Small bowel diaphragm disease (DD) is a relatively rare clinical entity described first in 1988 by Lang et al. [1], characterized by short length circumferential lesions involving predominantly small intestine resulting in multiple stenosis of the lumen. The most common cause is believed to be the use of nonsteroid antiinflammatory drugs (NSAIDs) [2]. Inhibition of cyclooxygenase-1 causing reduction in villous microcirculation combines with inhibitory action on the cellular oxidative processes of the epithelial cells to induce increased mucosal permeability which allows luminal aggressors (enteral bacteria, their products, and bile) to gain access to the mucosa and cause inflammation with expression of inducible nitric oxide synthase. Reactive oxygen species from neutrophils and injured endothelial cells add to the damage. Clinical presentations vary from vague intermittent abdominal discomfort to frank small intestinal obstruction, chronic iron deficiency anemia to gastrointestinal bleed. Diagnosis of DD is complicated, not only by the ambiguity of the symptoms, but also by the fact that most investigations are inconclusive. Radiographic studies with contrast media are notoriously inaccurate for the diagnosis of DD. They either do not show the diaphragms or show them so indistinctly that they are misinterpreted as exaggerated plicae circulares. Newer modalities like enteroscopy and capsule endoscopy aid the diagnosis. The typical histology is focal chronic injury of mucosa with inflammatory infiltrate, neurovascular/muscular hamartoma-like changes, and submucosal fibrosis. Treatment is by surgical resection or stricturoplasty/balloon dilatation, based on the involved portion of intestine and discontinuation of offending NSAIDs. Lang et al. have reported a symptom recurrence rate as high as 50 % after resection for DD [1].
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