Key result
In healthy volunteers, hydroxychloroquine combined with aspirin significantly increased inhibition of platelet aggregation compared with aspirin alone (31.2% ± 8.1% increase, P = .002).
Why the study?
Does hydroxychloroquine improve inhibition of platelet aggregation in healthy volunteers?
RCT (n=20)
1:1:1 ratio, incomplete block design
Does hydroxychloroquine improve inhibition of platelet aggregation in healthy volunteers?
Effect estimate: 31.2% ± 8.1% increase
p-value: p=.002
Hydroxychloroquine demonstrates antiplatelet properties and synergistic effects with aspirin in healthy volunteers, suggesting potential utility as an antiplatelet agent.
Hydroxychloroquine augments aspirin's platelet inhibition in volunteers; extends mechanistic data but leaves clinical translation untested.
BACKGROUND: With the inflammatory model of atherosclerosis taking center stage, anti-inflammatory drugs hold a promising place in the therapy of cardiovascular disease (CVD). Recent studies showed that hydroxychloroquine (HCQ) was protective against thrombovascular events in lupus erythematosus and traditional cardiovascular risk factors in patients with rheumatoid arthritis. Some preliminary experimental data have shown that it may prevent platelet activation too. OBJECTIVE: To evaluate the antiplatelet activity of HCQ when given alone and in combination with aspirin (ASA) and compare it with ASA alone and ASA plus clopidogrel (CLOP) in healthy human volunteers. METHODS: In part 1 of the study, 8 volunteers were given HCQ for 7 days. In part 2, 12 volunteers were randomly assigned in a 1:1:1 ratio to the 3 groups in which 2 of the 3 treatments, ASA, ASA plus CLOP, and ASA plus HCQ, were given in the 2 treatment periods separated by a 14-day washout period using the incomplete block design. Inhibition of platelet aggregation (IPA) was measured by light transmission aggregometry. RESULTS: When arachidonic acid (AA) was used as agonist, HCQ given alone showed a significant reduction in platelet aggregation (11.0% ± 4.2%, P = .03). The IPA was significantly increased when ASA plus HCQ was compared with ASA alone (31.2% ± 8.1%, P = .002). This synergistic effect was not seen with adenosine diphosphate and collagen as agonists. Levels of serum 11-dehydrothromboxane B2, a stable marker of thromboxane A2 production, were not significantly different between the groups. There was also a significant decrease in fibrinogen and erythrocyte sedimentation rate values when HCQ was used alone or in combination with ASA. CONCLUSION: This study suggests that HCQ has antiplatelet properties possibly through the AA pathway (downstream to thromboxane A2 production). With possible additional beneficial effects over the traditional CVD risk factors, larger studies in the future might explore HCQ's potential as an antiplatelet agent.
No takes yet. Share an insight, caveat, or question.
Achuthan et al. (2014) conducted an RCT in Healthy volunteers (n=20). Hydroxychloroquine (HCQ) alone and in combination with aspirin (ASA) vs. Aspirin (ASA) alone and ASA plus clopidogrel (CLOP) was evaluated on Inhibition of platelet aggregation (IPA) (31.2% ± 8.1% increase, p=.002). In healthy volunteers, hydroxychloroquine combined with aspirin significantly increased inhibition of platelet aggregation compared with aspirin alone (31.2% ± 8.1% increase, P = .002).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: