydr olase reduction in SS patients remain to be determined.