A109 CELIAC DISEASE IS A RARE CAUSE OF BENIGN DUODENAL STRICTURE

Abstract Background Benign duodenal stricture is an uncommon problem encountered by gastroenterologists. The most common cause is peptic ulcer disease (PUD). With the diagnosis and eradication of H. Pylori, early diagnosis of PUD and the use of PPIs to treat upper gastrointestinal inflammation, the incidence of benign duodenal stricture has dramatically decreased. Patients with duodenal stricture may present with early satiety, nausea, vomiting and weight loss. We present the case of a man with a refractory web-like stricture in the second part of the duodenum (D2) caused by Celiac disease. Aims To describe a rare endoscopic finding in a patient with Celiac disease Methods Case report with literature review Results We present a case of a 64 year old male was referred for consideration of duodenal stenting of a refractory stricture in the second part of the duodenum D2. The patient had a 1 year history of abdominal pain, early satiety and weight loss (10 lbs). He also reported intermittent episodes of diarrhea. Investigations included a CT scan of the abdomen which showed a stricture at the level of proximal D2 described as a “duodenal band”. Previous attempts at balloon dilation had not resulted in prolonged symptomatic or endoscopic improvement. Testing for H. Pylori was negative and he did not use NSAIDs. Upper endoscopy was performed to assess the stricture prior to consideration of stenting. This showed a tight web-like stricture in proximal D2. The stricture was balloon dilated up to 16.5 mm, enabling the endoscope to pass beyond it. The mucosa in D2 was atrophic with flattening of the folds and scalloping. There was no inflammation seen. Biopsies from D2 revealed moderate villous blunting and intraepithelial lymphocytosis. Celiac serology testing was abnormal, with an anti-tTG Ab level of 32 RU/ml which confirmed the diagnosis of Celiac disease. The balloon dilation and gluten-free diet resulted in resolution of his symptoms. Follow up endoscopy revealed normalization of his duodenal folds and biopsies. In addition, anti-tTG Ab level was normalized. Although stricture improved with prolonged patency, he still has mild recurrence of his stricture requiring balloon dilation on an annual basis. Conclusions This case describes a very uncommon complication of Celiac disease. The likely pathophysiology involves inflammation and potentially ulceration from Celiac disease, resulting in a benign stricture. There have been a few case reports describing duodenal strictures as a complication of Celiac disease. Treatment involves a gluten-free diet and endoscopic therapy. More severe cases of obstruction would likely require surgical intervention. In our case, the gluten-free diet and balloon dilation were successful and duodenal stenting was not necessary. Given the possibility of Celiac disease as a cause of duodenal stricture, it would be reasonable to biopsy D2 and check anti-tTG Ab in cases of duodenal stricture. Funding Agencies None

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