eISSN: 2084-9869
ISSN: 1233-9687
Polish Journal of Pathology
Current issue Archive Manuscripts accepted About the journal Supplements Editorial board Abstracting and indexing Subscription Contact Instructions for authors Ethical standards and procedures
SCImago Journal & Country Rank
1/2017
vol. 68
 
Share:
Share:
more
 
 
Short communication

Is there a correlation between autoimmune and alkaline gastritis?

Marina Perdiki
,
George Karamanolis
,
Ioannis Varbobitis
,
Evaggelia Kavoura
,
Ioanna Delladetsima

Pol J Pathol 2017; 68 (1): 73-74
Online publish date: 2017/05/23
Article file
- Is there.pdf  [0.16 MB]
Get citation
ENW
EndNote
BIB
JabRef, Mendeley
RIS
Papers, Reference Manager, RefWorks, Zotero
AMA
APA
Chicago
Harvard
MLA
Vancouver
 
 
Reactive gastropathy is a common diagnosis in gastric biopsies and reflects the stomach’s response to a variety of irritants including drugs, chronic alcohol consumption as well as reflux of duodenal contents into the stomach. The latter condition, known as alkaline gastritis, has been accepted by the Sydney System as a distinct entity [1]. It results from pyloric sphincter dysfunction caused by pyloroplasty, partial gastrectomy (Billroth I or II) and age-related sphincter soothing.
Studying routine gastric biopsies, we observed rather frequent coexistence of alkaline and autoimmune gastritis. As histological features of the antral mucosa in autoimmune gastritis (AIG) may have been overlooked, we retrospectively studied gastric biopsies in order to identify a possible correlation of alkaline gastritis with autoimmune gastritis, considering that such an association has not yet been reported.
From our archives, we retrieved 1149 gastric biopsies obtained over a one-year period (2014-2015). Biopsies from gastric stumps were not included. All autoimmune gastritis cases were re-evaluated and diagnosis was based on the following appropriate criteria: lesions confined to the corpus/fundus, intense lymphoplasmacytic infiltration of lamina propria, oxyntic glands atrophy, pseudopyloric and intestinal metaplasia [2, 3] as well as enterochromaffin-like (ECL) cell proliferation evaluated on immunohistochemically stained sections for chromogranin A. Histological diagnostic criteria for alkaline gastritis included no or mild inflammation, foveolar hyperplasia, elongation and tortuosity of gastric pits, mucosa villiform transformation, mucin paucity and angulated glands, edema with dilated capillaries and upward extension of smooth muscle fibers from the muscularis mucosa into the lamina propria.
Helicobacter pylori gastritis was found in 228 cases (19.8%), chemical/alkaline gastritis in 88 (7.66%) cases, and non-specific gastritis in 384 (33.4%) cases, whereas no histological changes were observed in 385 (33.5%) cases. Sixty four (5.57%) biopsies carried the diagnosis of autoimmune gastritis. Upon review of these 64 biopsies, atrophy of the oxyntic mucosa was severe in 50, moderate in 10 and mild in 4 cases, while 12 cases (19%) exhibited additional findings of mild and less frequently moderate alkaline gastritis of the antral mucosa (Fig. 1). The latter subgroup had no clinical history of drug or alcohol abuse. No significant correlation was found between coexistence of the aforementioned gastritis types and demographic and histological parameters.
Although the currently established histology of AIG is characterized by a relatively normal antral mucosa, our observations suggest alkaline gastritis to be a rather common additional finding. The only indication of the presence of alkaline gastritis is the reported observation of antral foveolar hyperplasia in AIG, which however was attributed to the trophic effect of hypergastrinemia [4]. The pathogenesis of alkaline gastritis has not been fully elucidated. Prolonged exposure of the gastric mucosa to bile contents and in particular to the toxicity of bile acids is considered to be a potential pathogenetic mechanism [5, 6]. The occurrence of alkaline gastritis in the context of AIG could be ascribed to hypochlorhydria and the ensuing deficient neutralization of the refluxed bile acids. A possible synergistic role of age-related pyloric sphincter dysfunction cannot be excluded. A prospective study should be performed in order to clarify the significance of our observation.

The authors declare no conflict of interest.

References

1. Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis. The update Sydney System. International Workshop on the Histopathology of Gastritis. Houston 1994. Am J Surg Pathol 1996; 20: 1161-1181.
2. Torbenson M, Abraham SC, Boitnott J, et al. Autoimmune gastritis: distinct histological and immunohistochemical findings before complete loss of oxyntic glands. Mod Pathol 2002; 15: 102-109.
3. Park JY, Lam-Himlin D, Vemulapalli R. Review of autoimmune metaplastic atrophic gastritis. Gastrointest Endosc 2013; 77: 284-292.
4. Coati I, Fassan M, Farinati F, et al. Autoimmune gastritis: Pathologist’s viewpoint. World J Gastroenterol 2015; 21: 12179-12189.
5. Santarelli L, Gabrielli M, Candelli M, et al. Post-cholocystectomy alkaline gastritis: a randomized trial comparing sucralfate versus rebeprazole or no treatment. Eur J Gastroenterol Hepatol 2003; 15: 975-979.
6. Vaezi MF, Richter JE. Role of acid and duodenogastroesophageal reflux in gastroesophageal reflux disease. Gastroenterology 1996; 111: 1192-1199.

Address for correspondence

Assoc. Prof. Ioanna Delladetsima
1st Department of Pathology
Athens Medical School
75 Mikras Asias St.
Athens 11527, Greece
tel. +30.210.7462158
fax +30.210.7462179
e-mail: jokadelladetsima@hotmail.com
Copyright: © 2017 Polish Association of Pathologists and the Polish Branch of the International Academy of Pathology This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (http://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
Quick links
© 2020 Termedia Sp. z o.o. All rights reserved.
Developed by Bentus.
PayU - płatności internetowe