P296. Association between autoantibodies against the gastric proliferative zone and inflammatory bowel disease
K. Tozawa1, K. Hori2, K. Kamikoduru2, Y. Yokoyama2, S. Nakamura2, H. Miwa3, K. Fukunaga2, T. Matsumoto2, 1Hyogo College of Medicine, Department of Internal Medicine, Nishinomiya, Hyogo, Japan, 2Hyogo College of Medicine, Department of Internal Medicine, Division of Lower Gastroenterology, Nishinomiya, Hyogo, Japan, 3Hyogo College of Medicine, Department of Internal Medicine, Division of upper Gastroenterology, Nishinomiya, Hyogo, Japan
Various autoantibodies have been detected in patients with inflammatory bowel disease (IBD), and we recently detected autoantibodies against the gastric proliferative zone in IBD patients. A microscopic finding termed focally enhanced gastritis (FEG) has also been observed in gastric biopsy samples from IBD patients. We previously noticed that FEG was localized at the level of the foveolar isthmi; i.e., between the foveolae and the glandular layer, and that FEG displayed a similar localization to autoantibodies against the gastric proliferative zone. Therefore, we assumed that a link exists between FEG and autoantibodies against the gastric proliferative zone. In this study, we retrospectively investigated 1) the prevalence of anti-gastric proliferative zone antibodies (GPZA) in IBD and 2) the associations between GPZA-positivity and the clinical characteristics of IBD, including endoscopic IBD lesions and FEG.
We reviewed a total of 110 Crohn's disease (CD) patients and 128 ulcerative colitis (UC) patients who underwent esophagogastroduodenoscopy (EGD) with biopsy from October 2003 to September 2008, and serum samples were collected from each patient. We tested for circulating autoantibodies against stomach tissue using an indirect immunofluorescence technique.
GPZA were detected in 28 (25.5%) of 110 patients with CD, 21 (16.4%) of 128 patients with UC, and 2 (1.8%) of 110 controls. The IBD patients displayed a significantly greater autoantibody positivity rate than the controls (P < 0.001). However, no correlation was detected between GPZA positivity and the frequencies of particular clinical symptoms, upper digestive tract lesions, or FEG in either the UC or CD patients. On the other hand, GPZA positivity was associated with perianal disease (p < 0.049) and the administration of immunosuppressive medications (p = 0.017) in CD.
Autoantibodies that reacted with the gastric proliferative zone were detected in the sera of IBD patients. Although the specificity of GPZA for IBD is high, its sensitivity is low; therefore, GPZA are not useful as a diagnostic tool for IBD. However, the presence of these autoantibodies might be important for the pathogeneses of substantial subsets of IBD or act as a marker for distinguishing certain types of the disease.