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Mediators of Inflammation
Volume 9 (2000), Issue 3-4, Pages 197-200

Platelet-activating factor acetylhydrolase and haemophagocytosis in the sepsis syndrome

1Department of Haematology, Dupuytren University Hospital, Limoges, France
2Intensive Care Unit, Dupuytren University Hospital, Limoges, France
3EP CNRS 118, Faculty of Medicine, 2 rue Dr Marcland, Limoges 87025, France

Copyright © 2000 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Sepsis syndrome (SS) is associated with depressed PAF acetylhydrolase, the enzyme responsible for the degradation of platelet activating factor. PAF acetylhydrolase is in a large part produced by macrophages, whose inadequate activation with haemophagocytosis is frequent in patients with SS.

The aim of this study was to test the hypothesis that PAF acetylhydrolase levels could be affected in these critically ill patients, because of the large amounts produced by activated macrophages in vitro and in vivo in animal models.

The levels of serum PAF acetylhydrolase were assessed in 90 SS patients, who were divided into three groups: patients with (n = 34) or without haemophagocytosis (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 values were obtained in 59 randomly selected blood donors.

Circulating levels of PAF acetylhydrolase were significantly (p = 0.0001) decreased in patients with SS (57 ± 3 nnol/ml/min, n = 90) when compared with healthy subjects (69 ± 3 nmol/ml/min, n = 59). PAF acetylhydrolase levels were greater in the presence of a haemophagocytosis but without statistical significance (64.2 ± 6.5 vs 50.1 ± 2.8: p = 0.25).

Despite the fact that macrophagic activation stimulates the in vitro release of PAF acetylhydrolase, no difference was found between patients with or without haemophagocytosis. The mechanism and the role of the PAF acetylhydrolase reduction in SS patients remain to be determined.