Objective. Low-dose enteric-coated aspirin is increasingly being used for prevention of cardiovascular disease. The aim of this study was to evaluate whether geranylgeranylacetone (GGA) could prevent aspirin-induced small bowel injury. Material and methods. This was a prospective, randomized, double-blind, pilot study of GGA versus placebo in subjects taking low-dose enteric-coated aspirin. Young healthy volunteers were enrolled and each received 100 mg of enteric-coated aspirin per day plus either GGA (150 mg/day) or matching placebo for 7 days. Video capsule endoscopy of the small bowel and the Gastrointestinal Symptom Rating Scale (GSRS) questionnaire were performed before and after the administration of aspirin. Results. Twenty volunteers were evaluated. There was no significant difference in the number of lesions in any category between those receiving or not receiving GGA. Large erosions or ulcers were observed in 12 (60%; 95% confidence interval 36%-80%) aspirin users. Mucosal breaks were most frequently found in the latter half of the proximal small bowel. Conclusions. Short-term administration of low-dose enteric-coated aspirin was associated with visible small bowel damage in the majority of users. We could not prove that aspirin-induced small bowel mucosal injury was prevented by GGA.

Co-treatment of ARB reduces peptic ulcer and bleeding among patients taking low dose aspirin. RAS may play an important role in the development of upper GI mucosal injury induced by low dose aspirin.

Hypoacidity related to corpus atrophy as well as taking PPI seems to be preventively associated with development of peptic ulcer among low dose aspirin users.

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 nonaspirin NSAID-related GI bleeding. The polymorphisms of interleukin-1b (IL-1b) and tumor necrosis factor-a (TNF-a) have been associated with development of peptic ulcer or gastric cancer. In a recent investigation, carriage of the IL-1b-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.

Checking the progress of the capsule with the external real-time viewer improved the diagnostic yield and completion rate of CE.