Tanen David A, Danish D Christopher, Reardon Jacqueline M, Chisholm Christopher B, Matteucci Michael J, Riffenburgh Robert H
Department of Emergency Medicine, Naval Medical Center San Diego, San Diego, CA 92134, USA.
Ann Pharmacother. 2008 Oct;42(10):1396-401. doi: 10.1345/aph.1L128. Epub 2008 Aug 12.
Oral acetylsalicylic acid (aspirin) is the primary antiplatelet therapy in the treatment of acute myocardial infarction and acute coronary syndrome. Methyl salicylate (MS; oil of wintergreen) is compounded into many over-the-counter antiinflammatory muscle preparations and has been shown to inhibit platelet aggregation locally and to be absorbed systemically.
To assess the ability of topically applied MS to inhibit systemic platelet aggregation for patients who are unable to tolerate oral drug therapy.
A randomized, prospective, blinded, crossover study was conducted in 9 healthy men, aged 30-46 years. All subjects ingested 162 mg of aspirin or applied 5 g of 30% MS preparation to their anterior thighs. There was a minimum 2-week washout period between study arms. Blood and urine were collected at baseline and at 6 hours. An aggregometer measured platelet aggregation over time against 5 standard concentrations of epinephrine, and a mean area under the curve (AUC) was calculated. Urinary metabolites of thromboxane B(2) were measured by a standard enzyme immunoassay. Differences in and between groups at baseline and 6 hours were tested by the Wilcoxon signed-rank test.
Baseline platelet aggregation did not differ significantly between the 2 arms of the study (median AUC [% aggregation(*)min]; binominal confidence intervals): aspirin 183; 139 to 292 versus MS 197; 118 to 445 (p = 0.51). Both aspirin and MS produced statistically significant platelet inhibition; aspirin decreased the AUC from 183; 139 to 292 to 85; 48 to 128 (p = 0.008) and MS decreased the AUC from 197; 118 to 445 to 112; 88 to 306 (p = 0.011). No significant difference was detected between baseline and 6-hour thromboxane levels for either aspirin (p = 0.779) or MS (p = 0.327).
Topical MS and oral aspirin both significantly decrease platelet aggregation in healthy human volunteers.
口服乙酰水杨酸（阿司匹林）是治疗急性心肌梗死和急性冠状动脉综合征的主要抗血小板疗法。水杨酸甲酯（MS；冬青油）被配制成许多非处方抗炎肌肉制剂，并已被证明可局部抑制血小板聚集并被全身吸收。
评估局部应用MS对无法耐受口服药物治疗的患者全身血小板聚集的抑制能力。
对9名年龄在30 - 46岁的健康男性进行了一项随机、前瞻性、双盲、交叉研究。所有受试者口服162毫克阿司匹林或在其大腿前部涂抹5克30%的MS制剂。研究组之间至少有2周的洗脱期。在基线和6小时时采集血液和尿液。用血小板聚集仪测量血小板随时间对5种标准浓度肾上腺素的聚集情况，并计算曲线下平均面积（AUC）。通过标准酶免疫测定法测量血栓素B₂的尿代谢产物。用Wilcoxon符号秩检验来检验基线和6小时时组内及组间的差异。
研究的两组之间基线血小板聚集无显著差异（中位数AUC[聚集百分比*分钟]；二项式置信区间）：阿司匹林组为183；139至292，而MS组为197；118至445（p = 0.51）。阿司匹林和MS均产生了具有统计学意义的血小板抑制作用；阿司匹林使AUC从183；139至292降至85；48至128（p = 0.008），MS使AUC从197；118至445降至112；88至306（p = 0.011）。阿司匹林（p = 0.779）或MS（p = 0.327）在基线和6小时时的血栓素水平之间均未检测到显著差异。
局部应用MS和口服阿司匹林均可显著降低健康人类志愿者的血小板聚集。
