Crohn Disease: A Case of Rare, Isolated Duodenal Involvement

Abstract

Crohn disease is a chronic inflammatory condition that may present or recur in any region of the gastrointestinal (GI) tract. Gastroduodenal Crohn disease occurs in only 0.5% to 4% of all Crohn cases, with duodenal isolated disease accounting for less than 0.07% of all cases. The diagnosis of Crohn disease is based on clinical, laboratory, endoscopic, and histopathologic findings. Nugent and Roy criteria for gastroduodenal Crohn must include either 1. histologic finding of noncaseating granulomatous inflammation of the stomach or duodenum and absence of other systemic granulomatous disorders or 2. confirmed Crohn disease of the GI tract and radiographic or endoscopic findings of diffuse inflammation of the stomach or duodenum consistent with Crohn disease. A 37 year old male with history of GERD and Crohn disease presented to the ED for vomiting, abdominal pain, diarrhea, bright red blood in stool, and a 50-60 lb unintentional weight loss. PE was benign. CT abd/pel was unremarkable. Colonoscopy revealed stenosis of the ileocecal valve preventing intubation, likely from chronic inflammation. Upper endoscopy revealed first portion duodenitis with edematous stenosis and partial gastric outlet obstruction. Gastric biopsies resulted as active H. pylori gastritis. Duodenal biopsies showed duodenitis with ulceration and granulation tissue. The patient was treated with Protonix, Amoxil, and Biaxin for H. pylori and Asacol for the Crohn's flare. Follow-up EGD and biopsies showed persistent Crohn of the duodenum. Historically, Duodenal Crohn Disease (DCD) has been very difficult to treat. A large portion of the patient population fail medical therapy and require invasive intervention. Recent research has addressed the question of whether H. pylori plays a provocative vs protective role in IBD. In this case, an argument could be made that the H. pylori was the catalyst for the rare isolated case of DCD. According to Papamichael et al, H. pylori infection may invoke changes of gastric and intestinal permeability or immunological derangements from the absorption of bacterial particles. Reversely, the fact that the DCD did not respond to medical therapy after eradication of the H. pylori promotes the theory of H. pylori producing a protective environment. As evidenced by this case, further research involving the etiology and pathogenesis of rare, isolated DCD is critical to the management of the patient.