The aim of this study was to observe the histological features of chronic gastritis and associated effects due to Helicobacter pylori infection in 176 randomly selected antral biopsy specimens of chronic gastritis cases. The specimens were reviewed for the presence or absence of H.pylori. The activity (neutrophilic infiltration) of gastritis and the presence or absence of mucosa-associated lymphoid tissue (MALT) were also noted. Chi-square test (Pearson value) was used to analyze categorical variables. H.pylori was detected in 110 (62.5%) cases of chronic gastritis. There was a significant association between H.pylori infection and activity of chronic gastritis (p=0.002). Lymphoid aggregates were significantly more frequently noted in H.pylori-positive patients (68.2%) vs. H.pylori negative group (47%), (p=0.005). It is concluded that H.pylori is significantly associated with active chronic gastritis and with formation of mucosa-associated lymphoid tissue (MALT), which may develop into gastric lymphoma (MALT type)

Hussainy, Akbar Shah

Yakoob, Mohammad Yawar

English

eCommons@AKU

eCommons@AKUDepartment of Pathology and Laboratory Medicine Medical College, PakistanNovember 2010Chronic gastritis and Helicobacter pylori: ahistopathological study of gastric mucosal biopsiesMohammad Yawar YakoobAga Khan UniversityAkbar Shah HussainyAga Khan UniversityFollow this and additional works at: http://ecommons.aku.edu/pakistan_fhs_mc_pathol_microbiolPart of the Microbiology Commons, and the Pathology CommonsRecommended CitationYakoob, M., Hussainy, A. (2010). Chronic gastritis and Helicobacter pylori: a histopathological study of gastric mucosal biopsies.JCPSP: Journal of the College of Physicians and Surgeons Pakistan, 20(11), 773-775.Available at: http://ecommons.aku.edu/pakistan_fhs_mc_pathol_microbiol/485Journal of the College of Physicians and Surgeons Pakistan  2010, Vol. 20 (11): 773-775 773Helicobacter (H.) pylori is a spiral shaped, basophilic, gramnegative bacillus that resides exclusively in the gastricmucosa. It is found in all parts of the world. It is believedthat half of the world’s population is infected with H.pylori,with the burden of disease being highest in thedeveloping countries.1 In India, for example, 80% of thepopulation is infected with this bacterium and most ofthem have been infected since 10 years of age.2 Theinfection with this bacterium is related to overcrowdingand poor hygienic conditions. Possible modes oftransmission generally described are through directperson-to-person contact between family members andalso through contaminated food and water.3Chronic gastritis is chronic inflammation of the gastricmucosa. Although a variety of etiological factors areassociated with chronic gastritis, Helicobacter pylori is theprimary cause. The inflammatory infiltrate is usuallycharacterized by an increase in chronic cells (lymphocytesand plasma cells) in the lamina propria.4 Presence ofpolymorphonuclear leukocytes indicates an activecomponent.4 H.pylori was the first bacterium observed tobehave as a carcinogen. It is implicated as a riskfactor/etiologic agent in a variety of other gastro-intestinal disorders, including peptic ulcers and cancerslike gastric MALTomas and adenocarcinomas.5,6 Giventhe importance of this bacterium in causing gastricpathology, this study was undertaken to observe thehistological features of chronic gastritis, with specialemphasis on presence or absence of H.pylori, activity(neutrophilic infiltration) of gastric mucosa and presenceor absence of lymphoid aggregates. This was a retrospective cohort study conducted at theAga Khan University Hospital in Pakistan. The record ofhistopathology laboratory identified 1080 cases ofchronic gastritis during a one-year period, of which 176cases were randomly selected (every sixth case). Theendoscopically derived antral biopsy slides of thesepatients were retrieved. All the slides were hematoxylinand eosin (H&E) stained. The slides were reviewed bythe authors for presence or absence of H.pylori. Theactivity of gastritis (neutrophilic infiltration) was gradedon a scale of 0 –3, as shown in Table I. The data wereentered and analyzed in SPSS Windows 11.5. Chi-square test (Pearson value) was used for categoricalvariables. Student’s t-test was used to compare means.A p-value of less than 0.05 was considered statisticallysignificant. The mean age of the study sample was 39.6 ± 15.2years (n = 173, range = 4-76 years). The data on agewere missing for 3 cases. The male to female ratio was1.2:1. H.pylori was detected in 110 of 176 (62.5%) casesof chronic gastritis. The mean age of patients in H.pylori-ABSTRACTThe aim of this study was to observe the histological features of chronic gastritis and associated effects due to Helicobacterpylori infection in 176 randomly selected antral biopsy specimens of chronic gastritis cases. The specimens were reviewedfor the presence or absence of H.pylori. The activity (neutrophilic infiltration) of gastritis and the presence or absence ofmucosa-associated lymphoid tissue (MALT) were also noted. Chi-square test (Pearson value) was used to analyzecategorical variables. H.pylori was detected in 110 (62.5%) cases of chronic gastritis. There was a significant associationbetween H.pylori infection and activity of chronic gastritis (p=0.002). Lymphoid aggregates were significantly morefrequently noted in H.pylori-positive patients (68.2%) vs. H.pylori negative group (47%), (p=0.005). It is concluded thatH.pylori is significantly associated with active chronic gastritis and with formation of mucosa-associated lymphoid tissue(MALT), which may develop into gastric lymphoma (MALT type).Key words: H.pylori.   Chronic active gastritis.   Mucosa-associated lymphoid tissue (MALT).   Neutrophilic infiltration activity.Department of Pathology and Microbiology, The Aga KhanUniversity Hospital, Karachi.Correspondence: Dr. Mohammad Yawar Yakoob, The Aga Khan University, Stadium Road, P.O. Box. 3500,Karachi-74800, Pakistan.E-mail: myyakoob@mail.harvard.eduReceived  April 22, 2010; accepted  August 16, 2010.Chronic Gastritis and Helicobacter pylori: A HistopathologicalStudy of Gastric Mucosal BiopsiesMohammad Yawar Yakoob and Akbar Shah HussainySHORT COMMUNICATIONTable I: Helicobacter pylori infection and activity of chronic gastritis.Activity of gastritis*0 1 2 3H.pylori positive 21 (11.9%) 13 (7.4%) 60 (34.1%) 16 (9.1%) 110H.pylori negative 26 (14.8%) 14 (7.9%) 20 (11.4%) 6 (3.4%) 66Total # 47 27 80 22 176* Activity of Gastritis:Activity refers to presence of neutrophils in the lamina propria (LP) (9). The activity wasgraded on a scale of 0-3 (modified from Bayerdorffer E, et al.) (9).0: Chronic inflammatory cells with no  neutrophilic infiltration (chronic gastritis only).1: Neutrophils in LP only.2: Neutrophils in LP and glandular epithelial lining only (cyrptitis).3: Neutrophils in LP,  glandular epithelial lining and lumina (cryptitis and crypt abscesses).positive (38.9 ± 15.1 years, range=4 - 76) and H.pylorinegative groups (40.9 ± 15.6, range=13-74) was notmarkedly different (p=0.4). Sixty (55%) patients withH.pylori positivity were males, compared to 36 (54.5%) inthe other group (p=0.95). Table I shows the activity ofgastritis in H.pylori-positive and negative groups. H.Pyloriinfection was significantly associated with the activity ofgastric inflammation (Pearson χ2=15.1, df=3, p=0.002).Lymphoid aggregates were also significantly noted inthe H.pylori positive cases more frequently, compared tothe negative ones (Pearson χ2=7.8, df=1, p=0.005).Table I also shows the gastric antral biopsy specimenshowing lymphoid follicle with germinal center.H.pylori was detected in 110/176 (62.5%) specimens ofchronic gastritis. This is comparable to figures of 50.4%and 66.9% reported in two studies from India.7,8 The useof histology for detecting H.pylori, however, has its owninherent limitations. It may fail to detect organismsbecause of patchy distribution of bacteria and/orsampling error. Low density infections may, therefore,have been missed. Other specific stains, like Giemsa,for detecting H.pylori were not used in this study.Absence of H.pylori in histological specimens withchronic gastritis, however, may point towards othercauses. It may indicate covert use of non-steroidal anti-inflammatory drug (NSAID) by the patient, when theappropriate history is not available. Presence ofgranulomas can suggest Crohn’s disease. Similarly,lymphocytic gastritis can be associated with glutenenteropathy and eosinophilic gastritis with an allergiccondition. This study showed a significant association betweenH.pylori infection and activity of chronic gastritis. This isin agreement with results of other studies on thetopic.9,10 H.pylori may produce gastric epithelial celldamage directly or by stimulating host immune response.Adherence of the organism produces loss of microvilliand irregularity of the luminal border.4 It is also known torelease vacuolating cytotoxins and enzymes, includingurease, which have toxic effects on the epithelium.H.pylori induces epithelial cells to release chemokinesincluding GRO-α and IL-8 which are chemotactic forneutrophils.4 IL-8 also causes neutro-phils to producereactive oxygen radicals (ROR) which cause tissuedamage. Other factors released (RANTES and MIP-1α)recruit monocytes and lymphocytes which also releasepro-inflammatory mediators and act as antigen presentingcells to initiate specific immunity (T-lymphocytes andplasma cells).4Lymphoid aggregates were significantly more frequentin H.pylori infected slides. This is in contrast to the resultof an Indian study, which failed to show a significantassociation between H.pylori infection and lymphoidaggregates.11 This study, however, supports the findingsof other studies on the subject.10 The normal humanstomach is devoid of organized MALT. In vitro studieshave demonstrated H.pylori specific CD4+ T-cell cloneshave been obtained from gastric biopsies of infectedpatients. These T-lymphocytes extend antigen dependenthelper function for B-cell proliferation. The germinalcentre is a morphologic indication of lymphocyteresponse to antigen. The presence of a germinal centrerepresents a cascade of events that include proliferationof lymphocytes, differentiation of plasma cells, andantibody production. The significant association ofH.pylori and MALT in this study indicates that thebacterium may induce local humoral and T-cellresponse in the gastric mucosa. H.pylori infection triggersthe development of MALT tissue, which can act as anidus in which a lymphoma might develop.In conclusion, H.pylori is significantly associated withactivity of chronic gastritis and mucosa-associatedlymphoid tissue. Absence of H.pylori in histologicalspecimens may either indicate inappropriate specimenor point towards other causes of chronic gastritis likeNSAID use by the patient. Acknowledgements: We thank Dr. Zubair Ahmed,Assistant Professor, Department of Pathology, forcritically reviewing this article and Mr. Salman Sabir(Department of Community Health Sciences, Division ofBiostatistics and Epidemiology) for his assistance withthe data analysis.REFERENCES1. Dorer MS, Talarico S, Salama NR. Helicobacter pylori'sunconventional role in health and disease. PLoS Pathog 2009;5:e1000544. Epub 2009 Oct 26.2. Poddar U, Yachha SK. Helicobacter pylori in children: an Indianperspective. Indian Pediatr 2007; 44:761-70. 3. Salih BA. Helicobacter pylori infection in developing countries: theburden for how long? Saudi J Gastroenterol 2009; 15:201-7.4. Bodger K, Crabtree JE. Helicobacter pylori and gastric inflammation.Br Med Bull 1998; 54:139-50.774 Journal of the College of Physicians and Surgeons Pakistan  2010, Vol. 20 (11): 773-775Figure 1: Gastric antral biopsy; low power view showing lymphoid folliclewith germinal center 4X.Mohammad Yawar Yakoob and Akbar Shah Hussainy 5. Pinto-Santini D, Salama NR. The biology of Helicobacter pyloriinfection, a major risk factor for gastric adenocarcinoma. CancerEpidemiol Biomarkers Prev 2005; 14:1853-8.6. Santacroce L, Cagiano R, Del Prete R, Bottalico L, Sabatini R,Carlaio RG, et al. Helicobacter pylori infection and gastric MALTomas:an up-to-date and therapy highlight. Clin Ter 2008; 159:457-62.7. Satoskar A, Vora IM. Incidence of Helicobacter pylori associatedgastritis in the urban population from India. Trop Geogr Med 1994;46:167-8.8. Maitra TN, Ghosh S. Gastritis and Helicobacter (Campylobacter)pylori: merely one more piece in the jigsaw puzzle or thefinal answer? Indian J Pathol Microbiol 1991; 34:67-79.9. Bayerdorffer E, Lehn N, Hatz R, Mannes GA, Oertel H,Sauerbruch T, et al. Difference in expression of Helicobacter pylorigastritis in antrum and body. Gastroenterology 1992; 102:1575-82.10. Lo CC, Hsu PI, Lo GH, Lai KH, Cheng JS, Tseng HH, et al.Comparison of clinical, serological and histological findingsbetween non-ulcer dyspepsia patients with and withoutHelicobacter pylori infection. J Gastroenterol Hepatol 2001; 16:276-81.11. Amarapurkar AD, Prabhu SR, Amarapurkar DN. Histologicalspectrum of lymphoid follicles and aggregates in Helicobacterpylori gastritis. Trop Gastroenterol 1997; 18:22-3.Journal of the College of Physicians and Surgeons Pakistan  2010, Vol. 20 (11): 773-775 775l l l l lOl l l l lChronic gastritis and Helicobacter pylori: a histopathological study of gastric mucosal biopsies

Chronic gastritis and Helicobacter pylori: a histopathological study of gastric mucosal biopsies

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Chronic gastritis and Helicobacter pylori: a histopathological study of gastric mucosal biopsies

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