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The role of capsule endoscopy in suspected celiac disease patients with positive celiac serology



The role of capsule endoscopy in suspected celiac disease patients with positive celiac serology



Digestive Diseases and Sciences 56(2): 499-505



Endomysial antibody (EMA) and tissue transglutaminase (tTG) antibody testing is used to screen subjects with suspected celiac disease. However, the traditional gold standard for the diagnosis of celiac disease is histopathology of the small bowel. As villous atrophy may be patchy, duodenal biopsies could potentially miss the abnormalities. Capsule endoscopy can obtain images of the whole small intestine and may be useful in the early diagnosis of celiac disease. To evaluate suspected celiac disease patients who have positive celiac serology and normal duodenal histology and to determine, with capsule endoscopy, whether these patients have any endoscopic markers of celiac disease. Twenty-two subjects with positive celiac serology (EMA or tTG) were prospectively evaluated. Eight of the subjects had normal duodenal histology and 14 had duodenal histology consistent with celiac disease. All subjects underwent capsule endoscopy. Endoscopic markers of villous atrophy such as loss of mucosal folds, scalloping, mosaic pattern, and visible vessels were assessed. Eight subjects with normal duodenal histology had normal capsule endoscopy findings. In the 14 subjects with duodenal histology that was consistent with celiac disease, 13 had celiac disease changes seen at capsule endoscopy. One subject with normal capsule endoscopy findings showed Marsh IIIc on duodenal histology. Using duodenal histology as the gold standard, capsule endoscopy had a sensitivity of 93%, specificity of 100%, PPV of 100%, and NPV of 89% in recognizing villous atrophy. Capsule endoscopy is useful in the detection of villous abnormalities in untreated celiac disease. Patients with positive celiac serology (EMA or tTG) and normal duodenal histology are unlikely to have capsule endoscopy markers of villous atrophy.

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Accession: 056473871

Download citation: RISBibTeXText

PMID: 20552401

DOI: 10.1007/s10620-010-1290-6


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