Suboptimal Inhibition of Platelet Cyclooxygenase 1 by Aspirin in Systemic Lupus Erythematosus: Association With Metabolic Syndrome1. Issue 2 (February 2014)

• Record Type: Journal Article
• Authors: Kawai, Vivian K.; Avalos, Ingrid; Oeser, Annette; Oates, John A.; Milne, Ginger L.; Solus, Joseph F.; Chung, Cecilia P.; Stein, C. Michael
• Is Part Of: Arthritis care & research. Volume 66:Issue 2(2014:Feb.)
• Page Start: 285
• Page End: 292
• Publication Date: 2014-02
• Subjects: Arthritis -- Periodicals; Rheumatism -- Periodicals; 616.72
• DOI: 10.1002/acr.22169
• Languages: English
• ISSNs: 2151-464X

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="acr22169-sec-0001" sec-type="section"> <title>Objective</title> <p>Low‐dose aspirin prevents platelet aggregation by suppressing thromboxane A<sub>2</sub> (TXA<sub>2</sub>) synthesis. However, in some individuals TXA<sub>2</sub> suppression by aspirin is impaired, indicating suboptimal inhibition of platelet cyclooxygenase 1 (COX‐1) by aspirin. Because patients with systemic lupus erythematosus (SLE) have increased risk of thrombotic events, many receive aspirin; however, the efficacy of aspirin in SLE has not been determined. We examined the hypothesis that aspirin response is impaired in SLE.</p> </sec> <sec id="acr22169-sec-0002" sec-type="section"> <title>Methods</title> <p>We assessed the effect of aspirin by measuring concentrations of the stable metabolite of TXA<sub>2</sub>, serum thromboxane B<sub>2</sub> (sTXB<sub>2</sub>), before and after treatment with daily aspirin (81 mg) for 7 days in 34 patients with SLE and 36 control subjects. The inability to suppress sTXB<sub>2</sub> synthesis to <10 ng/ml represents suboptimal inhibition of platelet COX‐1 by aspirin.</p> </sec> <sec id="acr22169-sec-0003" sec-type="section"> <title>Results</title> <p>Aspirin almost completely suppressed sTXB<sub>2</sub> in control subjects to median 1.5 ng/ml (interquartile range [IQR] 0.8–2.7) but had less effect in patients with SLE (median 3.1 ng/ml [IQR 2.2–5.3]) (<italic>P</italic> = 0.002). A suboptimal effect of aspirin was present in 15% (5 of 34) of the patients with SLE but not in control subjects (0 of 36) (<italic>P</italic> = 0.023). Incomplete responders were more likely to have metabolic syndrome (<italic>P</italic> = 0.048), obesity (<italic>P</italic> = 0.048), and higher concentrations of C‐reactive protein (CRP) (<italic>P</italic> = 0.018).</p> </sec> <sec id="acr22169-sec-0004" sec-type="section"> <title>Conclusion</title> <p>The pharmacologic effect of aspirin is suboptimal in 15% of patients with SLE but in none of the control subjects, and the suboptimal response was associated with metabolic syndrome, obesity, and higher CRP concentrations.</p> </sec> </abstract>