Nonsteroidal antiinflammatory drug‐induced small intestinal inflammation and blood loss. Effects of sulfasalazine and other disease‐modifying antirheumatic drugs

Hayllar, Jeremy; Smith, T.; Macpherson, Andrew J.; Price, Ashley B.; Gumpel, M.; Bjarnason, Ingvar

doi:10.1002/art.1780370806

Cited by 67 publications

(50 citation statements)

References 20 publications

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“…Misoprostol, metronidazole and sulfasalazine have all been suggested to be beneficial in treatment or prevention of NSAID-enteropathy in humans, but the studies suggesting this had significant limitations (open-label, not controlled, and/or small sample sizes) [22,24,[109][110][111] . Misoprostol, H2RA and sucralfate were found to be ineffective in reducing NSAID-induced intestinal permeability in humans [112,113] , though in one, open-label study misoprostol reduced the elevated intestinal permeability induced by indomethacin [114] .…”

Section: Nsaid-enteropathymentioning

confidence: 99%

Mechanisms, prevention and clinical implications of nonsteroidal anti-inflammatory drug-enteropathy

Wallace¹

2013

WJG

151

148

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This article reviews the latest developments in understanding the pathogenesis, detection and treatment of small intestinal damage and bleeding caused by nonsteroidal anti-inflammatory drugs (NSAIDs). With improvements in the detection of NSAID-induced damage in the small intestine, it is now clear that this injury and the associated bleeding occurs more frequently than that occurring in the stomach and duodenum, and can also be regarded as more dangerous. However, there are no proven-effective therapies for NSAIDenteropathy, and detection remains a challenge, particularly because of the poor correlation between tissue injury and symptoms. Moreover, recent studies suggest that commonly used drugs for protecting the upper gastrointestinal tract (i.e. , proton pump inhibitors) can significantly worsen NSAID-induced damage in the small intestine. The pathogenesis of NSAIDenteropathy is complex, but studies in animal models are shedding light on the key factors that contribute to ulceration and bleeding, and are providing clues to the development of effective therapies and prevention strategies. Novel NSAIDs that do not cause small in- FRONTIER

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Section: Nsaid-enteropathymentioning

confidence: 99%

Mechanisms, prevention and clinical implications of nonsteroidal anti-inflammatory drug-enteropathy

Wallace¹

2013

WJG

151

148

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“…And long-term administration of prophylactic drugs is needed for chronic users of NSAIDs or aspirin, especially patients with experience of small intestinal bleeding. Until recently, some trials showed the efficacy of metronidazole, sulfasalazine, and misoprostol for treatment of NSAID-induced injury [45][46][47]. However, in these studies, efficacy was indirectly evaluated by measuring several markers such as hemoglobin levels and fecal excretion of radiolabeled neutrophils, so their effectiveness has not yet been fully confirmed.…”

Section: Prevention and Treatment Of Small Intestinal Mucosal Injury mentioning

confidence: 99%

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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“…However, even if temporary cessation of the NSAIDs is possible, long-term cessation of NSAIDs is frequently impossible, and long-term administration of prophylactic drugs is needed for chronic users of NSAIDs or aspirin, especially patients who experience small intestinal bleeding. Some trials have shown the efficacy of metronidazole, sulfasalazine and misoprostol for treatment of NSAIDinduced injury (11)(12)(13). Clinically, proton pump inhibitors (PPIs) and PG analogs are the first-choice drugs for the prevention of NSAID-induced peptic ulcers and bleeding (14).…”

Section: Discussionmentioning

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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Nonsteroidal antiinflammatory drug‐induced small intestinal inflammation and blood loss. Effects of sulfasalazine and other disease‐modifying antirheumatic drugs

Cited by 67 publications

References 20 publications

Mechanisms, prevention and clinical implications of nonsteroidal anti-inflammatory drug-enteropathy

Mechanisms, prevention and clinical implications of nonsteroidal anti-inflammatory drug-enteropathy

Present status and strategy of NSAIDs-induced small bowel injury

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

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