Assessment of Cell Proliferation in Helicobacter pylori associated gastric epithelial diseases

  • Neeraj Dhameja Department of Pathology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, UP, India.
  • Ritambra Nada Professor, Department of Histopathology, PostGraduate Institute of Medical Education and Research, Chandigarh
  • Deepak Kumar Bhasin Professor and Head, Department of Gastroenterology, PostGraduate Institute of Medical Education and Research, Chandigarh.
  • Kusum Joshi Professor &Head, Department of Histopathology, PostGraduate Institute of Medical Education and Research, Chandigarh.
Keywords: Atrophy, Carcinoma, Chronic active gastritis, Dysplasia, Intestinal metaplasia, Helicobacter pylori, Proliferative Index

Abstract

Background: Alterations in cell proliferation and apoptosis as a result of Helicobacter Pylori infection can contribute to carcinogenesis. This study was planned to assess cellular proliferation during chronic active gastritis with or without H. Pylori, atrophy, intestinal metaplasia, dysplasia and carcinoma. Effect of H. Pylori eradication on cell proliferation was also studied.Methods: Ki67 immunostaining was done to calculate proliferative index (PI) in H. pylori associated gastric diseases.  Gastric biopsies of 160 patients with dyspepsia were selected comprising of 20 cases each of  following groups 1) Normal control 2) H .pylori positive chronic  active gastritis before  and after treatment  3)H. pylori negative chronic active gastritis  4) Atrophy  5) Intestinal metaplasia  6) Dysplasia  7) Gastric adenocarcinoma Result: There was increased proliferative index (PI) in H. pylori positive and negative chronic active gastritis as compared to normal controls. However, the PI in H. pylori positive chronic active gastritis was significantly higher than  that of H. pylori negative chronic active gastritis. Increased proliferation was persistent in atrophy, intestinal metaplasia, dysplasia and carcinoma. There was significant  increase in PI in foveolar regions in chronic active gastritis, intestinal metaplasia and dysplasia . After H. pylori eradication, there was marked reduction in  PI. Conclusion: H. pylori infection results in increased gastric epithelial cell proliferation which persists in the premalignant stages of atrophy, intestinal metaplasia, dysplasia and carcinoma. Presence of H. pylori augments proliferation resulting from inflammation and eradication of H. pylori reduces proliferation.. This increased proliferation may be one of the mechanism of H. pylori associated  carcinogenesis.

Author Biography

Neeraj Dhameja, Department of Pathology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, UP, India.
Assistant Professor, Department of Pathology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, UP, India.

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Published
2016-05-07
Issue
Vol 3 No 2 (2016)
Section
Original Article

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