Saudi Journal of Gastroenterology
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Year : 1999  |  Volume : 5  |  Issue : 1  |  Page : 15-17
Association of gastric lymphoid follicles and Helicobacter pylori infection


1 Department of Histopathology, Central Lab & Blood Bank, Riyadh, Saudi Arabia
2 Department of Medicine, College of Medicine, KSU, Riyadh, Saudi Arabia

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Date of Submission10-Dec-1997
Date of Acceptance17-Jun-1998
 

   Abstract 

Lymphoid tissue is normally absent in the gastric mucosa; however, lymphoid follicles are very frequently noted in Helicobacter-associated gastritis. We reviewed 237 cases of chronic gastritis with lymphoid follicles. Out of this 227 cases (95.8%) were found to have H. pylori infection. The significance of this finding and its possible relationship to primary gastric lymphoma are discussed.

How to cite this article:
Afzal M, Baez-Giangreco A, Joarder MI, Laajam MA. Association of gastric lymphoid follicles and Helicobacter pylori infection. Saudi J Gastroenterol 1999;5:15-7

How to cite this URL:
Afzal M, Baez-Giangreco A, Joarder MI, Laajam MA. Association of gastric lymphoid follicles and Helicobacter pylori infection. Saudi J Gastroenterol [serial online] 1999 [cited 2021 Sep 28];5:15-7. Available from: https://www.saudijgastro.com/text.asp?1999/5/1/15/33520


Helicobacter pylori, a fastidious gram negative micro-aerophilic spiral organism, is the causative agent of chronic gastritis, peptic ulcer disease and it is also implicated in the development of gastric cancer [1] . Recently a number of reports have described high prevalence of lymphoid aggregates in H. pylori associated gastritis [2],[3],[4] . Since the development of mucosa-associated lymphoid tissue (MALT) in the stomach in association with H. pylori may provide some clues about the pathogenesis of gastric lymphoma, we undertook a restrospective study to verify that observation in our gastric biopsy material.


   Material and Methods Top


This is a retrospective study conducted at the Histopathology Department of the Riyadh Central Laboratory. All the endoscopic gastric biopsies cases carrying non neoplastic diagnoses and done over a period of six months from May 1996 to November 1996 were retrieved from our files. A total of 500 cases were collected. We routinely make duplicate Hematoxylin/Eosin stained slides and perform Giemsa and modified Gram stains to check for H. pylori on all endoscopic gastric biopsies [Figure - 1],[Figure - 2]. All the available slides and reports were reviewed by two pathologists, independently. No additional slides or special stains were made. For the purpose of this study chronic gastritis was considered to be present when a definitive increase in mononuclear inflammatory cells (lymphocytes & plasma cells) was seen in the lamina propria. Lymphoid hyperplasia was noted to be present when lymphoid follicles were seen with or without germinal centers. The Chi-square was used to analyze the results. The P­value 0.05 or less is considered significant.


   Results Top


A total of 500 cases of chronic gastritis were reviewed. Lymphoid hyperplasia was noted in 237 (48%) cases and in this group H. pylori was detected in 227 (95.8%). In the remaining 263 cases of chronic gastritis without lymphoid follicles, 226 (85.9%) showed H Pylori (P-value > 0.1) [Table - 1]. The average number of biopsy fragments for each patient was two. A positive relationship was noted between the density of H.pylori and degree of inflammation. The age ranged from less than 10 to 90 years. with median age of 30 years. Sex distribution showed male preponderance with ratio of 1.5: 1.


   Discussion Top


Lymphoid follicles in the gastric mucosa represent a common response to H. pylori infection. The range of this response varies from 27% to 100 % in previous publications [3],[5],[6] . In our study it was about 50%. It appears that this percentage increases when additional efforts such as deeper sections, repeat of special stains and/or new biopsies are carried out [7],[8] . The presence of lymphoid follicles in the gastric mucosa appears to be a strong predictor of H. pylori infection since in our group of 237 cases with follicular gastritis, 227 were positive for H. pylori infection (95.8%). Probably if we consider others factors such as inadequate sampling or antibiotics taken before biopsies. the percentage of association of follicular gastritis and presence of H. pylori will be higher almost approaching 100%.

In a more comprehensive study Genta et al [7] using a similar approach reported that in a group of 110 gastric biopsies showing chronic gastritis with lymphoid hyperplasia, 91.8% were found to have H. pylon. Their results are fairly comparable to ours [Table - 2]. They concluded that finding even a single lymphoid follicle in a gastric biopsy specimen is associated with a very high probability (>90%) of detecting H. pylori in the same or in another synchronous biopsy specimen obtained from that patient. Our study supports that conclusion. Lymphoid follicle are absent in the normal stomach [9] , therefore their appearance in the stomach with H. pylori associated gastritis, is an issue of considerable interest. The development of mucosa associated lymphoid tissue is a necessary first step in the development of primary MALT lymphoma in various organs such as lung, thyroid or stomach that are normally devoid of MALT [10],[11] . Therefore, association in the stomach mucosa suggests a causal relationship between H. pylori and the origin of gastric MALT lymphoma.

This concept is enforced by epidemiological evidence of high incidence of primary gastric lymphoma in areas of high prevalence of H. pylori infection in some parts of the world [12] and that H. pylori infection is present in nearly all patients with gastric MALT lymphoma. Furthermore, in vitro studies by Hussell and associates [13] showed that addition of H. pylori to low grade gastric MALT lymphoma cells resulted inactivation, proliferation and production of tumor immuno globulin. A.C. Whatherpoon and colleague [14] , reported tumor regression after cure of H. pylori infection in five out of six patients with low grade gastric MALT lymphoma. Other studies have also reported similar tumor regression after treatment of H. pylori infection [15] .

In conclusion the present study supports other reports that H pylori infection causes appearance of gastric MALT. This provides the necessary background where other as yet unidentified factors may act leading to the development of lymphoma in a small proportion of cases. Also it supports the concept that eradication of H. pylori results in prevention or regression of previously developed MALTOMA of the stomach. Further studies and therapeutic trials would help further clarify this relationship.

 
   References Top

1.Appelman HD. Gastritis, terminology. etiology and clinicopathological correlations, another biased view. Hum. Pathol. 1994;25:1006-19.  Back to cited text no. 1    
2.Eidt S, Stolte M. Prevalence of lymphoid follicles and aggregates in Helicobacter pylori gastritis in antral and body mucosa. J. Clin. Pathol. 1993;46:832-5.  Back to cited text no. 2    
3.Wyatt JI, Rathbohe G.J. Immune response of the gastric mucosa to Campylobacter pylori. Scand. J. Gastroenterol. 1988;23(suppl.) 44-9.  Back to cited text no. 3    
4.Wotherspoon A, Ortiz-Hidalgo C, Diss T, Falzon MR, Isaacson PG. Helicobacter pylori associated gastritis and Primary B-cell gastric lymphoma. Lancet 1991;338:1175-6.  Back to cited text no. 4    
5.Stolte M, Eidt S. Lymphoid follicles in the antral mucosa: immune response to Campylobacgter pylori. J. Clin. pathol. 1989;42:1269-71.  Back to cited text no. 5    
6.Genta RM, Hammer HW, Graham DY. Gastric lymhoid follicles in Helicobacter pylori infection: Frequency, distribution and response to triple therapy. Hum. Pathol. 1993;24:577-83.  Back to cited text no. 6    
7.Genta RM, Hammer HW. The significance of lymphoid follicles in the interpretation of gastric biopsy specimens. Arch. Pathol. Lab. Med. 1994;119:740-3.  Back to cited text no. 7    
8.Ibrahim BH, Amin JT, Sarkar C. Helicobacter pylon: Associated chronic antral gastritis in Kuwait. A Histopathological study. Ann. Saudi Med. 1995;16: 570-4.  Back to cited text no. 8    
9.Owen DA. : Normal histology of the stomach. Am. J. surg. Pathol. 1986;10:49-61.  Back to cited text no. 9    
10.Hyjek E, Isaacson PG. Primary B-cell Lymphoma of the thyroid and its relationship to Hashimoto" thyroiditis. Human Pathol. 1988;19:1315-26.  Back to cited text no. 10    
11.Hyjek E, Smith WJ, Isaacson PG. Primary B-cell lymphoma of salivary glands and its relationship to myoepithelial sialoadenitis. Hum. Pathol. 1988;19:766-76.  Back to cited text no. 11    
12.Doglioni C, Wotherspoon AC, Moschini A. et al. High incidence of primary gastric lymphoma in northeastern Italy. Lancet 1992;834-5.  Back to cited text no. 12    
13.Hussel T, Isaacson PG, Crabtree JE, Spencer J. The response of cells from low grade B-cell gastric lymphomas of mucosa associated lymphoid tissue to Helicobacter pylori. Lancet 1993;342:571-4.  Back to cited text no. 13    
14.Wotherspoon AC, Doglioni C, de-Boni M, Spencer J. Isaacson PG. Antibiotic treatment for low grade gastric MALT lymphoma. Lancet 1994;343:1503.  Back to cited text no. 14    
15.Bayderdorffer E, Neubauer A, Rudolph B. et al. For MALT Lymphoma Study Group. Regression of primary gastric lymphoma of mucosa-associated lymphoid tissue type after cure ofHelicobacter pylori infection. Lancet 1995;345:1591-4.  Back to cited text no. 15    

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Correspondence Address:
Mohammad Afzal
P.O. Box 60179, Riyadh, 1545
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


PMID: 19864754

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