1. ¹Otsuka Pharmaceutical Co., Ltd., Osaka, Japan
2. ²Takeda Pharmaceutical Company, Osaka, Japan
3. ³Astellas Pharma Inc., Tokyo, Japan
4. ⁴Dainippon Sumitomo Pharma Co., Ltd., Osaka, Japan
5. ⁵Tanabe Seiyaku Co., Ltd., Osaka, Japan
6. ⁶Senju Pharmaceutical Co., Ltd., Osaka, Japan
7. ⁷Sanwa Kagaku Kenkyusho Co., Ltd., Nagoya, Japan
8. ⁸Shionogi & Co., Ltd., Osaka, Japan
9. ⁹Takara Bio Inc., Otsu, Japan
10. ¹⁰Hitachi, Ltd., Kawagoe, Japan
11. ¹¹Maruyama Hospital, Hamamatsu, Japan
12. ¹²Osaka University, Suita, Japan

Correspondence: Dr T Fujiwara, Department of Clinical Research and Development, Otsuka Pharmaceutical Co. Ltd., 3-2-27, Otedori Chuo-ku, Osaka, 540-0021, Japan. E-mail: fujiwaratu@otsuka.jp

Received 28 November 2005; Revised 26 October 2006; Accepted 30 October 2006; Published online 23 January 2007.

Abstract

Aspirin prevents the production of thromboxane A₂ (TXA₂) by irreversibly inhibiting platelet cyclooxygenase, exhibiting antiplatelet actions. This agent has been reported to prevent relapse in patients with ischemic heart disease or cerebral infarction via this action mechanism. However, there are individual differences in this action, and aspirin is not effective in some patients, which is referred to as 'aspirin resistance'. In this study, we analyzed laboratory aspirin resistance by platelet aggregation in 110 healthy adult Japanese males using 24 single-nucleotide polymorphisms (SNPs) of nine genes involved in platelet aggregation/hemorrhage. Among SNPs involved in platelet aggregation, aspirin was less effective for 924T homozygote of a TXA₂ receptor, 924T>C, and 1018C homozygote of a platelet membrane glycoprotein GPIb, 1018C>T, suggesting that 924T and 1018C alleles are involved in aspirin resistance.