Brief Report Open Access
Copyright ©The Author(s) 1997. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 15, 1997; 3(2): 113-113
Published online Jun 15, 1997. doi: 10.3748/wjg.v3.i2.113
Study on clinical pathology and immunohistochemistry of chronic erosive gastritis
Chang-Shu Ke, Dao-Fen Li, Wei Wang, Yi-Ming Wang, Department of Pathology and Gastroenterology, Wuhan General Hospital of Chinese PLA, Guangzhou Command Area, Wuhan 430070, Hubei Province, China
Author contributions: All authors contributed equally to the work.
Received: November 10, 1996
Revised: January 31, 1997
Accepted: March 1, 1997
Published online: June 15, 1997

Abstract

AIM: To study the clinical pathology of chronic erosive gastritis (CEG) and determine the expression of epithelial tumor markers, oncoprotein p21 and carcinoembryonic antigen (CEA), and G cells by immunohistochemistry.

METHODS: Gastric mucosal biopsies from 40 CEG cases were examined. Histopathology and Helicobacter pylori (Hp) infection were determined by light microscopy. Thirty-one biopsies from CEG cases were immunostained with antibodies against p21, CEA, proliferation cell nuclear antigen (PCNA), and gastrin using the labeled streptavidin-biotin (LSAB) method.

RESULTS: A total of 35/40 (87.5%) CEG lesions showed antral location; 75% of the lesions were associated with different degrees of atrophic change. Twenty percent presented with mild and moderate atypia of mucosal epithelia and 27.5% showed intestinal metaplasia. Acute inflammatory changes were observed in 25% of the cases. Hp was identified in 40.0% of the specimens. Immunohistochemistry studies showed that 67.7% of the CEG mucosal epithelial samples expressed oncoprotein p21 and 29.0% expressed CEA, rates significantly higher than those observed in control samples from a chronic superficial gastritis group. However, PCNA and gastrin expression in mucosal G cells was not significantly different between CEG samples and samples from the control group (P > 0.05).

CONCLUSION: CEG is a chronic gastric mucosal proliferative lesion that expresses higher levels of p21 and CEA than control samples. Our observations suggest that antral location of the lesion and Hp infection do not participate in the pathological process of CEG.

Key Words: Gastritis/pathology, Chronic disease



Footnotes

Original title: China National Journal of New Gastroenterology (1995-1997) renamed World Journal of Gastroenterology (1998-)

S- Editor: Filipodia L- Editor: Jennifer E- Editor: Liu WX

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