Saudi Journal of Gastroenterology
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Year : 1999  |  Volume : 5  |  Issue : 2  |  Page : 81-84
Comparison of H. pylori-gastritis among young and old patients by using "the modified Sydney system of classification and grading"

Department of Pathology, College of Medicine, King Saud University, Abha, Saudi Arabia

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Date of Submission23-Jun-1998
Date of Acceptance12-Dec-1998


It is well known that the age at which H. pylori infection is acquired is crucial in the genesis of gastric cancer () . The aim of the study is to compare antral biopsies from younger (age range 3 - 20 years) and older (age range 51 - 60 years) patients infected with H. pylori. The biopsies were graded for five parameters according to the guidelines from "The modified Sydney System of Classification and Grading of gastritis" (2). There was no significant difference in three parameters i.e. H. pylori density, neutrophilic activity and chronic inflammation between the two age groups. Two parameters i.e. the mucosal atrophy and intestinal metaplasia were, however, more prevalent in older age group. They are considered preneoplastic for gastric cancer. This study demonstrated that the intensity of inflammation is not age related. Preneoplastic changes do, however, begin to emerge later in life.

How to cite this article:
Khan AR. Comparison of H. pylori-gastritis among young and old patients by using "the modified Sydney system of classification and grading". Saudi J Gastroenterol 1999;5:81-4

How to cite this URL:
Khan AR. Comparison of H. pylori-gastritis among young and old patients by using "the modified Sydney system of classification and grading". Saudi J Gastroenterol [serial online] 1999 [cited 2022 Dec 7];5:81-4. Available from:

H. pylori is considered to be a definite cause of gastric cancer [3] . The development of cancer depends upon the time at which the infection is acquired, earlier in life or later [1] . Childhood infection predisposes patients to gastric cancer [1] . Once the infection is acquired in childhood, it persists for life if not treated, and the morphology of the acute gastritis frequently changes to chronic gastritis and later to atrophy and intestinal metaplasia. Grading of the gastritis is useful in evaluation of the severity of the disease. The modified Sydney system describes practical guidelines for grading histopathological features of the gastritis by using visual analogue scale. There are some limitations to this system such as difficulties of its usage in routine and every day reporting in a busy histopathology laboratory. However, the system has been found useful and reproducible for treatment protocols and research purposes. This study is particularly important for the Asir region of Saudi Arabia because of the high incidence of gastric cancer reported from that part of the Kingdom [4]

   Patients and Methods Top

From March 1995 to August 1996, the surgical pathology laboratory of Asir Central Hospital received 528 endoscopic biopsies for investigation of H. pylori infection. These patients were referred to the gastroenterologists for dyspeptic symptoms. Only Two endoscopic specimens were submitted to the histopathology laboratory. The Sydney system, however, requires taking two biopsies from both antral and fundic (body) mucosa. The latter are more useful in those patients who had been previously treated with antisecretory drugs. Our patients had received no prior treatment, therefore, two biopsies from antrum were considered sufficient. All the endoscopic biopsies were fixed in 10 % formalin and were routinely stained with Hematoxylin and Eosin. When the organism could not be identified by the routine stains, additional specific stains were performed such as Giemsa or modified Wright's stain (Diff-Quik(&). The usefulness of Diff-Quik® stain for detection of H. pylori has been documented [5] . We collected all histopathological slides from 31 consecutive H. pylori-positive specimens in a younger age group (3-20 years) and also from 37 cases of an older age group (51-60 years). These slides were graded for the following features: H. pylori density, neutrophilic activity, chronic inflammation, intestinal metaplasia and glandular atrophy. A visual analogue scale was used to assess the severity of the inflammatory changes and grading was done as follows: l:mild, 2:moderate, and 3:severe. H. pylori density was measured by the number of bacteria present on the surface epithelium [Figure - 1]. The neutrophilic activity was counted by the number of neutrophils seen in the lamina propria, or within the glandular epithelium [Figure - 2]. Chronic inflammation was graded according to the number of mononuclear leukocytes in the lamina propria. These mononuclear cells included lymphocytes, plasma cells and macrophages. About 2 to 5 of these cells in the lamina propria per high­power field( x40 objective) are expected in normal biopsies but more than five are considered abnormal. The lymphoid follicles, which are defined as intramucosal aggregates of lymphocytes with germinal centers, were recorded but not graded. Grading of lymphoid follicles was not indicated because its prevalence is determined by the number of specimens taken and not by the severity of the infection. Mucosal atrophy was confirmed in cases showing decrease in the number of mucosal glands and fibrosis of the lamina propria. The intestinal metaplasia was recognized morphologically by the presence of goblet cells and absorptive cells [Figure - 3].

Data were analyzed using the SPSS software program. Mann-Whitney test was used for the comparison of quantitative data between the two groups of patients, while Chi-Squire test was used for comparison of qualitative data. The difference was considered statistically significant at P-value of less than 0.05.

   Results Top

A comparison of scores from younger and older patients is shown in [Table - 1]. No significant differences were noted in the scores of H. pylori density, neutrophilic activity, or chronic inflammatory cell infiltration between the two groups. The intestinal metaplasia was not seen in any young patient (0%) but mild, focal metaplastic changes were seen in 8 (22%) older patients (P<0.05). The atrophic changes were seen in 7 (19%)of 37 older patients but only in one (3%)of 31 younger patients (P<0.05). The lymphoid follicles were observed with almost equal frequency in both groups, 52% in biopsies from younger patients and 57% from older patient's biopsies (P>0.05).

   Discussion Top

The incidence of gastric cancer is high in Saudi Arabia [4],[7],[8],[9]. In studies from the Southern region of Saudi Arabia, stomach cancer ranks as sixth among all malignancies [4] and second among gastrointestinal malignancies [6] . A similar high incidence has also been reported from other regions of Saudi Arabia [7],[8],[9] . International agency for research on cancer has classified H. pylori as a definite cause of gastric adenocarcinoma in humans [1] . Epidemiological studies have shown that areas with high gastric cancer rates often have correspondingly high prevalence of H. pylon [10] . It is possible that H. pylori infection, in conjunction with some other unknown factors, is responsible for the high incidence of gastric cancer reported from this region through development of intestinal metaplasia and glandular atrophy in older population.

H. pylori infection is acquired in early childhood period in the developing countries [11] . Once acquired, the infection persists for life if not treated [12] . The bacterial colonization in the gastric mucosa invokes an inflammatory response by producing urease as well as some cytokines. The earliest stage is known as acute gastritis in which numerous neutrophils are seen in the lamina propria and invading the glandular epithelium. The intensity of neutrophilic activity seems, however, to be independent of the density of H. pylori infection and probably depends upon some other unknown factors such as virulence of the organisms [13] . With the passage of time, neutrophilic inflammatory cells begin to infiltrate the lamina propria. This stage, known as chronic active gastritis, probably persists as long as H. pylori remain present on the mucosal surface. After an unknown but probably considerable length of time the mucosal glands are gradually destroyed and fibrosis begins to emerge in the lamina propria. With the onset of glandular atrophy some of the preserved mucosal glands develop intestinal metaplastic changes. Surprisingly, the density of H. pylori as well as mucosal inflammatory cells tend to decrease in grade after the occurrence of glandular atrophy and intestinal metaplasia [14].

Our study has demonstrated that the intensity of H. pylori organisms, neutrophilic activity and inflammatory changes remain the same in young and old patients. The metaplastic changes and glandular atrophy were, however, significantly higher among older patients. Since the development of the latter two conditions is directly related to the duration of infection, it seems that our older patients probably have been harboring the infection for a considerable length of time. In order to determine whether these changes could be reversed if H pylori infection is appropriately treated, Tucci et al [15] , evaluated 12 patients for H. pylori intensity, neutrophilic activity, lymphocytic infiltration, glandular atrophy and intestinal metaplasia. Six of these patients were treated with oral course of amoxicillin, metronidazole and bismuth and six did not receive any treatment. Glandular atrophy improved in those patients who received the treatment; conversely, no substantial change in histological findings was observed in those patients who did not receive treatment.

Since the lymphoid follicles are found in 100% specimens from H. pylori-positive cases [16] , therefore, we did not think that grading of a feature whose prevalence is determined by number of biopsy specimens taken is necessary. In this study the number of lymphoid follicles was similar in both groups, indicating the abscence of a sampling bias during endoscopic examination.

In conclusion, this study demonstrated that the severity of H. pylori gastritis does not change with age, but preneoplastic changes begin to emerge later in life, thus predisposing patients to gastric cancer.

   References Top

1.Parsonnet J. Helicobacter pylori in the stomach-A paradox unmasked. N Engl J Med. 1996;335:278-80.  Back to cited text no. 1    
2.Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis. The updated Sydney system. Am J Surg Pathol. 1996;20:1161-81.  Back to cited text no. 2    
3.Ho SB. Premalignant lesions of the stomach. Semin Gastrointest Dis. 1996;7:61-73.  Back to cited text no. 3    
4.Khan AR, Hussain NK, Al-Saigh AA, Malatani T, Sheikha AA. Pattern of cancer at Asir Central Hospital, Abha, Saudi Arabia. Ann Saudi Med. 1991;11:285-8.  Back to cited text no. 4    
5.Mendoza M., Martin-Rabadan P, Carrion-I, Morillas JD, Lopez-Alonso G, Diaz-Rubio M. Helicobacter pylori infection. Rapid diagnosis with brush cytology. Acta Cytol. 1993;37:181-5.  Back to cited text no. 5    
6.Morad N, Khan AR, Al-Saigh AA, Malatani T, Hussain N. Pattern of primary gastrointestinal tract cancer in southern province. Ann Saudi Med. 1992;12:259-63.  Back to cited text no. 6    
7.Rabadi SJ. Cancer at Dhahran Health Center, Saudi Arabia. Ann Saudi Med. 1987;7:288-93.  Back to cited text no. 7    
8.Koreich AM, Karawi M. Gastrointestinal tract malignancies: Pattern of disease at Armed Forces Hospital (Abstract). Ann Saudi Med. 1988;8:A75.  Back to cited text no. 8    
9.Bedikian AY. Survey of alimentary malignancies at King Faisal Specialist Hospital and Research Center. Ann Saudi Med. 1987;7:277-81.  Back to cited text no. 9    
10.Webb PM, Forman D. Helicobacter as a risk factor for gastric cancer. Baillieres Clin Gastroenterol. 1995;9:563-82.  Back to cited text no. 10    
11.Neale KR, Logan RP. The epidemiology and transmission of Helicobacter pylori infection in children. Aliment Pharmacol Ther. 1995;9:77-84.  Back to cited text no. 11    
12.Lee A, Buck F. Vaccination and mucosal responses to Helicobacter pylori infection. Aliment Pharmacol Ther. 1996;10:129-38.  Back to cited text no. 12    
13.Phull PS, Price AB, Stephens J, Rathbone BJ, Jacyna MR. Histolory of chronic gastritis with and without duodenitis in patients with Helicobacter pylori infection. J. Clic Pathol. 1996;49:377-80.  Back to cited text no. 13    
14.Sipponen P, Kekki M, Seppala K, Siurala M. The relationship between chronic gastritis and gastric acid secretion. Aliment Pharmacol Ther. 1996;10:103-11.  Back to cited text no. 14    
15.Tucci A, Biasco G, Paparo GF. Effect of eradication of Helicobacter pylori in patients with fundic atrophic gastritis. N Engl J Med. 1997;336:957-8.  Back to cited text no. 15    
16.Genta RM, Hamner W. The significance of lymphoid follicle in the interpretation of gastric biopsy specimens. Arch Pathol Lab Med 1994;118:740-3.  Back to cited text no. 16    

Correspondence Address:
Abdur Rauf Khan
Department of Pathology, College of Medicine, King Saud University, P.O. Box 641, Abha
Saudi Arabia
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Source of Support: None, Conflict of Interest: None

PMID: 19864749

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