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Tranexamic acid bolus plus drip paradoxically increases complement activation: A PATCH trial secondary study.

Nicolle Barmettler1, Elizabeth R Maginot, Ernest E Moore

  • 1Division of Acute Care Surgery, Department of Surgery (N.B., E.R.M., F.I.G., C.M.W., T.B.M., A.C., K.S.S., D.H., G.E.V., R.H., C.D.B.), University of Nebraska Medical Center, Omaha, Nebraska; Department of Surgery (E.E.M., J.G.C.), Ernest E Moore Shock Trauma Center, Denver Health; Department of Surgery (H.B.M.), AdventHealth Porter, Denver, Colorado; Department of Cardiology (D.F.D.), Bern Center for Precision Medicine, University Hospital of Bern, Bern, Switzerland; School of Medicine and Psychology (R.G.), Australian National University, Canberra, Australia; Department of Biological Sciences, Hunter College (I.M.B.), New York, New York; The Australian Centre for Blood Diseases (R.L.M.), Monash University; Emergency and Trauma Centre (B.M.), Alfred Health, Melbourne, Australia; Department of Surgery (M.A.S.), Uniformed Services University of Health Sciences, Bethesda, Maryland; Section of Trauma and Acute Care Surgery, Department of Surgery (S.E.R.), University of Chicago Pritzker School of Medicine, Chicago, Illinois; Sauaia Statistical Solutions, L.L.C. (A.S.), Denver, Colorado; and Department of Cellular and Integrative Physiology (C.D.B.), University of Nebraska Medical Center, Omaha, Nebraska.

The Journal of Trauma and Acute Care Surgery
|February 3, 2026
PubMed
Summary
This summary is machine-generated.

Tranexamic acid (TXA) did not reduce early complement activation in trauma patients. Paradoxically, TXA increased complement activation at 24 hours, suggesting a complex role in the inflammatory response and questioning optimal dosing strategies.

Keywords:
Tranexamic acidcomplement activationfibrinolysis

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Area of Science:

  • Trauma and Emergency Medicine
  • Immunology
  • Pharmacology

Background:

  • Tranexamic acid (TXA) shows modest survival benefits in polytrauma, but its effects may extend beyond hemostasis.
  • Plasmin activates complement proteins, and TXA inhibits plasmin generation.
  • This study investigated TXA's impact on complement activation in trauma patients.

Purpose of the Study:

  • To determine if TXA administration reduces complement activation in polytrauma patients.
  • To explore the relationship between TXA, plasmin, and complement pathways post-trauma.

Main Methods:

  • Plasma samples from 53 polytrauma patients in the PATCH trial (TXA vs. placebo) were analyzed.
  • Complement activation markers (C3a, C5a, sC5b-9) and plasmin-antiplasmin levels were measured at ED, 8, and 24 hours.
  • Statistical comparisons were made between TXA and placebo groups.

Main Results:

  • No significant difference in complement activation or plasmin-antiplasmin levels between TXA and placebo groups at early time points (ED, 8 hours).
  • A significant increase in C3a and C5a levels was observed in the TXA group at 24 hours post-admission.
  • These findings suggest TXA may paradoxically enhance complement activation later after trauma.

Conclusions:

  • TXA administration paradoxically increased complement activation at 24 hours in polytrauma patients.
  • These results indicate TXA's involvement in the inflammatory pathway post-trauma.
  • Optimal TXA dosing strategies in trauma require further investigation due to delayed inflammatory effects.