Cell proliferation and inflammation on biopsy samples with multifocal atrophic gastritis before and 1 year after Helicobacter pylori eradication.
BACKGROUND
Results of clinical trials that have assessed whether gastric cancer is preventable with Helicobacter pylori eradication therapy remain inconclusive. These trials have used atrophy, intestinal metaplasia, and dysplasia as histopathologic end points that reflect possible preneoplastic lesions. Trial results would be more compelling if cell proliferation and inflammatory markers improved simultaneously with histopathologic lesions.


OBJECTIVE
To study the presence of cell proliferation markers and type of inflammatory cells in biopsy specimens with gastritis, atrophy, and intestinal metaplasia before and 1 year after H pylori therapy and to determine if immunohistochemistry can be used to study these.


METHODS
We evaluated 12 subjects with gastritis and 16 with gastritis and multiple foci of atrophy and intestinal metaplasia by using immunohistochemical assays for tumor suppressor protein p53, proliferation marker Ki-67, cell cycle regulator cyclin D1, T and B lymphocytes, macrophages, and TUNEL (terminal deoxynucleotide transferase deoxyuridine triphosphate nick end labeling) assay for apoptosis. The biopsy specimens were selected from a randomized clinical trial that studied improvement of histopathologic gastric lesions after H pylori eradication.


RESULTS
Groups of surface epithelial cells that expressed p53 and Ki-67 were observed more often in subjects with atrophy and intestinal metaplasia compared with those with gastritis alone. T lymphocytes in the lamina propria were frequently observed 1 year after treatment in subjects with atrophy and intestinal metaplasia.


CONCLUSIONS
Immunohistochemical assays for cell proliferation and inflammatory cell markers showed different distribution patterns in these gastric biopsy specimens. The presence of T lymphocytes and groups of cells that expressed proliferation markers in subjects with multiple foci of atrophy and intestinal metaplasia needs further study.
Guarner
Jeannette
J
Infectious Diseases Pathology Activity, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA. jguarner@cdc.gov
Bartlett
Jeanine
J
Seitz
Roslyn
R
Whistler
Toni
T
Herrera-Goepfert
Roberto
R
Mohar
Alejandro
A
Sanchez
Luz
L
Halperin
David
D
Parsonnet
Julie
J
D017209:Apoptosis; D015415:Biomarkers / Q000378:metabolism; D001706:Biopsy; D049109:Cell Proliferation; D005753:Gastric Mucosa / Q000378:metabolism / Q000473:pathology*; D005757:Gastritis, Atrophic / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D016481:Helicobacter Infections / Q000150:complications / Q000188:drug therapy / Q000473:pathology*; D016480:Helicobacter pylori; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D019394:Ki-67 Antigen / Q000378:metabolism; D013601:T-Lymphocytes / Q000378:metabolism / Q000473:pathology; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
D015415:Biomarkers; D019394:Ki-67 Antigen; D016159:Tumor Suppressor Protein p53