P074 Histopathologic evaluation and lymphocyte subpopulations of the upper digestive tract of Crohn’s disease

A. Martin Cardona1,2, A. Carrasco García1,2, E. Tristán Lopez3, Y. Zabana Abdo1,2, M. Aceituno Quintanilla1,2, C. Ferrer Cassadó4, D. Horta Sangenis1, L. Ruiz-Campos1, C. Loras Alastruey1,2, X. Andujar Murcia1,2, O. Benítez Leiva1, F. Fernández-Bañares1,2, M. Esteve Comas1,2

1Hospital Universitari Mútua Terrassa, Digestive Diseases Department, Terrassa, Spain, 2Centro de Investigación biomédica en red de enfermedades hepáticas y digestivas CIBERehd, Terrassa, Barcelona, Spain, 3Hospital Universitari Mútua Terrassa, Laboratori de Recerca. Fundació Mútua de Terrassa, Terrassa, Spain, 4Hospital Universitari Mútua Terrassa, Department of Pathology, Terrassa, Spain


The histology of the duodenum of Crohn’s disease (CD) has been scarcely explored. Lymphocytic enteritis (LE) and duodenal atrophy were described in CD but the prevalence is unknown and in some cases it raises the differential diagnosis with celiac disease. It is unknown if there is a cytometric-specific pattern of lymphocyte subpopulations of CD as it occurs in celiac disease (increased TCRγδ+ and decreased CD3− lymphocytes) (Fernández-Bañares F. PLoS One 2014). Objectives: Duodenal evaluation of CD: (1) histopathology, (2) lymphocyte subpopulations and (3) association of histopathological abnormalities with clinical parameters.


A total of 134 patients (82 CD, 52 celiac) and 13 controls were prospectively included. Endoscopic, histopathological and clinical parameters were recorded: calprotectin, Harvey–Bradshaw activity index, Montreal classification, treatment regimen, celiac disease work-up, H. pylori and stool parasites. Lymphocyte subpopulations [CD4+, CD8+, DP(CD4+CD8+), DN(CD4-CD8−), TCRγδ and CD3−] were evaluated by flow cytometry. Kruskal–Wallis and U of Mann–Whitney were used as statistical method.


Twenty-five CD patients (30.5%) showed macroscopic involvement of the upper digestive tract (L4). The histopathological study was normal in 46 (56.1%) and showed abnormalities in 36 [7.3% chronic inflammatory infiltrate (of these one granulomas and three LE); 36% isolated LE]. In 20 cases, LE was considered to be due to CD (62.5%), while in 12 (37.5%) it was due to H. pylori (n = 8), NSAIDs (n = 2) and parasites (n = 2). The gastric and oesophageal mucosa showed abnormalities in 64.2% (chronic gastritis) and 15.4%, respectively. No relationship was found between histopathological abnormalities, activity, treatment and the outcome of CD. CD4+ and CD8+ subpopulations did not differ from controls and CD at diagnosis, but they have an increased ‘helper’ response (CD4+) and a reduced suppressor response (CD8+) in previously diagnosed CD (p < 0.0001). There were no differences in DP(CD4+CD8+), whereas DN(CD4−CD8−) were increased in both early and late CD (p = 0.008 vs. controls). Celiac disease presented much more marked changes than CD with decreased ‘helper’ CD4+, suppressors CD8+ and DP(CD4+CD8+) (p < 0.0001 vs. controls and CD), whereas DN(CD4−CD8−) were much more increased than in CD (p < 0.0001). The characteristic celiac cytometric pattern was not detected in CD.


LE (not atrophy) is a frequent finding in the duodenum of CD. Despite being indistinguishable from celiac LE, the immune response is completely different and could be used for diagnostic purposes. The increase in ‘atypical’ DN lymphocytes from the early CD suggests that it is an intrinsic immune alteration that deserves further characterisation by using multiparametric cytometry.