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FRI0178 Followup of platelet activation in a patient with antiphospholipid syndrome upon tirofiban treatment
  1. A Perniok1,
  2. A Messis1,
  3. C Specker2,
  4. M Siebler3,
  5. M Schneider2
  1. 1Department of Medicine II, University of Cologne, Cologne, Germany
  2. 2Department of Rheumatology, University of Düsseldorf, Düsseldorf, Germany
  3. 3Department of Neurology, University of Düsseldorf, Düsseldorf, Germany

Abstract

Background Patients with primary or secondary antiphospholipid syndrome (APS) often suffer from stroke leading to high degree of disability. Though it is well known that phospholipid antibodies induce a procoagulatory scenario, antibody status does not well characterise patients at risk. Using transcranial Doppler ultrasound of intracerebral arteries we could detect microembolic signals correlating well with phospholipid antibody titer as well as with history of stroke. In these patients we could also demonstrate elevated levels of platelet activation markers (p-selectin) as well as increased platelet leukocyte aggregation. Tirofiban is a potent, highly selective and reversible inhibitor of platelet gpIIb/IIIa receptor which binds fibrinogen on platelet surface.

Objectives We treated a patient with primary APS and refractory transitory ischaemic attacks with tirofiban and detected microembolic signals as well as platelet activation markers and platelet-leukocyte aggregations (PLA).

Methods In fresh venous citrate-anticoagulated whole blood expression of gp Ib (CD41), gp IIb/IIIa (CD42b), fibrinogen binding and p-selectin (CD62p) was analysed using a flowcytometric double staining method. In parallel we detected PLA by determining percentage of platelet marker/leukocyte marker (CD42b/CD45) double posi-tive leukocytes.

Results Upon Tirofiban treatment we found a reduction of platelet activation markers (p-selectin, fibrinogen binding, CD63). Under steady state conditions with tirofiban expression of platelet activation markers and platelet leukocyte interaction normalised completely compared to normal healthy donors. The morning after each infusion there was a rebound phenomenon, which could also be observed in platelet activation markers and PLA. This rebound phenomenon could be reproduced upon sequential administration of tirofiban in parallel with rate of microembolic events.

Conclusion In a patient with primary APS therapeutic intervention with tirofiban, a reversible inhibitor of platelet gpIIb/IIIa receptor, induced a clinical improvement of transitory ischaemic attacks. In parallel with clinical improvement there was a modulation of microembolic signals as well as platelet activation markers and PLA. Flowcytometric measurement of platelet activation can be a useful tool in monitoring platelet hyperreactivity in APS upon therapeutic intervention.

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