Detection of platelet inhibition is of clinical relevance in the preinterventional risk-benefit assessment in chronic
low-back-pain patients scheduled for invasive
pain therapy. We evaluated the sensitivity of various point-of-care platelet function tests for the detection of platelet inhibition induced by
nonopioid analgesic drugs. After Institutional Review Board approval and informed consent, citrated whole blood from 40 patients with chronic unspecific
low back pain was investigated before and 30 min after
intravenous infusion of the study medication consisting of
diclofenac 75 mg (plus orphenadrin 30 mg;
Neodolpasse; Fresenius Kabi Austria GmbH, Austria),
parecoxib 40 mg (
Dynastat; Pharmacia Europe EEIG, UK),
paracetamol 1 g (Perfalgan; Bieffe Medital S.P.A., Italy), or
normal saline in a randomized, cross-over, double-blinded, placebo-controlled study. Platelet function was assessed using the PFA-100 platelet function analyzer and thromboelastometry, as well as impedance aggregometry (in the last 17 patients recruited after it became commercially available). Sensitivity for detecting
diclofenac-induced platelet inhibition was 85% for the PFA-100 using
epinephrine as agonist and 94% for
arachidonic acid-induced impedance aggregometry.
ADP-induced platelet function tests, as well as
cytochalasin D-modified thromboelastometry were unreliable. All tests had a low incidence of false-positive test results after
normal saline.
Paracetamol and
parecoxib had no significant platelet inhibiting effect. The PFA-100 using
epinephrine as agonist and
arachidonic acid-induced impedance aggregometry are recommended for the detection of
cyclooxygenase-I-inhibiting effects of nonsteroidal anti-inflammatory drugs such as
diclofenac. Our findings confirm that a single rescue dose of
paracetamol and
parecoxib has no antiplatelet effect.