Effect of a Specific Cyclooxygenase-Gene Polymorphism (A-842G/C50T) on the Occurrence of Peptic Ulcer Hemorrhage

Oijen, Martijn G.H. van; Laheij, R.J.F.; Koetsier, M.I.A.; Kleine, Evelien de; Morsche, R.H.M. te; Kerkhoven, Lieke A. S. van; Jansen, J. B. M. J.; Drenth, Joost P.H.

doi:10.1007/s10620-006-9475-8

Cited by 30 publications

(36 citation statements)

References 15 publications

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“…Only a few studies have examined the physiologic consequences of genetic variation in COX-1. The previous data on genetic diversity of COX-1 in Western populations showed an inverse association between the prevalence of A-842G/C50T polymorphism and bleeding peptic ulcer disease, but the data lacked statistical significance [21]. In contrast, a recent Japanese study indicated an association of T-1676C polypmorphism with NSAID-induced ulcer [24].…”

Section: Discussionmentioning

confidence: 88%

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The preventive factors for aspirin-induced peptic ulcer: aspirin ulcer and corpus atrophy

et al. 2009

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Section: Discussionmentioning

confidence: 88%

“…For polymorphism of UGT 1A6, CYP2C9, TNF-a, and COX-1 PCR reactions were carried out separately using the primers described in Table 1 for multiplex amplification. PCR-restriction fragment length polymorphism (RFLP) was performed as described previously [20][21][22].…”

Section: Genotypingmentioning

confidence: 99%

The preventive factors for aspirin-induced peptic ulcer: aspirin ulcer and corpus atrophy

et al. 2009

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“…On the other hand, although the T-1676C promoter polymorphism did not affect the two Sp1 binding sites that were reported to be essential for COX-1 transcription (14), putative transcription factor (GATA-1, CdxA) binding sites were altered by this polymorphism (15). The relationship between the A-842G/C50T polymorphism and human disorders was investigated in several reports (8,(16)(17)(18), whereas only a few studies have researched the association of the T-1676C polymorphism with human diseases. Shi et al reported that the COX-1 polymorphisms including the T-1676C polymorphism do not appear to play a substantial role in genetic predisposition for asthma or asthma severity (9).…”

Section: Discussionmentioning

confidence: 99%

“…This fact suggests that the -842G carrier has a higher risk of developing NSAID-induced ulcer. Although Oijen et al reported that the COX-1 A-842G/C50T polymorphism did not influence the risk for developing peptic ulcer bleeding (8), the role of this polymorphism on the development of peptic ulcers still remains unclear. In addition, Shi et al have investigated the association of 4 of 20 known informative and potentially functional polymorphisms in the COX-1 gene with asthma (9).…”

Section: Introductionmentioning

confidence: 99%

Association between genetic polymorphisms in thecyclooxygenase-1 gene promoter and peptic ulcers in Japan

et al. 2007

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Abstract. Cyclooxygenase-1 (COX-1) has been regarded as a constitutively expressed enzyme that generates prostaglandins for gastrointestinal integrity. We attempted to clarify the association between potentially functional polymorphisms (T-1676C and A-842G/C50T) in the COX-1 gene promoter and gastroduodenal disorders in a Japanese population. The study was performed with 480 stocked DNAs from subjects (gastric ulcers in 93 subjects and duodenal ulcers in 44) with no evidence of gastric malignancy. We employed the PCR-SSCP method to detect gene polymorphisms. The severity of histological chronic gastritis in antral biopsy specimens was classified according to the updated Sydney system. The T-1676C polymorphism was not associated with either gastric mucosal atrophy or infiltration of inflammatory cells into gastric mucosa. In non-NSAID (non-steroidal antiinflammatory drug) users, male gender and Helicobacter pylori (HP) infection were significantly associated with both gastric and duodenal ulcers, whereas the -1676T allele carrier was significantly associated with only gastric ulcers (OR, 2.86; 95% CI, 1.29-6.34). In NSAID users, the number of -1676T alleles was significantly associated with developing gastroduodenal ulcers (OR, 5.80; 95% CI, 1.59-21.1), whereas male gender and HP infection were not. The -842T/ C50T polymorphism was not detected in any of the 480 Japanese subjects. In conclusion, a carrier of the -1676T allele in the COX-1 gene promoter, as well as HP infection and male gender, seem to be significant risk factors for developing gastric ulcers, and the number of -1676T alleles was also a significant risk factor for the NSAID-induced ulcer, whereas the frequency of the A-842G polymorphism was thought to be very rare in the Japanese population.

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“…31,32 The previous data show an inverse association between the prevalence of A-842G/C50T polymorphism and bleeding peptic ulcer disease, but lack statistical significance. 33 In contrast, a recent Japanese study indicated a possible association of COX-1 T-1676C polymorphism with NSAID-induced peptic ulcer. 34 However, there are no data supporting a significant association among aspirin users.…”

Section: Genetic Polymorphisms and Aspirin-induced Peptic Ulcer Coxmentioning

confidence: 92%

Risk and preventive factors of low‐dose aspirin‐induced gastroduodenal injuries: A comprehensive review

Shiotani

Manabe

Kamada

et al. 2012

J of Gastro and Hepatol

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The risk of peptic ulcer complications, particularly bleeding, is increased in association with the use of low-dose aspirin (LDA). Risk factors for upper gastrointestinal (GI) ulcer or bleeding among LDA users include a history of prior GI events, older age, chronic renal failure, combined antithrombotic therapy and nonsteroidal anti-inflammatory drugs (NSAIDs). Helicobacter pylori and aspirin seem to be independent risk factors for peptic ulcer and bleeding. The studies report conflicting findings about the effect of H. pylori infection on NSAID-related ulcers, and proton-pump inhibitors (PPIs) seem to be superior to eradication only to prevent recurrent ulcer bleeding with LDA. Previous studies indicate that hypoacidity related to corpus atrophy, as well as taking PPIs and co-treatment with angiotensin type 1 receptor blockers (ARBs) and statins seem to reduce peptic ulcer among LDA users. In addition, the interleukin-1b (IL-1b)-511 T allele and angiotensinogen (AGT)-20 CC, which work as the high-producer allele of IL-1b and AGT, are significantly associated with ulcer or ulcer bleeding. The SLCO1B1*1b haplotype, which has the highest transport activity, may diminish the preventive effect of statins or ARBs. The data are still lacking and further prospective studies are needed to identify the specific risk or protective factors for upper GI ulcer and its complications associated with LDA.Key words angiotensin type 1 receptor blocker, angiotensinogen, aspirin, interleukin-1b, polymorphism, SLCO1B*1b, statins.

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Effect of a Specific Cyclooxygenase-Gene Polymorphism (A-842G/C50T) on the Occurrence of Peptic Ulcer Hemorrhage

Cited by 30 publications

References 15 publications

The preventive factors for aspirin-induced peptic ulcer: aspirin ulcer and corpus atrophy

The preventive factors for aspirin-induced peptic ulcer: aspirin ulcer and corpus atrophy

Association between genetic polymorphisms in thecyclooxygenase-1 gene promoter and peptic ulcers in Japan

Risk and preventive factors of low‐dose aspirin‐induced gastroduodenal injuries: A comprehensive review

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