H Pylori
Copyright ©The Author(s) 2003. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 15, 2003; 9(12): 2706-2710
Published online Dec 15, 2003. doi: 10.3748/wjg.v9.i12.2706
Epithelial cell proliferation and glandular atrophy in lymphocytic gastritis: Effect of H pylori treatment
Johanna M. Mäkinen, Seppo Niemelä, Tuomo Kerola, Juhani Lehtola, Tuomo J. Karttunen
Johanna M. Mäkinen, Tuomo J. Karttunen, Department of Pathology, University of Oulu, Oulu, Finland
Seppo Niemelä, Juhani Lehtola, Department of Internal Medicine, Oulu University Hospital, Oulu, Finland
Tuomo Kerola, Department of Pathology, Länsi-Pohja Central Hospital, Kemi, Finland
Author contributions: All authors contributed equally to the work.
Correspondence to: Tuomo J. Karttunen, Department of Pathology, P.O. Box 5000 (Aapistie 5), FIN-90014 University of Oulu, Finland. tuomo.karttunen@oulu.fi
Telephone: +358-8-537-5951 Fax: +358-8-537-5953
Received: August 11, 2003
Revised: August 27, 2003
Accepted: October 12, 2003
Published online: December 15, 2003
Abstract

AIM: Lymphocytic gastritis is commonly associated with Helicobacter pylori infection. The presence of glandular atrophy and foveolar hyperplasia in lymphocytic gastritis suggests abnormalities in cell proliferation and differentiation, forming a potential link with the suspected association with gastric cancer. Our aim was to compare epithelial proliferation and morphology in H pylori associated lymphocytic gastritis and H pylori gastritis without features of lymphocytic gastritis, and to evaluate the effect of H pylori treatment.

METHODS: We studied 14 lymphocytic gastritis patients with H pylori infection. For controls, we selected 14 matched dyspeptic patients participating in another treatment trial whose H pylori infection had successfully been eradicated. Both groups were treated with a triple therapy and followed up with biopsies for 6-18 months (patients) or 3 months (controls). Blinded evaluation for histopathological features was carried out. To determine the cell proliferation index, the sections were labeled with Ki-67 antibody.

RESULTS: Before treatment, lymphocytic gastritis was characterized by foveolar hyperplasia (P = 0.001) and glandular atrophy in the body (P = 0.008), and increased proliferation in both the body (P = 0.001) and antrum (P = 0. 002). Proliferation correlated with foveolar hyperplasia and inflammation activity. After eradication, the number of intraepithelial lymphocytes decreased in the body (P = 0.004) and antrum (P = 0.065), remaining higher than in controls (P < 0.001). Simultaneously, the proliferation index decreased in the body from 0.38 to 0.15 (P = 0.043), and in the antrum from 0.34 to 0.20 (P = 0.069), the antral index still being higher in lymphocytic gastritis than in controls (P = 0.010). Foveolar hyperplasia and glandular atrophy in the body improved (P = 0.021), reaching the non-LG level.

CONCLUSION: In lymphocytic gastritis, excessive epithelial proliferation is predominantly present in the body, where it associates with foveolar hyperplasia and glandular atrophy. These characteristic changes of lymphocytic gastritis are largely related to H pylori infection, as shown by their improvement after eradication. However, some residual deviation was still seen in lymphocytic gastritis, indicating either an abnormally slow improvement or the presence of some persistent abnormality.

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