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P129. There is a different tissue transglutaminase (tTG) distribution in coeliac disease (CD) and inflammatory bowel disease (IBD) duodenal mucosa

M.M. Bosca Watts1, S. Navarro2, M. Minguez1, J. Santiago1, A. Rodriguez1, J. Tosca1, R. Romero3, C. Mongort2, F. Mora1, 1University Clinic Hospital of Valencia, Gastroenterology and Hepatology, Valencia, Spain, 2University Clinic Hospital of Valencia, Pathology Department, Valencia, Spain, 3Politecnic University of Valencia, Faculty of Statistics, Valencia, Spain

Background

tTG is a ubiquitous molecule found in inflammation, regeneration and apoptotic processes, of special interest in CD because it is the target of the anti-tTG antibodies. The tTG distribution in the enterocytes and the role of this distribution as a diagnostic marker of CD is controversial.

Since IBD's mark is an altered inflammation, in which tTG (among others) can be found, we hypothesized that a qualitative observation of the tTG in the duodenal wall could help differentiate between CD and IBD.

Methods

With immunohistochemistry (IMC) techniques, we applied anti-tTG (TGase1-Kit LSAB2, Santa Cruz Biotech, Ca USA) on paraffin sections of duodenal mucosae biopsies of 54 IBD patients (34 Crohn's Disease [CrD] and 20 Ulcerative Colitis [CU]) and 12 CD patients. A qualitative scale was used to describe the amount of stain due to anti-tTG + tTG complexes. Cytoplasmic staining was graded as 0–3, and apical border staining as 0, 1, 1.5, 2 and 3 (1.5: heterogeneous distribution of tTG). A pathology-trained gastroenterologist and an expert pathologist, blind to the CD or IBD diagnosis, described the results according to their degree of staining in the cytoplasm and the brush border.

Statistical analysis was performed using the SPSS (PASW 17.0) and Statsgraphics Plus (5.1) programs.

Results

Globally (CD+IBD), 90% had cytoplasm grade 2 or 3 staining, while only 23% of the biopsies presented apical border grade 2 or 3. None of the 12 CD patients or the 7 IBD patients with biopsy compatible with CD presented intense brush border staining (>1.5), while 15 of the 47 (32%) did. Of these 15, 13 were CrD patients and 2 UC. Through ANOVA, we observed that the cytoplasm was significantly more intensively stained in IBD patients than in controls (p = 0.0345), with no difference found between CrD or UC. As expected, IBD patients had a more intensively stained brush border with respect to CD patients (p = 0.0392), mainly due to CrD biopsies with grade 2 and 3 apical border staining (p = 0.0555).

Conclusion

With IMC and a simple qualitative scale to describe the stain, we have observed that tTG tends to deposit in the brush border of the enterocytes of CrD patients, whereas the distribution in CD patients is different and does not show the same tendency. Duodenal biopsies from IBD patients showed a stronger cytoplasmic and apical border staining than CD patient biopsies.