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J Jones, GK Turnbull, DA Maltajalian

Division of Gastroenterology, Department of Medicine and Department of Pathology, Dalhousie University, Halifax, Nova Scotia

Celiac disease is characterized by malabsorption as a result of inflammatory injury to the small intestinal mucosa after ingestion of gluten or related rye and barley proteins. The classic lesion of untreated celiac disease consists of mucosal architectural changes including variable degrees of villous atrophy, hyperplastic and mitotically active crypts, increased lymphocytic infiltration in the lamina propria, and lymphocytic damage of enterocytes. Granulomatous inflammation is said not to be a feature of Celiac Disease.
We report a 52 year-old man who presented with complaints of intermittent blood per rectum and frequent, loose stools. He had no other gastrointestinal symptoms, no significant weight loss and no constitutional symptoms. He was found to have a microcytic anemia with a Hb of 126 g/L and a ferritin of 4ug/L. Vitamin B12 and red blood cell folate levels were normal. AST was increased slightly to 43 U/L. Albumin was decreased at 29g/L. There was no IgA deficiency. The anti-tissue trans-glutaminase test was positive. A full colonoscopic evaluation with ileal intubation and biopsy was normal. The patient went on to have a gastroduodenoscopy which revealed some mild erythema of the gastric body as well as multiple small, superficial, erosions with overlying white plagues in the duodenal bulb. The mucosa of the second part of the duodenum appeared diffusely atrophic. A subsequent upper gastrointestinal xray with small bowel follow-through was normal. Distal duodenal biopsies showed villous atrophy with crypt hyperplasia and increased crypt mitotic activity. There were increased intraepithelial lymphocytes and increased numbers of lymphocytes and plasma cells in the lamina propria. Both superficial and deep mucosal, non-caseating, epithelioid granulomas were present. Gastric mucosal biopsies showed foci of early granulomas composed of small aggregates of epithelioid histiocytes. There were no parasites and special stains showed no fungi, acid-fast bacilli, no evidence of Wipple's disease and H. pylori organisms were not seen. Investigations looking for other causes of granulomatous inflammation were negative. A gluten-free diet was started with complete resolution of symptoms.
This is only the second reported case of gastroduodenal granulomatous inflammation in association with celiac disease reported in the literature (Gut 1977;18:814-816). In our case there is no evidence of Crohn's disease or a secondary disease process to explain the granulomas. We conclude that the granulomas are present as a result of an altered chronic inflammatory response to celiac disease in this patient. Although rare, gastroduodenal granulomas may be a feature of celiac disease and not necessarily diagnostic of gastroduodenal Crohn's disease.