Epithelial cell proliferation and glandular atrophy in lymphocytic gastritis: Effect of H pylori tre

来源 :World Journal of Gastroenterology | 被引量 : 0次 | 上传用户:meihong
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AIM:Lymphocytic gastritis is commonly associated withHelicobacter pylori infection.The presence of glandularatrophy and foveolar hyperplasia in lymphocytic gastritissuggests abnormalities in cell proliferation and differentiation,forming a potential link with the suspected association withgastric cancer.Our aim was to compare epibhelial cell proliferationand morphology in H pylori associated lymphocytic gastritisand H pylori gastritis without features of lymphocytic gastritis,and to evaluate the effect of H pylori treatment.METHODS:We studied 14 lymphocytic gastritis patientswith H pylori infection.For controls,we selected 14 matcheddyspeptic patients participating in another treatment trialwhose H pylori infection had successfully been eradicated.Both groups were treated with a triple therapy and followedup with biopsies for 6-18 months (patients) or 3 months(controls).Blinded evaluation for histopathological featureswas carried out.To determine the cell proliferation index,the sections were labeled with Ki-67 antibody.RESULTS:Before treatment,lymphocytic gastritis wascharacterized by foveolar hyperplasia (P=0.001) and glandularatrophy in the body (P=0.008),and increased proliferation inboth the body (P=0.001) and antrum (P=0.002).Proliferationcorrelated with foveolar hyperplasia and inflammationactivity.After eradication therapy,the number ofintraepithelial lymphocytes decreased in the body (P=0.004)and antrum (P=0.065),remaining higher than in controls(P<0.001).Simultaneously,the proliferation index decreasedin the body from 0.38 to 0.15 (P=0.043),and in the antrumfrom 0.34 to 0.20 (P=0.069),the antral index still beinghigher in lymphocytic gastritis than in controls (P=0.010).Foveolar hyperplasia and glandular atrophy in the bodyimproved (P=0.021),reaching the non-LG level.CONCLUSION: In lymphocytic gastritis, excessive epithelialcell proliferation is predominantly present in the body, where it associates with foveolar hyperplasia and glandular atrophy. These characteristic changes of lymphocytic gastritis are largely related to H pylori infection, as shown by their improvement after eradication. However, some residualdeviation was still seen in lymphocytic gastritis, indicating either an abnormally slow improvement or the presence of some persistent abnormality. AIM: Lymphocytic gastritis is commonly associated with Helicobacter pylori infection. The presence of glandularatrophy and foveolar hyperplasia in lymphocytic gastritissuggests abnormalities in cell proliferation and differentiation, forming a potential link with the suspected association with gastric cancer. Our aim was to compare epibial cell proliferation and morphology in H pylori associated lymphocytic gastritis and H pylori gastritis without features of lymphocytic gastritis, and to evaluate the effect of H pylori treatment. METHODS: We studied 14 lymphocytic gastritis patients with H pylori infection. For controls, we selected 14 matched dyspeptic patients participating in another treatment trial Hose H pylori infection had successfully been eradicated. Both groups were treated with a triple therapy and followed with biopsies for 6-18 months (patients) or 3 months (controls). Bllinded evaluation for histopathological features was carried out. To determine the cell proliferation index, the sectio ns were labeled with Ki-67 antibody .RESULTS: Before treatment, lymphocytic gastritis was characterized by foveolar hyperplasia (P = 0.001) and glandularatrophy in the body (P = 0.008), and increased proliferation inboth the body P = 0.002) .Proliferationcorrelated with foveolar hyperplasia and inflammationactivity. After eradication therapy, the number of invitro lymphocytes decreased in the body (P = 0.004) and antrum (P = 0.065), remaining higher than in controls the proliferation index decreased in the body from 0.38 to 0.15 (P = 0.043), and in the antrum from 0.34 to 0.20 (P = 0.069), the antral index still beinghigher in lymphocytic gastritis than in controls (P = 0.010) .Foveolar hyperplasia and glandular reaching the non-LG level. CONCLUSION: In lymphocytic gastritis, excessive epithelial cell proliferation is predominantly present in the body, where it associates with foveolar hyperplasia and glandular atrophy. These characteristic changes of lymphocytic gastritis are largely related to h pylori infection, as shown by their improvement after eradication. However, some residualdeviation was still seen in lymphocytic gastritis, indicating either an abnormally slow improvement or the presence of some persistent abnormality.
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