Abstract
Introduction : The risk for coronary artery disease (CAD) and mortality has increased in patients with rheumatoid arthritis (RA). Aspirin has anti-thrombotic effects and causes reduction in CAD occurrence in high-risk individuals. The objective of present project was evaluating the influence of low-dose aspirin on inhibition of platelet aggregation in patients with RA. Methods: Forty-eight subjects with RA diagnosed based on the American College of Rheumatology/European League Against Rheumatism (ACR/EULAR) 2010 criteria and age- and sex-matched healthy participants were studied. All subjects received 81 mg/day aspirin for 10 days. Level of the serum thromboxane B2 (sTxB2), a permanent metabolite of thromboxane A2 (TxA2), was measured before and after therapy using enzyme-linked immunosorbent assay (ELISA) kit. The impotency to decrease sTxB2 production to less than 10 ng/ml indicates suboptimal suppression of platelet aggregation via aspirin. Results: Low-dose aspirin decreased sTxB2 significantly compared with baseline in patients with RA [median interquartile range (IQR): 25.72 (11.78, 90.10) to 7.74 (5.80, 8.82), P < 0.001] and in healthy controls [median (IQR): 40.50 (33.25, 50.90) to 7.30 (4.75, 8.85), P < 0.001]. No remarkable changes were seen in sTxB2 between patients and controls after adjustment (P > 0.050). Pharmacologic influence of aspirin was suboptimal in 6.25% of cases in the presence of higher erythrocyte sedimentation rate (ESR) and in 2.7% of controls. Low-dose aspirin decreased sTxB2 significantly only in patients with Framingham Risk Score (FRS) < 10%. Conclusion: Low-dose aspirin decreased sTxB2 level and suppressed platelet aggregation and therefore, was effective in primary prevention of cardiovascular (CV) events in patients with RA; however, additional studies are required to reach accurate conclusions.
Highlights
Forty-eight subjects with Rheumatoid arthritis (RA) diagnosed based on the American College of Rheumatology/European League Against Rheumatism (ACR/EULAR) 2010 criteria and ageand sex-matched healthy participants were studied
Patients with RA are at high risk of mortality in comparison with general community mainly attributed to atherosclerosis, coronary artery disease (CAD)
In order to calculate the high CAD risk caused by RA, the European League Against Rheumatism (EULAR) suggested models of CAD risk score, adjusted for patients with RA by proposing a 1.5 multiplication factor whenever the patient has 2 out of 3 criteria including: duration of disease ≥ 10 years, positive rheumatoid factor (RF) or anti-cyclic citrullinated peptide antibodies, and demonstrating extra-articular signs.[3]
Summary
Sciences and all subjects signed informed consent before inclusion in the research. this study was recorded on the Iranian Registry of Clinical Trials (IRCT). Data were presented as median (interquartile range or IQR); *Wilcoxon signed-rank test sTXB2: Serum thromboxane B2; BMI: Body mass index; TG: Triglyceride; HDL-C: High-density lipoprotein cholesterol; DAS-28: Disease activity score 28; CRP: C-reactive protein; Anti-CCP: Anticyclic citrullinated peptide; ESR: Erythrocyte sedimentation rate; FRS: Framingham risk score. Metabolites in urine do not reflect a particular eicosanoid biosynthesis site and urine Tx-M is not an authentic marker of aspirin action on platelets.[25,26] various tests examine different facets of aspirin reaction[14,22] like Tx generation from sources independent of extra-platelet and COX-1.14,24,27-29 Overall, one of the most particular tests for pharmacological action of aspirin is sTxB2 suppression.[21,22] In another study by Smith et al.,[25] MetS had strong association with less effective COX-1 inhibition This controversy between findings from different studies might be because of variations in studied individuals, physiological circumstances (e.g., different types of disease), disease duration, baseline TxB2 status, dosage and duration of aspirin therapy, variation between individuals in reaction to aspirin, and different tests for response to aspirin assessment.
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Journal of Analytical Research in Clinical Medicine
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
