In:
Journal of Gastroenterology and Hepatology, Wiley, Vol. 25, No. s1 ( 2010-05)
Abstract:
There are a few studies of the association between genetic polymorphisms and the risks of acetylsalicylic acid (aspirin)‐induced ulcer or its complications. Two single nucleotide polymorphisms (SNP) of cyclooxygenase‐1 (COX‐1), A‐842G and C50T, exhibited increased sensitivity to aspirin and had lower prostaglandin synthesis capacity, lacking statistical significance in the association with bleeding peptic ulcer. A recent Japanese study indicated that the number of COX‐1‐1676T alleles was a significant risk factor for peptic ulcer in users of non‐steroidal anti‐inflammatory drugs (NSAIDs). There are some genetic polymorphisms for aspirin resistance, such as platelet membrane glycoproteins, thromboxane A2 (TXA2) receptor, platelet activating factor acetylhydrolase and coagulation factor XIII; however, data on the frequency of gastrointestinal (GI) events in these variants are lacking. Carrying the CYP2C9 variants is reported a significantly increased risk of non‐aspirin NSAID‐related GI bleeding. The polymorphisms of interleukin‐1β (IL‐1β) and tumor necrosis factor‐α (TNF‐α) have been associated with development of peptic ulcer or gastric cancer. In a recent investigation, carriage of the IL‐1β‐511 T allele was significantly associated with peptic ulcer among low‐dose aspirin users. Hypoacidity in corpus gastritis related to polymorphisms of pro‐inflammatory cytokines seems to reduce NSAIDs or aspirin‐related injury. Data on which polymorphisms are significant risk factors for GI events in aspirin users are still lacking and further large‐scale clinical studies are required.
Type of Medium:
Online Resource
ISSN:
0815-9319
,
1440-1746
DOI:
10.1111/jgh.2010.25.issue-s1
DOI:
10.1111/j.1440-1746.2009.06212.x
Language:
English
Publisher:
Wiley
Publication Date:
2010
detail.hit.zdb_id:
2006782-3
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