Intest Res.  2017 Oct;15(4):446-455. 10.5217/ir.2017.15.4.446.

Non-steroidal anti-inflammatory drug-induced enteropathy

Affiliations
  • 1Department of Gastroenterology, Ajou University School of Medicine, Suwon, Korea. shsj9128@ajou.ac.kr

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs) are well known to be associated with serious upper gastrointestinal complications, such as peptic ulcer, bleeding, perforation, and obstruction. Recently, attention has been mainly focused on the small bowel injuries caused by NSAIDs, and new endoscopic techniques such as capsule endoscopy and double balloon endoscopy can help in detecting such injuries. This article reviewed the epidemiology, pathogenesis, clinical manifestations, diagnosis, and treatment of small bowel injuries caused by NSAIDs. Small bowel injures by NSAIDs might occur with a similar frequency and extent as those observed in the upper gastrointestinal tract. The pathogenesis of NSAID-induced enteropathy is complex and not clearly understood. The various lesions observed in the small bowel, including petechiae, reddened folds, loss of villi, erosions, and ulcers can be detected by capsule endoscopy. A drug that could prevent or treat NSAID-induced enteropathy has not yet been developed. Therefore, further investigations should be performed to elucidate the pathogenesis of such enteropathy and develop suitable preventive and treatment strategies.

Keyword

Anti-inflammatory agents, non-steroidal; Small intestine injury; Capsule endoscopy

MeSH Terms

Anti-Inflammatory Agents, Non-Steroidal
Capsule Endoscopy
Diagnosis
Endoscopy
Epidemiology
Hemorrhage
Peptic Ulcer
Purpura
Ulcer
Upper Gastrointestinal Tract
Anti-Inflammatory Agents, Non-Steroidal

Figure

  • Fig. 1 Putative pathophysiology of NSAID-induced enteropathy. NSAIDs decrease PG synthesis, resulting in the reduction of mucus and blood flow of the intestinal mucosa and directly damage the small bowel epithelium. These injuries cause increased intestinal permeability of bile acid, bacteria, proteolytic enzymes, and toxins. Therefore, neutrophils and many inflammatory mediators are activated and various clinical manifestations, such as erosion, ulceration, bleeding, and protein loss develop. Additionally, enterohepatic circulation of NSAIDs and bile augments the damage to the small bowel. TLR4, Toll-like receptor 4. Adapted from Wallace JL. Br J Pharmacol 2012;165:67-74.18

  • Fig. 2 Capsule endoscopic images of various intestinal mucosal lesions by NSAID. (A) Small bowel petechiae, (B) small bowel erosion, (C) small bowel ulcer, (D) small bowel ulcer with adherent blood clots, (E) small bowel active bleeding, and (F) small bowel stricture with adherent clots.


Cited by  1 articles

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