Key result
Low-dose aspirin profoundly decreases thromboxane B2 but fails to reduce CRP versus placebo.
Why the study?
Elevated CRP increases the risk of thrombotic cardiovascular events, and low-dose aspirin may prevent thrombosis by reducing inflammation, but prior studies examining aspirin's effect on CRP levels yielded conflicting results.
Does low-dose aspirin reduce serum C-reactive protein and thromboxane B2 concentrations in healthy volunteers?
RCT (n=57)
Does low-dose aspirin reduce serum C-reactive protein and thromboxane B2 concentrations in healthy volunteers?
p-value: p=<0.001
Low-dose aspirin effectively inhibits platelet COX-1 activity but does not reduce systemic inflammation as measured by serum CRP levels in healthy individuals.
Low-dose aspirin should not be used to target CRP in primary prevention; challenges anti-inflammatory mechanism beyond antiplatelet effects in healthy adults.
OBJECTIVES: We performed a placebo-controlled study to evaluate the effect of low-dose aspirin on serum C-reactive protein (CRP) levels. BACKGROUND: Elevated circulating concentrations of CRP, an inflammatory marker, increase the risk of thrombotic cardiovascular diseases such as myocardial infarction (MI). Moreover, low-dose aspirin therapy has been reported to be more effective in preventing MI in men with higher CRP levels than it is in those with lower levels, raising the possibility that aspirin prevents thrombosis by reducing vascular inflammation. The effect of low-dose aspirin therapy on serum CRP levels in men has been addressed recently, but the results of the two studies conflict. METHODS: Effects of aspirin (81 mg every day or 325, 81 or 40 mg every-third-day given for 31 days) on serum CRP, using a highly-sensitive assay, and on serum platelet-cyclo-oxygenase (COX)-1-derived thromboxane (Tx) B2 concentrations were studied simultaneously in 57 healthy volunteers (30 men and 27 women). RESULTS: Trough platelet COX-1-derived serum Tx B2 concentrations decreased by 100% with daily aspirin and by 90%, 84% and 78% with 325, 81 and 40 mg aspirin every-third-day (p < 0.001). However, there were no significant changes in serum CRP levels from baseline with daily low-dose aspirin therapy, with any of the every-third-day aspirin regimens or with placebo treatment. CONCLUSIONS: Low doses of aspirin that markedly inhibit platelet COX-1 activity, as manifested by a profound decline in platelet-derived serum Tx B2 concentrations, have no detectable effect on serum CRP levels in healthy men and women.
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Feldman et al. (2001) conducted an RCT in Healthy volunteers (n=57). Aspirin vs. Placebo was evaluated on Serum C-reactive protein (CRP) and platelet COX-1-derived thromboxane (Tx) B2 concentrations (p=<0.001). Low-dose aspirin profoundly decreased serum thromboxane B2 concentrations (p<0.001) but had no detectable effect on serum C-reactive protein levels compared to placebo.
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