Nonsteroidal antiinflammatory drug-induced intestinal inflammation in humans

Bjarnason, Ingvar; Zanelli, G. D.; Smith, T.; Prouse, P.; Williams, Peter; Smethurst, Paul; DELACEY, G; Gumpel, M.; Levi, A J

doi:10.1016/0016-5085(87)90909-7

Cited by 337 publications

(159 citation statements)

References 30 publications

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“…It has been reported that gold salts, which are disease-modifying anti-rheumatic drugs (DMARDs), frequently cause inflammation of the digestive organs (10)(11)(12). In addition, some non-steroidal anti-inflammatory drugs (NSAIDs) are thought to cause intestinal inflammation (13). In the present case, drug-induced colitis was not plausible because the drugs the patient had taken (other than diclofenac) have not been reported to cause colitis.…”

Section: Discussionmentioning

confidence: 64%

Ulcerative Colitis Occurring in the Course of Rheumatoid Arthritis: A Case Successfully Treated with Mesalamine Enema

et al. 2004

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We report a case of ulcerative colitis (UC) that occurred during the course of rheumatoid arthritis (RA). A 29-year-old woman with a 25-year history of RA was hospitalized for high fever, abdominal pain and hematochezia. Colonoscopy revealed erosive and reddish mucosa from the distal transverse colon to rectum. Histology revealed cryptitis (mainly caused by neutrophils), mild crypt abscess and goblet cell depletion. She was diagnosed with left-sided UC and treated with mesalamine enema. The abdominal symptoms and colonoscopic findings were greatly ameliorated. We conclude that the mesalamine enema was effective in this case of UC occurring during the course of RA.

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Section: Discussionmentioning

confidence: 64%

Ulcerative Colitis Occurring in the Course of Rheumatoid Arthritis: A Case Successfully Treated with Mesalamine Enema

et al. 2004

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“…Measurement of inflammation is by qualitative indium-111-labeled neutrophil scintigraphy. In 50% of patients on NSAIDs for more than 6 months, this method of scintigraphy consistently shows accumulation of the labeled white cells on the terminal ileum, halted by the ileocecal valve, after 20 h [40]. The 4-day fecal excretion of 111 In also confirms low-level inflammation in NSAID users compared to that in inflammatory bowel disease.…”

Section: Diagnosis Of Nsaids-induced Small Intestinal Injurymentioning

confidence: 64%

Present status and strategy of NSAIDs-induced small bowel injury

et al. 2009

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Non-steroidal anti-inflammatory drugs (NSAIDs) are well known to cause gastroduodenal mucosal lesions as an adverse effect. Recently, the serious problem of NSAID-induced small intestinal damage has become a topic of great interest to gastroenterologists, since capsule endoscopy and balloon enteroscopy are available for the detection of small intestinal lesions. Such lesions have been of great concern in clinical settings, and their treatment and prevention must be devised as soon as possible. The prevalence of NSAIDs-induced small intestinal injury is higher than had been expected. Recent studies show that more than 50% of patients taking NSAIDs have some mucosal damage in the small intestine. The gross appearance of NSAIDinduced enteropathy varies, appearing variously as diaphragm-like strictures, ulcers, erosions, and mucosal redness. To investigate NSAID-induced enteropathy, and to rule out other specific enteropathies, other useful methods (in addition to capsule endoscopy and balloon enteroscopy) include such modalities as radiological examination of the small intestine, the permeability test, scintigraphy or the fecal excretion test using 111 Indium-labeled white blood cells, and measurement of the fecal calprotectin concentration. Diaphragm-like strictures and bleeding from mucosal breaks may be treatable with interventional enteroscopy. Misoprostol, metronidazole, and sulfasalazine are frequently used to treat NSAID-induced enteropathy, but have undesirable effects in some cases. In the experimental model, we confirmed that several existing drugs for gastroduodenal ulcers prevented indomethacin-induced small intestinal injury. Such drugs may be useful for preventing the adverse effects of NSAIDs not only in the stomach but also in the small intestine. We hope to examine these drugs in future clinical studies.

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“…In two retrospective studies of 268 and 188 patients, hospitalization due to intestinal perforations or hemorrhage were twice as likely to develop in patients on NSAIDs than in controls [30] . Bjarnason et al [31] reported that up to 70% of patients receiving long-term NSAID therapy, including diclofenac therapy, developed small intestinal NSAID enteropathy. Numerous studies have demonstrated that an increase in intestinal permeability is the central mechanism that translates biochemical damage to tissue damage in the pathogenesis of NSAID enteropathy.…”

Section: Discussionmentioning

confidence: 99%

A protective effect of melatonin on intestinal permeability is induced by diclofenac via regulation of mitochondrial function in mice

Qiao

Diao

et al. 2011

Acta Pharmacol Sin

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Aim: This study investigated the effect of intragastrically administered melatonin on intestinal mucosal permeability induced by diclofenac in mice. Methods: Intestinal mucosal permeability was induced in mice by intragastric administration of diclofenac (2.5 mg/kg). Melatonin was given intragastrically (10 mg/kg) once per day for 3 d after diclofenac administration. The small intestine was examined macroscopically and microscopically for pathologic injury to the intestinal mucosa. Intestinal mucosal permeability was evaluated by Evans blue and FITC-dextran methods. Mitochondrial functional parameters, including mitochondrial membrane potential, mitochondrial ATPase and succinate dehydrogenase (SDH) activity, were assessed. The malondialdehyde (MDA) and myeloperoxidase (MPO) levels were determined from small intestinal mucosal homogenates. Results: As compared with control mice, the permeability, pathologic score, MDA and MPO levels and ulceration of the intestinal mucosa were increased significantly by diclofenac treatment, and a broadened junctional complex and enlarged intercellular space were observed by transmission electron microscopy (TEM). Melatonin treatment significantly reduced the intestinal mucosal permeability, pathologic score, MDA, and MPO levels and ulceration of the intestinal mucosa. By TEM, the small intestine villus morphology and intercellular spaces were nearly normal in melatonin-treated mice. At the level of the mitochondria, melatonin treatment significantly restored the activities of ATPase and SDH. Conclusion: The intestinal damage and increased intestinal permeability induced by diclofenac in mice was limited by melatonin; moreover, melatonin preserved several aspects of mitochondrial function.

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Nonsteroidal antiinflammatory drug-induced intestinal inflammation in humans

Cited by 337 publications

References 30 publications

Ulcerative Colitis Occurring in the Course of Rheumatoid Arthritis: A Case Successfully Treated with Mesalamine Enema

Ulcerative Colitis Occurring in the Course of Rheumatoid Arthritis: A Case Successfully Treated with Mesalamine Enema

Present status and strategy of NSAIDs-induced small bowel injury

A protective effect of melatonin on intestinal permeability is induced by diclofenac via regulation of mitochondrial function in mice

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