Objective. Platelets are involved in various thrombotic events, often by means of platelet-derived microparticles (PMPs). It is likely that platelets are also involved in inflammation. Because inflammatory processes play a central role in rheumatoid arthritis (RA), we sought to determine whether PMPs are present in this disease.Methods. This descriptive, cross-sectional study included 19 RA patients and 10 healthy controls. Nine of the patients had active RA (erythrocyte sedimentation rate [ESR] >28 mm/hour and/or C-reactive protein [CRP] level >28 mg/liter, >9 painful joints, and >6 swollen joints), and 10 had inactive disease (ESR <27 mm/hour, CRP <27 mg/liter, no tender joints, and no swollen joints). Platelet counts and PMP numbers were determined using cell counter and flow cytometry, respectively.Results. Platelet counts in the 3 groups were similar. However, levels of PMPs in RA patients were significantly higher than those in healthy controls (median 616 versus 118 ؋ 10 6 /liter; P ‫؍‬ 0.005). PMP levels were higher in patients with active RA than in those with inactive RA (median 2,104 versus 504 ؋ 10 6 /liter; P > 0.05). Moreover, PMP levels correlated with disease activity (r ‫؍‬ 0.67, P ‫؍‬ 0.05).

In RA patients, meloxicam, a representative of the selective COX-2 inhibitors, does not interfere with platelet function and thromboxane levels, in contrast with naproxen (a non-selective COX inhibitor).

NSAID use during coumarin therapy considerably increases the bleeding risk compared with coumarin therapy alone. Although in daily practice these medications are frequently prescribed concomitantly, our results underscore the contraindication of concomitant use of NSAIDs and coumarin derivatives.

Objective-To test the hypothesis that nabumetone (a partially selective cyclooxygenase-(COX)-2 inhibitor) has less effect on platelet aggregation than naproxen (a non-selective COX-inhibitor) in patients with rheumatoid arthritis (RA). Methods-A crossover study in 10 RA patients was performed, using either nabumetone or naproxen for two weeks, and, after a washout period of two weeks, the other drug during another two weeks. Platelet aggregation studies were performed and bleeding time was assessed before and after each treatment period. Results-Maximum platelet aggregation induced by epinephrine and by collagen was significantly more reduced after the use of naproxen than of nabumetone; secondary aggregation induced by ADP and epinephrine disappeared more often by naproxen than by nabumetone. Bleeding times were not influenced. Conclusion-COX dependent platelet aggregation in RA patients seems to be more inhibited by naproxen than by nabumetone. This may be relevant for patients requiring non-steroidal anti-inflammatory drug treatment but who have an increased risk of bleeding as well.

No abstract