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. 2000 Oct;53(10):784–787. doi: 10.1136/jcp.53.10.784

Cell proliferation in type C gastritis affecting the intact stomach

D Mac 1, P Willis 1, R Prescott 1, S Lamonby 1, D Lynch 1
PMCID: PMC1731098  PMID: 11064674

Abstract

Aims—Type C gastritis caused by bile reflux has a characteristic appearance, similar to that seen in other forms of chemical gastritis, such as those associated with NSAIDs or alcohol. An increase in mucosal cell proliferation increases the likelihood of a neoplastic clone of epithelial cells emerging, particularly where there is chronic epithelial injury associated with bile reflux. It has been shown previously that type C gastritis is associated with increased cell proliferation in the postsurgical stomach. The aim of this study was to determine cell proliferation in type C gastritis caused by bile reflux affecting the intact stomach.

Methods—Specimens from 15 patients with a histological diagnosis of type C gastritis on antral biopsy were obtained from the pathology archives between 1994 and 1997. A control group of nine normal antral biopsies was also selected and all underwent MIB-1 immunostaining. The gastric glands were divided into three zones (zone 1, gastric pit; zone 2, isthmus; and zone 3, gland base) and the numbers of positively staining nuclei for 500 epithelial cell nuclei were counted in each zone to determine the percentage labelling index (LI%).

Results—Cell proliferation was significantly higher in all three zones of the gastric glands with type C gastritis compared with controls as follows: zone 1, median LI% in type C gastritis 64.7 (range, 7.8–99.2), controls 4.7 (range, 2.0–11.3); zone 2, median LI% in type C gastritis 94.7 (range, 28.8–98.7), controls 40.2 (range, 23.1–70.3); and zone 3, median LI% in type C gastritis 20.0 (range, 1.3–96.0), controls 2.6 (range, 0.9–8.7).

Conclusions—Bile reflux is thought to act as a promoter of gastric carcinogenesis in the postsurgical stomach. The same may be true in the intact stomach.

Key Words: cell proliferation • epithelial kinetics • chemical gastritis

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Figure 1 MIB-1 immunostaining of gastric glands in (A) type C gastritis (B) normal mucosa.

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Figure 2 Haematoxylin and eosin staining of gastric glands in (A) type C gastritis (B) normal mucosa.

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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