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Secretory phospholipase A2 activity correlates with postinjury multiple organ failure

Partrick, David A. MD; Moore, Ernest E. MD; Silliman, Christopher C. MD, PhD; Barnett, Carlton C. MD; Kuypers, Frans A. PhD

Clinical Investigations

Postinjury multiple organ failure (MOF) may result from overwhelming systemic hyperinflammation. Secretory phospholipase A2 (sPLA2) produces many inflammatory lipid mediators, and levels have been correlated with both the severity of patient injury and postinjury mortality. The objective of this study was to characterize the plasma activity of sPLA2 type IIa in severely injured patients and to determine whether the activity of this enzyme correlates with the subsequent development of MOF.

Patients Seventeen severely injured patients at known risk for MOF had blood sampled on postinjury days 0, 1, 2, 3, and 5.

Design sPLA2 activity was sequentially measured and correlated with MOF scores.

Results Six patients (35%) developed MOF. In comparison with non-MOF patients, MOF patients had elevated sPLA2 activity beginning 36 hrs postinjury (MOF sPLA2, 2.4 ± 0.97, vs. non-MOF sPLA2, 0.86 ± 0.16 active units (AU);p < .05) and continuing over the ensuing 5 days. To rule out the possibility that stored blood components required for patient resuscitation was the source of sPLA2, the sPLA2 was measured in packed red blood cells, platelet concentrates, and fresh frozen plasma over the routine storage time. None of the products tested had elevated levels of sPLA2 compared with fresh plasma from healthy adult volunteers.

Conclusions We conclude that increased sPLA2 activity is associated with the development of postinjury MOF.

From the Department of Surgery, Denver Health Medical Center (DAP, EEM, CCB), Bonfils Blood Center and the Department of Pediatrics (CCS), University of Colorado Health Sciences Center, Denver, CO; and the Children’s Hospital Oakland Research Institute (FAK), Oakland, CA.

Supported, in part, by National Institutes of Health grants P50GM49222, T32GM08315, MO1RR01271, HL20985, a grant from The National Blood Foundation, and a Clinical Associate Physician Award (M01-RR00069) from the General Clinical Research Centers Program, National Centers for Research Resources, National Institutes of Health.

Address request for reprints to: Frans A. Kuypers, PhD, Children’s Hospital Oakland Research Institute, 5700 Martin Luther King Jr. Way, Oakland, CA 94609. E-mail:

© 2001 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins