Purpose of review The review describes the effects of NSAID gastrointestinal toxicity on the small bowel, wherein injury is as prevalent as in the gastroduodenum. This is well documented by capsule endoscopy, which also provides an endoscopic endpoint for novel treatment strategies. Recent findings Appreciation of the prevalence of NSAID enteropathy has grown with capsule endoscopy and the use of composite end points that include obscure haemoglobin decreases in clinical studies. Along with dual cyclo-oxygenase isoform inhibition, gram-negative antigen presentation plays a role in the pathogenesis of NSAID enteropathy. The concomitant use of proton pump inhibitor (PPI) agents with both selective and nonselective NSAIDs in gastroduodenal protection exacerbates endoscopic enteropathy, which is thought to be due to intestinal dysbiosis. Strategies for small bowel mucosal protection include prostaglandin repletion and augmenting the intestinal flora. Summary NSAID- related enteropathy is common and often presents subclinically. The most common presentation is anaemia, which may be less common in those on cyclo-oxygenase (COX)-2 inhibitors than nonselective NSAIDs. PPI use worsens NSAID enteropathy with more occult bleeding and ulceration and has been linked to gram-negative intestinal dysbiosis. If NSAID cessation is not possible, COX-2 inhibition without PPI therapy should be considered in patients with upper gastrointestinal risk factors. Mucoprotective agents such as misoprostol and rebamipide show promise and probiotics may have a future role.