Proposed mechanisms:
(1) direct mucosal injury following chronic use of high doses
(2) enteric coating with release of drug in the small bowel
(3) excretion of absorbed NSAID into the bile
(4) inhibition of prostaglandin synthesis
(5) inhibition of COX-1 and/or COX-2 isoforms
(6) effect on other signal transduction pathways
Clinical features:
(1) The patient has a history of daily NSAID therapy for several weeks to several years.
(2) One or more luminal diaphragms may form in the upper and/or lower GI tract. The finding of one diaphragm does not preclude additional ones in other portions of the GI tract. Often multiple strictures may be limited to a short length of the small bowel.
(3) The patient may present with GI bleeding, obstruction and/or vague abdominal complaints.
(4) Imaging studies are unreliable in identifying lesions. Patients may present with a history of extensive evaluation with negative findings.
(5) An endoscopic video capsule may be able to localize lesions beyond the reach of standard endoscopes.
Clinical findings:
(1) obstruction
(2) abdominal pain
(3) nausea and vomiting
(4) diarrhea
(5) iron-deficiency anemia
(6) low grade GI bleeding
(7) protein-losing enteropathy
Intraoperative bowel palpation or intraluminal endoscopy is necessary to identify lesions since:
(1) there are no serosal signs of disease
(2) multiple diaphragms may be present
A resected diaphragm is a thin and concentric membranous band with a residual lumen. It may show submucosal fibrosis and/or hamartomatous proliferation of nerves, blood vessels and smooth muscle.
Diagnosis usually requires exclusion of other conditions that can explain obstruction or GI bleeding as well as occult malignancy.
