Gastrointestinal: Eosinophilic enteritis manifesting as brown‐pigmented duodenal ulcers

Abstract

A 31-year-old man was investigated for chronic lower abdominal pain and leucocytosis. Clinical examination revealed diffuse abdominal tenderness. He has chronic hepatitis B, history of epididymo-orchitis and deep vein thrombosis. Abdominal X-ray was unremarkable and abdominal CT showed increased density of the mesenteric fat with mesenteric lymphadenopathy. EGD showed duodenal ulceration (Figure 1) and colonoscopy was normal. His full blood picture revealed eosinophilia of 6.8 × 109 /L, a remarkable increase from his previous blood test in 2000 which on retrospect, demonstrated eosinophilia of 0.7–1.4 × 109. His duodenal (Figure 2A, H&E stain 200 × magnification, black arrow) and terminal ileal (Figure 2B, H&E stain 400 × magnification, white arrow) biopsies demonstrated eosinophilic infiltration in the lamina propria and submucosa affecting the Burner's glands. Extracellular eosinophilic staining constituents were present. He was treated with proton pump inhibitor and recovered. Eosinophilic enteritis is an increasing recognized condition affecting mainly the stomach and small intestine. There is no consensus as to what constitute eosinophilic enteritis but Talley et al. have identified 3 main diagnostic criteria: (1) the presence of gastrointestinal symptoms, (2) biopsies demonstrating eosinophilic infiltration of one or more areas of the gastrointestinal track, and (3) no evidence of parasitic or extra intestinal disease (as opposed to secondary eosinophilic gastrointestinal disorders). Peripheral eosinophilia is seen in less than 50% of the time. Clinical manifestations depend on level of eosinophilic infiltration. Mucosal layer disease presents as luminal symptoms like diarrhea, vomiting, malabsorption, weight loss and colicky abdominal pain. Muscular layer disease presents as hypertrophy leading to intestinal obstruction. Serosal layer disease, the rarest of all, presents as ascites. This is the form of eosinophilic enteritis that escape diagnosis as biopsy of the mucosal layer often fail to demonstrate presence of eosinophils in the superficial layers. Eosinophilic enteritis may be treated with steroid with 90% rapid symptom resolution, and rarely azathioprine is required. Mast cell stabilizers such as cromolyn and ketotifen have been used with mixed results. A leukotriene receptor antagonist, montelukast has also been tried. Surgical interventions may be required for cases present as intestinal obstruction or perforation. Contributed by