Table of Contents  
Year : 2014  |  Volume : 7  |  Issue : 4  |  Page : 463-467  

Evaluation of gastric biopsies in chronic gastritis: Grading of inflammation by Visual Analogue Scale

Department of Pathology, Kasturba Medical College, Mangalore, Karnataka, India

Date of Web Publication25-Jun-2014

Correspondence Address:
Shrijeet Chakraborti
Department of Pathology, Kasturba Medical College - Mangalore, Lighthouse Hill Road, Mangalore, Karnataka - 575 001
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0975-2870.135268

Rights and Permissions

Introduction: Gastritis is a common condition with many etiologies and the classification of the same poses a great challenge to the pathologist. Aim: This study was undertaken to classify gastritis according to the Sydney system guidelines including graded and non-graded variables and simultaneously find association of Helicobacter pylori (H. pylori) with each of these variables. Materials and Methods: A total of 100 biopsies of chronic superficial gastritis received over a period of two years were studied, prospectively. Histology was evaluated with Hematoxylin and eosin, and Giemsa stains, and Gomori's staining method for demonstration of reticulin fibres. Rapid Urease test results obtained from gastroenterology department were compared with histopathology. Chi-square test was used to analyze the correlation between the various variables. Results: Gastritis cases showed a male preponderance and the most common presenting complaint was dyspepsia. H. pylori gastritis usually shows increased neutrophilic activity but can also present with increased mononuclear inflammatory infiltrate and lymphoid follicles in chronic gastritis. Intestinal metaplasia and atrophy indicates the chronicity of the disease. H. pylori were noted in the areas away from the metaplastic gastric epithelium. Conclusion: The study showed that histopathology is the most sensitive test for diagnosing H. pylori on endoscopic biopsies. Though, rapid urease test kit gives gastroenterologist a rapid diagnosis, its specificity is low, and hence should be combined with histopathology, which is the gold standard for diagnosis.

Keywords: Chronic superficial gastritis, Giemsa stain, H. pylori, Sydney system

How to cite this article:
Pruthi S, Nirupama M, Chakraborti S. Evaluation of gastric biopsies in chronic gastritis: Grading of inflammation by Visual Analogue Scale. Med J DY Patil Univ 2014;7:463-7

How to cite this URL:
Pruthi S, Nirupama M, Chakraborti S. Evaluation of gastric biopsies in chronic gastritis: Grading of inflammation by Visual Analogue Scale. Med J DY Patil Univ [serial online] 2014 [cited 2021 Sep 17];7:463-7. Available from:

  Introduction Top

Since the discovery of Helicobacter pylori (H. pylori) in the gastric mucosa by Warren and Marshall in 1983, H. pylori have brought about a complete revision of concepts of chronic gastritis and its consequences. [1] H. pylori is a spiral to curved, gram negative, rod-shaped bacterium, and is strongly associated with chronic active gastritis as well as gastric adenocarcinoma and mucosa associated lymphatic tissue lymphoma (MALToma). In an attempt to remove diagnostic confusion, the Sydney System for the grading and classification of chronic gastritis was introduced in 1990, and was later updated in 1994, provides the framework for a standardized description of chronic gastritis, which is not only confined to etiological categories, but also useful in clinicopathological research and provides a sound basis for routine diagnosis. To address the topographical differences in the distribution of gastritis, the Sydney System has a morphological section which attempts to produce a 'flexible matrix of rules' by which five histological variables are graded independently on a simple four point scale (absent or normal, mild, moderate and marked or severe abnormality). Sydney System now being used internationally has histological component which combines topographical, morphological, and etiological information. [2]

  Materials and Methods Top

In the Department of Pathology, Kasturba Medical College, Mangalore, a total of 110 gastric biopsies for gastritis were received from 2010 to 2012, and studied prospectively. Inclusion criteria for the study: (i) cases of all ages and both sexes with upper gastrointestinal symptomatology (ii) both in-patients and out-patients, and with (iii) full mucosal thickness endoscopic biopsies incorporating muscularis mucosae. Exclusion criteria included cases with superficial gastric biopsy specimens. The patient's age, sex, detailed clinical history, upper gastrointestinal endoscopy findings and other relevant laboratory investigations were recorded. The results of rapid urease test were recorded from the Gastroenterology department. The test was considered positive when the urea block of the test kit changed color from yellow to pink at room temperature, within 24 hours. The endoscopic biopsies were taken from the antrum, corpus, and edge of ulcer if any or areas of mucosal abnormalities. Serial sections of 4-5μ thickness, obtained formalin fixed paraffin embedded tissue and stained with hematoxylin and eosin (H and E). The histopathological findings were studied. Giemsa stain was done for each of the biopsy specimen to demonstrate H. pylori. The grades of H. pylori density, neutrophilic activity, mononuclear cell (MNC) infiltration, intestinal metaplasia (IM) and glandular atrophy were determined in biopsy tissue fragments using the Updated Sydney classification system and Visual Analogue Scale, and scored as normal, mild, moderate or marked. Stain for demonstration of reticulin by Gomori's method was also performed to study the reticulin frame work in the gastric biopsies showing gastric atrophy to differentiate atrophy from the separation of the glands by dense inflammation.

Statistical analysis was done using percentage, mean, sensitivity, specificity, positive and negative predictive value. Chi-square test was used to analyze the correlation between the various variables. The p value of <0.05 was considered significant.

  Results Top

The 10 superficial mucosal biopsies were excluded from this study, and the remaining 100 cases were analyzed. Gastritis cases were distributed over a wide age group ranging from 16-81 years with a mean age of 55 years. Maximum numbers of cases, that is 28% belonged to age group of 61-70 years, followed by 23% cases in 51-60 years age group, and 13% each in 31-40, 41-50, and 71-80 years, age groups. Three cases were less than 20 years of age. Gastritis cases showed a male predominance with a male : female ratio of 2.3:1. Helicobacter pylori was detectable on HandE stained sections in only 8% of cases, whereas in total 47% cases it was demonstrable by Giemsa stain [Figure 1]a. Twelve (25.5%) cases showed H. pylori positivity and were in age group of 51-60 years, followed by 8 (17.02%) cases each in 31-40, 41-50 and 61-70 years age group. Clinical features were available in 81% cases, of which the most common presenting symptom was dyspepsia (33.3%), followed by abdominal pain (22.2%). Seven cases (8.6%) presented with hematemesis due to active bleeding gastric ulcer. Melena and anemia were presenting clinical features in 3 (3.7%) and 2 (2.46%) cases, respectively. The history of prolonged intake of non-steroidal anti-inflammatory drugs (NSAIDs) was seen found in 7 (8.64%) cases.
Figure 1: (a) H. pylori colononization of crypts (Giemsa ×400); a inset – corkscrew appearance (H and E ×40); (b) Dense mixed inflammation and crypt distortion; (c) Intra-epithelial neutrophilic infi ltrate (H and E ×400); (d) Lymphoplasmacytic infi ltrate (H and E ×400); (e) Intestinal metaplasia (H and E ×100); e inset – goblet cells (H and E ×400); (f) Lymphoid follicle (H and E ×100); (g) Foveolar hyperplasia with dense chronic infl ammation (H and E ×40)

Click here to view

Endoscopic findings were available in 77 cases, and showed antral ulcers / erosions in 36 (46.7%) cases. This was followed by gastric (fundus, incisura, lesser and greater curvature) ulcer / erosion in 25.9% cases, pre-pyloric and pyloric ulcer in 9.09% cases, normal mucosa and duodenal ulcer / erosion in 6.4% and 5.1% cases, respectively. As biopsy was done from the site of ulcer or erosion, so antrum was the most commonly biopsied site. Gastritis was seen histologically in all 5 cases of normal appearing mucosa on endoscopy, of which 3 cases (60%) were positive for H. pylori.

Mild density of H.pylori was seen in 28 (59.6%) cases and moderate density in 19 (40.4%) cases. Surface positivity of H. pylori was seen in 27 (57.4%) cases, surface and crypt positivity in 40.4%, and 2.2% showed positivity in crypts alone. Neutrophilic activity was mild, moderate and marked in 35, 14 and 6 cases, respectively [Figure 1]b, c. Mononuclear cells or lymphocytic infiltrate was seen in all the cases, with mild MNC infiltrate in 8% of cases. Moderate and marked lymphocytic infiltrate was noted 61% and 31% cases, respectively. Intestinal metaplasia was mild in 31% of the cases, moderate in 6% cases and absent in 63% cases. Only mild atrophy of the fundic and corpus mucosa was seen in 8% of the cases [Figure 2].
Figure 2: Grading of variables by Visual Analogue Scale

Click here to view

Helicobacter pylori on was identified in 16 (35.5%) of cases with absent neutrophilic activity. Similarly, H. pylori was detected in 34.2% of cases with mild neutrophilic activity, and 85.7% of cases with moderate neutrophilic activity. All six cases having marked neutrophilic activity showed H. pylori positivity. In 37.5% cases with mild, 33.3% of moderate and 80.6% of marked mononuclear cell or lymphocytic infiltrate, H. pylori was detected. The mononuclear cell infiltration was associated with plasma cells in all the cases [Figure 1]d. Density of H. pylori colonization increased with the severity of neutrophilic and mononuclear cell activity, and P value of <0.001 showed highly significant correlation between H. pylori density and acute and chronic inflammatory cell activity.

Intestinal metaplasia seen in 36 cases, was mild in 31 (86.1%) cases and moderate in 13.8% cases [Figure 1]e. The maximum cases were seen in 6th and 7th decades, with 27.7% and 33.3% cases were in the age group of 51-60 and 61-70 years, respectively. Intestinal metaplasia had a male predilection (M: F = 3:1). Helicobacter pylori was seen only in 10 (32.2%) cases with mild IM. Eight cases showed gastric atrophy and had male predilection (M: F = 3:1) and H. pylori were demonstrable in 5 cases (62.5%). Overall 8% cases showed gastric atrophy, of which 4 (50%) cases belonged to the 51-60 years age group, followed by 2 cases in 61-70 years, and 1 case each in 41-50 years and 71-80 years, age groups. In five out of eight (62.5%) cases of gastric atrophy showed H.pylori positivity. In 29 mucosal biopsies with lymphoid follicles [Figure 1]f H. pylori was seen in 16 (55.2%) cases. In 84% cases foveolar hyperplasia was seen, of which 39 (46.4%) cases showed H. pylori [Figure 1]g.

The result of rapid urease test was available for 19 cases, and was positive in 8 cases. Among the positive urease test cases H. pylori was seen in 5 (62.5%) cases. However, in urease test negative 11 cases, H. pylori was present in 3 (27%) cases. Sensitivity and specificity of rapid urease test is 62.5% and 37.5%. The positive and negative predictive value of the test was 62.5% and 72.7%, respectively.

  Discussion Top

H. pylori remain the world's commonest chronic bacterial infection. Reliability in assessing intestinal metaplasia and atrophy in histological specimens is especially important because these changes are associated with an increased risk of gastric cancer. Introduction of Sydney system classification of gastritis and H. pylori association with other variables (both graded and non-graded), has improved the knowledge and reproducibility of classification of gastritis. Staging would convey information on the topography and extension of the gastric atrophic changes, whereas grading should represent the semi-quantitative assessment of the combined severity of both mononuclear and granulocytic inflammation.

In this study, gastroenterologists didn't follow the Sydney system guidelines for sites of procuring full thickness mucosal biopsies. Hence, it wasn't possible to specify the predominant topographic sites for H. pylori, neutrophilic activity, MNC infiltrate, gastric atrophy or intestinal metaplasia. Helicobacter pylori colonization is pangastric in younger cases. [3] Antrum is the most common location in atrophic gastritis and intestinal metaplasia with H. pylori colonization. [4],[5]

Prevalence of H. pylori infection increases with increasing age [6],[7],[8],[9] and also prevalence of H. pylori infection is higher in males, [10] similar to the findings in this study. According to Mysorekar et al 52% of Indians with dyspepsia and 44% of control subjects have active H. pylori infection by second decade of life. [11] Histological gastritis was present in 66% of asymptomatic and endoscopically normal individuals, and H. pylori infection was noticed in 25% cases with histological normal gastric mucosa. [12] Endoscopic mucosal breaks (erosions) have a stronger association with histological gastritis. [13] In this study, all 7 cases with history of NSAID intake showed foveolar hyperplasia and 57.14% cases showed H. pylori. In cases with NSAID intake, H. pylori was more commonly found in the setting of abnormal endoscopic findings than with normal endoscopic findings. [14],[15],[16] Eradication of H. pylori in NSAID users is associated with healing of gastritis, inspite of continued NSAID use. [17]

In the present study, 25.9% of cases with ulcer/erosion showed H. pylori positivity, unlike in other studies where 90% of peptic ulcer cases had evidence of H. pylori infection. [18],[19],[20] The presence of H.pylori in 55.2% cases with lymphoid follicles is a finding, consistent with a study by Genta et al. [21]

The absence of the polymorphs and lymphocytes is associated with eradication of bacteria following treatment. [22] In this study biopsy evaluation of post-treatment cases wasn't done.

In the present study, 62.5% cases of gastric atrophy showed H. pylori positivity and most of the cases were in 6th and 7th decades, which suggest that it progresses as age advances in chronic gastritis patients. Similar studies have shown that the prevalence of atrophic gastritis increases with increasing age. [23] In contrast, other studies have shown that presence of atrophy is rare, despite the acquisition of H. pylori in younger age group. [24],[25]

Mysorekar et al., showed that there was a significant association between rapid urease test and histology results for the detection of H. pylori and found the sensitivity of test being 92.5% and specificity was 97.2%. [11] The low sensitivity and specificity in this study is attributable to the less number of cases in which data of rapid urease test result was available.

In a study of 645 gastric lymphoma cases, a positive association with a past history of gastric ulcer and H. pylori infection for gastric lymphoma was demonstrated. However duodenal ulcer history did not show any association with gastric lymphoma. [26] Simultaneous presentation of gastric carcinoma and lymphoma of the mucosa associated lymphoid tissue (MALToma), in a background of chronic gastritis and H. pylori has been reported. [27] Such associated lesions were not encountered in the present study.

  Conclusion Top

Histopathology is the most sensitive test for diagnosing H. pylori on endoscopic biopsies, and is the gold standard for diagnosis. H. pylori gastritis usually shows increased neutrophilic activity but can also present with increased mononuclear inflammatory infiltrate and lymphoid follicles in chronic gastritis. Intestinal metaplasia and atrophy indicates the chronicity of the disease. Association with neoplastic disorders mandates early diagnosis and treatment of H. pylori gastritis.

  References Top

1.Warren JR, Marshall BJ. Unidentified curve bacilli on gastric epithelium in active chronic gastritis. Lancet 1983;2:1273-5.  Back to cited text no. 1
2.Dixon MF, Genta RM, Yardley JH. Classification and grading of gastritis. The Updated Sydney System. International Workshop on the histopathology of gastritis, Houston 1994. Am J Surg Pathol 1996;20:1161-81.  Back to cited text no. 2
3.Zhang C, Yamada N, Wu YL. Comparison of Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer cases with chronic gastritis cases. World J Gastroenterol 2005;11:976-81.  Back to cited text no. 3
4.Goldstein NS. Chronic Inactive Gastritis and Coccoid Helicobacter pylori in cases treated for Gastroesophageal Reflux Disease or with H. pylori Eradication Therapy. Am J Clin Pathol 2002;118:719-26.  Back to cited text no. 4
5.Satoh K, Kimura K, Sipponen P. Helicobacter pylori infection and chronological extension of atrophic gastritis. Eur J Gastroenterol Hepatol 1995;7:11-5.  Back to cited text no. 5
6.Graham DY, Malaty HM, Evans DJ, Evans DG, Klein PD, Adam E. Epidemiology of Helicobacter pylori in an asymptomatic population in the United States: Effect of age, race, and socioeconomic status. Gastroenterology 1991;100:1495-501.  Back to cited text no. 6
7.Asaka M, Kimura T, Kudo M, Takeda H, Mitani S, Miyazaki T et al. Relationship of Helicobacter pylori to serum pepsinogens in an asymptomatic Japanese population. Gastroenterol 1992;102:760-6.  Back to cited text no. 7
8.Megraud F. Epidemiology of Helicobacter pylori infection. Gastroenterol Clin North Am 1993;22:73-7.  Back to cited text no. 8
9.Chen YY, Antonioli DA, Spechler SJ, Zeroogian JM, Goyal RK, Wang HH. Gastro esophageal reflux disease versus Helicobacter pylori infection as the chief cause of carditis. Mod Pathol 1998;11:950-6.  Back to cited text no. 9
10.Zhang C, Yamada N, Wu YL, Wen M, Matsuhisa T, Matsukura N. Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer. World J Gastroenterol 2005;11:791-6.  Back to cited text no. 10
11.Mysorekar VV, Chitralekha, Dandekar P, Prakash BS. Antral histopathological changes in acid peptic disease associated with helicobacter pylori. Indian J Pathol Microbiol 1999;42:427-35.  Back to cited text no. 11
[PUBMED]  Medknow Journal  
12.Prabhu SR, Ranganath S, Amarapurkar DN. Helicobacter pylori in normal gastric mucosa. JAPI 1994;42:863-4.  Back to cited text no. 12
13.Elta GH, Appleman HD, Behler EB. A study of the correlation between endoscopic and histological diagnosis in gastroduodenitis. Am J Gastroenterol 1987;82:353-8.  Back to cited text no. 13
14.Heresbach D, Raoul JL, Bretagns JF, Minet J, Donnio PY, Ramée MP, et al. Helicobacter pylori: A risk and severity factor of non-steroidal anti-inflammatory drug induced gastropathy. Gut 1992;33:1608-11.  Back to cited text no. 14
15.McCarthy DM. H. pylori infection and gastroduodenal injury by non-steroidal anti-inflammatory agents. Scand J Gastroenterol 1991;187:91-7.  Back to cited text no. 15
16.Dixon MF, Neville PM, Mapstone NP, Moayyedi P, Axon AT. Bile reflux gastritis and Barrett's esophagus: Further evidence of a role for duodenogastric-oesophageal reflux. Gut 2001;49:359-63.  Back to cited text no. 16
17.De Leest HT, Steen KS, Bloemena E, Lems WF, Kuipers EJ, Van de Laar MA, et al. Helicobacter pylori eradication in cases on long-term treatment with NSAIDs reduces the severity of gastritis: A randomized controlled trial. J Clin Gastroenterol 2009;43:140-6.  Back to cited text no. 17
18.Leung KM, Hui PK, Chan WY, Thomas TM. Helicobacter pylori-related gastritis and gastric ulcer - a continuum of progressive epithelial degeneration. Am J Clin Pathol 1992;98:569-74.  Back to cited text no. 18
19.Bell GD, Powell KU. Eradication of H. pylori and its effect in peptic ulcer disease. Scand J Gastroenterol 1993;28:7-11.  Back to cited text no. 19
20.Hui PK, Chan WY, Cheung PS, Chan JK. Pathologic changes of gastric mucosa colonized by Helicobacter pylori. Hum Pathol 1992;23:548-56.  Back to cited text no. 20
21.Genta RM, Hamner HW, Graham DY. Gastric lymphoid follicles in Helicobacter pylori infection: Frequency, distribution, and response to triple therapy. Hum Pathol 1993;24:577-83.  Back to cited text no. 21
22.Goldstein NS. Chronic Inactive Gastritis and Coccoid Helicobacter pylori in cases treated for Gastroesophageal Reflux Disease or with Helicobacter pylori Eradication Therapy. Am J ClinPathol 2002;118:719-26.  Back to cited text no. 22
23.Schlemper RJ, Werf van SDJ, Vandenbroucke JP, Biemond I, Lamers CB. Seroepidemiology of gastritis in Japanese and Dutch working populations: Evidence for the development of atrophic gastritis that is not related to Helicobacter pylori. Gut 1995; 37:199-204.  Back to cited text no. 23
24.Hussien NF, Napaki SM, Atherton JC. A study of Helicobacter pylori associated gastritis patterns in Iraq and their association with strain virulence. Saudi J Gastroenterol 2009;15:125-7.  Back to cited text no. 24
25.Turkay C, Erbayrak M, Bavbek N, Yendunya S, Eraslani E, Kasapolu B. Helicobacter pylori and histopathological findings in cases with dyspepsia. Turk J Gastroenterol 2011;22:122-7.  Back to cited text no. 25
26.Suzuki T, Matsuo K, Ito H, Hirose K, Wakai K, Saito T, et al. A past history of gastric ulcers and Helicobacter pylori infection increase the risk of gastric malignant lymphoma. Carcinogenesis 2006;27:1391-7.   Back to cited text no. 26
27. Sakai T, Ogura Y, Narita J, Suto T, Kimura D, Ainai S, et al. Simultaneous early adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma of the stomach associated with Helicobacter pylori infection. Gastric Cancer 2003;6:191-6.  Back to cited text no. 27


  [Figure 1], [Figure 2]

This article has been cited by
1 Histopathological Changes in Helicobacter pylori Associated Gastritis and Scope of Special Stain and Immunohistochemistry as Diagnostic Aids
Ruby Elizabeth Elias,Bindiya Gisuthan,Sreeganesh A.S
Journal of Evidence Based Medicine and Healthcare. 2020; 7(50): 3027
[Pubmed] | [DOI]
2 Histopathological Patterns of Gastric Mucosal Biopsies in Dyspepsia A Study of 550 Cases
K Suman,Namrata Rao
Journal of Medical Sciences and Health. 2020; 05(03): 1
[Pubmed] | [DOI]
Sampa Choudhury,Rajesh Singh Laishram,Punyabati P,Moirangthem G.S,Kaushik Debnath
Journal of Evidence Based Medicine and Healthcare. 2016; 3(55): 2829
[Pubmed] | [DOI]


    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

  In this article
Materials and Me...
Article Figures

 Article Access Statistics
    PDF Downloaded569    
    Comments [Add]    
    Cited by others 3    

Recommend this journal