Prevention of Traditional NSAID-Induced Small Intestinal Injury: Recent Preliminary Studies Using Capsule Endoscopy

Fujimori, Shunji; Takahashi, Yōko; Seo, Tsuguhiko; Gudis, Katya; Ehara, Akihito; Kobayashi, Tsuyoshi; Mitsui, Keigo; Yonezawa, Masaoki; Tanaka, Shu; Tatsuguchi, Atsushi; Sakamoto, Choitsu

doi:10.1159/000308361

Cited by 22 publications

(20 citation statements)

References 71 publications

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“…However, in the majority of patients, LDA is used as an antiplatelet agent and cannot be discontinued due to the increased risk of cardiovascular or cerebrovascular morbidity and mortality. Thus far, several studies have been conducted on the prevention and treatment regimens of NSAID-induced small-bowel mucosal injury [20,21,26,27,28,31,32,36,37,38,39,40]. Fujimori et al [26] have shown that rebamipide is effective for reducing the incidence of diclofenac-induced small intestinal injuries.…”

Section: Discussionmentioning

confidence: 99%

Comparison of Small-Bowel Mucosal Injury between Low-Dose Aspirin and Non-Aspirin Non-Steroidal Anti-Inflammatory Drugs: A Capsule Endoscopy Study

et al. 2014

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Background/Aims: The differences in the severity of small-bowel toxicity induced by aspirin and non-aspirin non-steroidal anti-inflammatory drugs (NSAIDs) remain unclear. This study aimed at clarifying these differences in small-bowel mucosal injury by using capsule endoscopy (CE). Methods: We retrospectively compared the records of 78 and 40 obscure gastrointestinal bleeding patients receiving low-dose aspirin (LDA) and non-aspirin NSAIDs, respectively. All patients were found to have small-bowel mucosal injuries on CE. The two groups were compared for the number of small-bowel mucosal injuries and CE scores on the basis of the findings of CE. Results: The mean numbers of reddened lesions in the LDA group and non-aspirin NSAID group were 2.49 ± 3.15 and 1.65 ± 3.04; the mean numbers of erosions/ulcers 1.56 ± 3.75 and 6.08 ± 10.4, and the mean CE scores 154 ± 294 and 520 ± 758, respectively. The mean number of reddened lesions was significantly higher and the mean number of erosions/ulcers and CE scores significantly lower in the LDA group than in the other non-aspirin NSAID group. Conclusion: Small-bowel mucosal injuries were significantly milder in the LDA group than in the non-aspirin NSAID group, though reddened lesions were more frequent in the LDA group.

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Section: Discussionmentioning

confidence: 99%

Comparison of Small-Bowel Mucosal Injury between Low-Dose Aspirin and Non-Aspirin Non-Steroidal Anti-Inflammatory Drugs: A Capsule Endoscopy Study

et al. 2014

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“…Many capsule endoscopic studies for healthy volunteers revealed that the concomitant administration of COX non-selective NSAIDs and proton pump inhibitor (PPI) can induce small intestinal mucosal injuries in over 50% of study subjects [6]. Hence, small intestinal mucosal injury is not infrequent with the treatment.…”

Section: Introductionmentioning

confidence: 99%

Pilot Study Indicates Helicobacter pylori Infection May Induce Small Intestinal Mucosal Injury

et al. 2018

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Background and Aim: Helicobacter pylori infection is a primary cause of gastroduodenal ulcers. To investigate whether there is an association between H. pylori infection and small intestinal mucosal injury. Methods: Patients were selected from a general pool of subjects who underwent capsule endoscopy for current or past obscure gastrointestinal bleeding. Characteristics including age, gender, history, treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) and/or acid suppressant, diagnosis, and H. pylori infection were investigated. Patients infected with H. pylori had positive test result, ranging 30 days before to 30 days after capsule endoscopy. Patients diagnosed with inflammatory diseases, malignant tumors, etc. were excluded. All video images were re-evaluated to count small intestinal mucosal breaks. Eligible patient variables were compared. Results: A total of 92 patients (30 infected with H. pylori/62 uninfected) were eligible. By univariate analysis of the number of mucosal breaks, patients treated with NSAIDs were found to have more mucosal breaks than patients untreated (38%: 8/21 vs. 18%: 13/71; p = 0.004), and the possible association was detected between patients infected with H. pylori and those who were not (67%: 14/21 vs. 37%: 26/71; p = 0.081). When comparing the H. pylori infected and uninfected patients, the rate of patients with mucosal breaks was greater in infected patients (47%: 14/30 vs. 11%: 7/62; p = 0.001). After excluding patients treated with NSAIDs, the number of mucosal breaks was also greater in patients infected with H. pylori (1.2 ± 1.5 vs. 0.38 ± 0.62; p = 0.001). Conclusion: There is a possibility that H. pylori infection induces small intestinal mucosal injury.

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“…However, NSAID-induced small intestinal lesions have drawn particular attention recently as a result of the development of the capsule endoscope and double-balloon endoscope [3,4,5,6]. These techniques have enabled the identification of previously undetectable lesions in the human small intestine and demonstrated that such lesions are more common than previously thought.…”

Section: Introductionmentioning

confidence: 99%

NSAID-Induced Small Intestinal Damage - Roles of Various Pathogenic Factors

Takeuchi

Satoh²

2015

Digestion

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Background/Aims: NSAID-induced enteropathy has been the focus of recent basic and clinical research subsequent to the development of the capsule endoscope and double-balloon endoscope. We review the possible pathogenic mechanisms underlying NSAID-induced enteropathy and discuss the role of the inhibition of COX-1/COX-2 and the influences of food as well as various prophylactic treatments on these lesions. Methods: Studies were performed in experimental animals. Results: Multiple factors, such as intestinal hypermotility, decreased mucus secretion, enterobacteria, and upregulation of iNOS/NO expression, are involved in the pathogenesis of NSAID-induced enteropathy, in addition to the decreased production of PGs due to the inhibition of COX. Enterobacterial invasion is the most important pathogenic event, and intestinal hypermotility, which was associated with this event, is essential for the development of these lesions. NSAIDs also upregulate the expression of COX-2, and the inhibition of both COX-1 and COX-2 is required for the intestinal ulcerogenic properties of NSAIDs to manifest. NSAID-induced enteropathy is prevented by PGE₂, atropine, ampicillin, and aminoguanidine as well as soluble dietary fiber, and exacerbated by antisecretory drugs such as proton pump inhibitors. Conclusion: These findings on the pathogenesis of NSAID-induced enteropathy will be useful for the future development of intestinal-sparing alternatives to standard NSAIDs.

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Prevention of Traditional NSAID-Induced Small Intestinal Injury: Recent Preliminary Studies Using Capsule Endoscopy

Cited by 22 publications

References 71 publications

Comparison of Small-Bowel Mucosal Injury between Low-Dose Aspirin and Non-Aspirin Non-Steroidal Anti-Inflammatory Drugs: A Capsule Endoscopy Study

Comparison of Small-Bowel Mucosal Injury between Low-Dose Aspirin and Non-Aspirin Non-Steroidal Anti-Inflammatory Drugs: A Capsule Endoscopy Study

Pilot Study Indicates Helicobacter pylori Infection May Induce Small Intestinal Mucosal Injury

NSAID-Induced Small Intestinal Damage - Roles of Various Pathogenic Factors

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