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SAT0537 Influence of meloxicam in orodispersible form on platelet aggregation and von willebrand factor in patients with osteoarthritis
  1. OS Khmel,
  2. VV Rodionova
  1. Occupational Diseases and Clinical Immunology, State Establishment “Dnipropetrovsk Medical Academy, of Health Ministry of Ukraine”, Dnepr, Ukraine

Abstract

Background Meloxicam, which selectively inhibits COX-2, can cause inhibition of the biosynthesis of vascular endothelium vasodilator - prostacyclin, without impacting significantly on production of thromboxane, which promotes vasoconstriction [1]. Therefore, the effect of Meloxicam on the possibility of thrombotic complications need to be learn more accurately.

Objectives To investigate the effect of orodispersible form of Meloxicam on platelet aggregation and von Willebrand factor in patients with knee osteoarthritis.

Methods The study included 24 patients with knee osteoarthritis (OA) of the II stage according to the Kellgren-Lawrence. The control group consisted of 15 healthy individuals. Patients were prescribed the orodispersible form of Meloxicam in dose of 15 mg 1 time per day orally during 10 days. The survey was carried out before and after treatment. Patients had all-clinical studies, questionnaires (visual analogue scale (VAS), Western Ontario and McMaster Universities Arthritis Index (WOMAC), questionnaire Lequesne), optical aggregometry with adenosine diphosphate (ADP), collagen, thrombin and ristocetin for revealing the level of von Willebrand factor.

Results As a result of treatment patients had a significant improvement of overall health and reduction of pain in knee joints according to the VAS (before treatment – 54.5 [50 – 71] mm, after treatment – 27 [18 – 41] mm; p≤0.05), WOMAC (before treatment – 143 [109 – 187] points, after treatment - 98 [13–168] points; p≤0.05), questionnaire Lequesne (before treatment – 16 [13 – 21] points, after treatment – 12 [3 – 22] points; p≤0.05). After treatment patients experienced a significant increase in the degree of platelet aggregation with ADP (before treatment – 52.6 [39.6 – 98.2]% after the treatment – 83.5 [41.3 – 127]%; p≤0.05), which may indicate a probable increase in the initiation of irreversible aggregation of circulating platelets. The degree of platelet aggregation with collagen also increased (before treatment – 46.5 [29.5 – 89]%, after treatment – 68.6 [37.9 – 115.4]%; p≤0.05), indicating the increased adhesion of platelets to collagen of the vascular endothelium. Before and after treatment, patients remained significantly elevated degree of aggregation with thrombin in comparison with the control group (before treatment – 65.6 [24.7 – 86.7], after treatment – 78 [62.3 – 92.7]%, control group – 37.8 [32.11 – 42.26]%; p≤0.05) which indicates the stimulation of the of the endothelin-1 synthesis with further infringements of procoagulants and anticoagulants. Von Willebrand factor, as an indirect indicator of endothelial damage, was significantly increased after treatment (before treatment – 151.4 [138.9 – 224]% after treatment – 206.8 [171.9 – 257.4]%), which may indicate increase of endothelial lesions because of meloxicam with further endothelial dysfunction (p≤0.05).

Conclusions Intake of the orodyspersible form of Meloxicam in patients with osteoarthritis can cause an increase of platelet aggregation and level of von Willebrand factor that may contribute to the vascular endothelial dysfunction and increase in risk of thrombosis.

References

  1. Wittenauer R., Smith L., Aden K. Update on 2004 Background Paper Written by Saloni Tanna, Pharm.D. MPH Background Paper 6.12 Osteoarthritis. Priority Medicines for Europe and the World “A Public Health Approach to Innovation”; 2013. P. 31.

References

Disclosure of Interest None declared

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