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Aspirin-induced peptic ulcer and genetic polymorphisms
Akiko Shiotani1, Takashi Sakakibara, Maki Nomura
1Department of Internal Medicine, Kawasaki Medical School, Matsushima Kurashiki City, Okayama, Japan. shiotani@med.kawasaki-m.ac.jp
Journal of Gastroenterology and Hepatology
|July 1, 2010
Summary
Genetic variations influence aspirin-induced ulcers. While some cyclooxygenase-1 (COX-1) and interleukin-1beta (IL-1beta) polymorphisms show associations, more research is needed to identify key risk factors for gastrointestinal events in aspirin users.
Area of Science:
- Pharmacogenomics
- Gastroenterology
- Molecular Biology
Background:
- Acetylsalicylic acid (aspirin) use is associated with gastrointestinal (GI) risks, including ulcers and bleeding.
- Genetic polymorphisms are increasingly studied for their role in drug response and adverse events.
- Existing research on genetic factors influencing aspirin-induced GI complications is limited.
Purpose of the Study:
- To review the current understanding of genetic polymorphisms associated with aspirin-induced ulcers and their complications.
- To identify specific genetic variants that may increase the risk of GI events in aspirin users.
- To highlight the need for further research in this field.
Main Methods:
- Literature review of studies investigating genetic polymorphisms and aspirin-induced GI events.
- Analysis of associations between specific gene variants (e.g., COX-1, IL-1beta, CYP2C9) and ulcer risk.
- Examination of data regarding other potential genetic factors like platelet glycoproteins and coagulation factors.
Main Results:
- Certain cyclooxygenase-1 (COX-1) polymorphisms (A-842G, C50T, -1676T) show potential links to aspirin sensitivity and peptic ulcer risk, though statistical significance varies.
- Interleukin-1beta (IL-1beta) polymorphisms, particularly the -511 T allele, are associated with peptic ulcer development in low-dose aspirin users.
- CYP2C9 variants increase the risk of GI bleeding with non-aspirin NSAIDs, and polymorphisms in other genes (TXA2 receptor, PAF acetylhydrolase) are implicated but lack GI event data.
- Hypoacidity linked to pro-inflammatory cytokine polymorphisms may offer some protection against NSAID/aspirin injury.
Conclusions:
- Genetic polymorphisms, particularly in COX-1 and IL-1beta, play a role in aspirin-induced GI events.
- Current data are insufficient to definitively identify all significant genetic risk factors for GI complications in aspirin users.
- Large-scale clinical studies are essential to elucidate the precise role of various genetic polymorphisms and guide personalized aspirin therapy.
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