Clinicopathological features of nonsteroidal antiinflammatory drug-induced small intestinal strictures

Bjarnason, Ingvar; Price, Ashley B.; Zanelli, G. D.; Smethurst, Paul; Burke, Michael; Gumpel, J M; Levi, A J

doi:10.1016/0016-5085(88)90568-9

Cited by 204 publications

(78 citation statements)

References 16 publications

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“…1a, 2f) is mentioned in medical textbooks as a typical NSAIDsinduced small-intestinal lesion. Since the identification of cases with NSAIDs enteropathy in the 1980s and 1990s [5][6][7][8], it has become evident that NSAIDs can damage the small intestine, resulting in a concentric ''diaphragm-like stricture''. However, multiple ulcers and erosions can also occur as NSAID-induced small intestinal lesions (Figs.…”

Section: Present Status Of Small Intestinal Mucosal Injury Caused By mentioning

confidence: 99%

“…It seems rational to regard aspirin as an agent that is less toxic to the small intestine in comparison with other NSAIDs because other NSAIDs, but not aspirin, undergo enterohepatic recirculation [5]. Enteric-coated aspirin was originally designed to cause fewer adverse effects on the stomach even when taken for a prolonged period of time.…”

Section: Present Status Of Small Intestinal Mucosal Injury Caused By mentioning

confidence: 99%

“…The diaphragm-like stricture is thought to be pathognomonic of NSAID injury, and is likely a scarring reaction secondary to ulcerative injury during long-term NSAIDs use [7]. Clinical presentation of diaphragm disease is nonspecific and may include obstructive symptoms, GI blood loss, or abdominal pain [5][6][7][8]. The histological features of the diaphragm-like strictures are fibrosis in the submucosa and thickening of the muscularis mucosa [79], while the proper muscle layer is intact.…”

Section: Prevention and Treatment Of Small Intestinal Mucosal Injury mentioning

confidence: 99%

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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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Section: Present Status Of Small Intestinal Mucosal Injury Caused By mentioning

confidence: 99%

Section: Present Status Of Small Intestinal Mucosal Injury Caused By mentioning

confidence: 99%

Section: Prevention and Treatment Of Small Intestinal Mucosal Injury mentioning

confidence: 99%

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Present status and strategy of NSAIDs-induced small bowel injury

et al. 2009

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“…The appearance of NSAIDinduced intestinal injury varies, appearing variously as diaphragm-like strictures, ulcers, erosions, and mucosal redness (2)(3)(4)(5). Herein, we present a case with an advanced anatomical impairment of the ileocecal valve deformation, presumably caused by enteric-coated acetyl salicylic acid (EC-ASA)-induced recurrent ulcers.…”

Section: Introductionmentioning

confidence: 99%

Asetil salisilik asit kullanımına bağlı oluşan ileoçekal valv ülserleri ve deformasyonu sonucunda gelişen çekumda çift lümen görünümü

Öztaş¹,

Akdoğan²,

Etık³

et al. 2015

Endoskopi Gastrointestinal

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The use of non-steroidal anti-inflammatory drugs, especially aspirin, has continued to increase with aging and related cardiovascular diseases. Since their well-known side effect is gastroduodenal mucosal injury, aspirin-induced intestinal damage has also become a growing problem. Herein, we present a case with an advanced anatomical impairment of the ileocecal valve deformation, presumably caused by enteric-coated acetyl salicylic acid induced recurrent ulcers.Keywords: Colonoscopy, intestinal ulcers, enteric-coated acetyl salicylic acid Günümüzde; non steroidal anti-inflamatuvar ilaçlar›n, özellikle aspirinin kullan›m› yafllanma ve yafllanmayla iliflkili kardiyovasküler hastal›klar›n s›kl›¤›n-daki art›flla birlikte giderek artmaktad›r. Aspirinin; gastroduodenal mukozal hasar yap›c› etkisi gibi en iyi bilinen yan etkisinin yan›nda yine aspirin nedeniyle oluflan intestinal hasar da daha s›k karfl›m›za ç›kmaktad›r. Burada muhtemelen enterik-kapl› asetil salisilik asit kullan›m› nedeniyle oluflan rekürran ülserlere ba¤l› geliflen ileoçekal valv deformasyonlu olguyu sunuyoruz.Anahtar kelimeler: Kolonoskopi, intestinal ülserler, enterik-kapl› asetil salisilik asit INTRODUCTIONThe prevalence of non-steroidal anti-inflammatory drugs (NSAIDs) (including aspirin)-induced intestinal injury is higher than had been expected (1). The appearance of NSAIDinduced intestinal injury varies, appearing variously as diaphragm-like strictures, ulcers, erosions, and mucosal redness (2-5). Herein, we present a case with an advanced anatomical impairment of the ileocecal valve deformation, presumably caused by enteric-coated acetyl salicylic acid (EC-ASA)-induced recurrent ulcers. CASE REPORTA 68-year-old male was admitted to the hospital with the complaints of weakness and dyspnea. He had a history of myocardial infarction 12 years ago, and he had been followed until the admission for congestive heart failure. He was still using medications intended for this disease, including 300 mg/day EC-ASA. He did not have any gastrointestinal complaints. On the laboratory examination, deep anemia was determined (hemoglobin: 6.8 g/dl, hematocrit level: 20%, and ferritin level: 2.4 ng/ml). Additionally, occult blood test in the stool examination was found to be positive. Subsequently, upper gastrointestinal endoscopy (revealing pangastritis) and colonoscopy were performed. During colonoscopy, double lumen appearance of the proximal side of the colon was determined ( Figure 1). During the procedure, it was realized that one of the lumens was the base of the cecum (larger arrow #1), and the other was the ileum (larger arrow #2). Both on the mucosa of the terminal ileum and the anatomically disrupted ileocecal valve, multiple ulcers were present (small arrows in Figure 1 and Figure 2). Biopsy specimens taken from the edges of the ulcers were reported as non-specific inflammatory findings. The valve deformation on the cecum resulted in pseudodiverticulum formation (larger arrow #3). Furthermore, two polyps on the cecum determined during colonoscopy we...

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“…Drugs such as non-steroi› dal anti-inflammatory drugs and enteric-coated po› tassium chloride are implicated [15,16]. Ischaemic ileitis and colitis are a common cause of intestinal strictures.…”

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confidence: 99%