Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver · 2026
Enterocyte proliferation as a new biomarker in potential coeliac disease.
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Ciccocioppo Rachele, D'Agate Cinzia, Galli Maria Vittoria, Macchioni Anna, Broggi Giuseppe, Zuliani Valeria, Frulloni Luca, Luciani Fabio, Bugatti Mattia, Benedetti Martina, Arshad Mamoona, Verlato Giuseppe, Villanacci Vincenzo
Аннотация
BACKGROUND: Potential coeliac disease is an increasingly diagnosed condition, and the dilemma whether start a gluten-free diet is still unsolved.
AIMS: We hypothesized that an exaggerated enterocyte turnover is responsible for an impairment of gut function leading to the development of symptoms and/or progression to villous atrophy.
METHODS: The proliferation and apoptotic rates of duodenal enterocytes, assessed by anti-Ki-67 and -Caspase-3 antibodies at immunohistochemistry, of 36 adult patients with potential coeliac disease were compared to those found in a group of 32 active coeliac patients and a group of 31 controls. Statistics was computed by Fisher's exact test, Wilcoxon-Mann-Whitney rank-sum test, and Kruskal-Wallis test as appropriate, post-hoc analysis was performed by Dunn's test with Bonferroni correction.
RESULTS: Nearly all patients with potential coeliac disease reported symptoms (31/36 = 86.1 %), and four out 36 developed active disease over time. A significant increase of enterocyte proliferation (p = 0.042), but not of apoptosis (p = 0.514), in comparison with control subjects was found. Notably, a significant correlation between Ki-67 expression and the progression to villous atrophy (p = 0.015) was evident.
CONCLUSIONS: The maintenance of mucosal architecture in potential coeliac disease is due to enterocyte hyper-proliferation that causes the presence of immature cells on the villous lining and correlates with the development of villous atrophy.
AIMS: We hypothesized that an exaggerated enterocyte turnover is responsible for an impairment of gut function leading to the development of symptoms and/or progression to villous atrophy.
METHODS: The proliferation and apoptotic rates of duodenal enterocytes, assessed by anti-Ki-67 and -Caspase-3 antibodies at immunohistochemistry, of 36 adult patients with potential coeliac disease were compared to those found in a group of 32 active coeliac patients and a group of 31 controls. Statistics was computed by Fisher's exact test, Wilcoxon-Mann-Whitney rank-sum test, and Kruskal-Wallis test as appropriate, post-hoc analysis was performed by Dunn's test with Bonferroni correction.
RESULTS: Nearly all patients with potential coeliac disease reported symptoms (31/36 = 86.1 %), and four out 36 developed active disease over time. A significant increase of enterocyte proliferation (p = 0.042), but not of apoptosis (p = 0.514), in comparison with control subjects was found. Notably, a significant correlation between Ki-67 expression and the progression to villous atrophy (p = 0.015) was evident.
CONCLUSIONS: The maintenance of mucosal architecture in potential coeliac disease is due to enterocyte hyper-proliferation that causes the presence of immature cells on the villous lining and correlates with the development of villous atrophy.