Journals / Dokuz Eylül Üniversitesi Tıp Fakültesi Dergisi / 2016 / Cilt: 30 - Sayı: 1

Analysis Of Inflammatory Cell Profile In Helicobacter Pylori Positive Gastrit Cases

Helikobakter Pylori Pozitif Gastrit Vakalarında İnflamatuar Hücre Analizi

Pages
9–17
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Additionally CD138 positive plasma cells were the most densely seen cell type in all the cases.Discussion and Conclusion: It is considered that in HP gastrits, the obvious increase of plasma cells and the decrease of CD5 positive lymphocytes in the group which has the most HP intensity might be playing a role in HP related stomach disease.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Introduction: Being the most frequent and important factor in the etiology of chronic active gastritis Helicobacter pylori can make up the basis for several diseases like peptic ulcer, adenocarcinoma, and MALT lymphoma.
📊
Key Findings & Data:Methods: 100 cases with Helicobacter pylori positive gastritis and 20 cases with Helicobacter pylori negative gastritis were included in the study.
💡
Conclusion & Impact:Additionally CD138 positive plasma cells were the most densely seen cell type in all the cases.Discussion and Conclusion: It is considered that in HP gastrits, the obvious increase of plasma cells and the decrease of CD5 positive lymphocytes in the group which has the most HP intensity might be playing a role in HP related stomach disease.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Helikobakter pylori · İnflamasyon · İmmünohistokimya

Abstract

Introduction: Being the most frequent and important factor in the etiology of chronic active gastritis Helicobacter pylori can make up the basis for several diseases like peptic ulcer, adenocarcinoma, and MALT lymphoma. It is important to determined the profile of inflammatory cell in Helicobacter pylori gastritis for lightening the pathogenesis of the diseases the Helicobacter pylori may cause. In this study the inflammatory cell profile of the cases with Helicobacter pylori gastritis was investigated. Methods: 100 cases with Helicobacter pylori positive gastritis and 20 cases with Helicobacter pylori negative gastritis were included in the study. In addition to these CD3, CD4, CD5, CD8, CD10, CD20, CD68, CD79 α and CD138 immunohistochemical stains, H&E and Giemsa stains were performed and detailed inflammatory cell analyse was done.Results: In immunohistochemical investigation, considering the CD3, CD20, CD68 and CD79α positivities, a significant difference was not determined between the groups. It was established that while the number of inflammatory cells positively reacted with CD10 and CD138 was increasing, the number of inflammatory cells positively reacted with CD4, CD5 and CD8 was decreasing significantly with the increasing amounts of Helicobacter pylori. Additionally CD138 positive plasma cells were the most densely seen cell type in all the cases.Discussion and Conclusion: It is considered that in HP gastrits, the obvious increase of plasma cells and the decrease of CD5 positive lymphocytes in the group which has the most HP intensity might be playing a role in HP related stomach disease.

Özet

Amaç: Helikobakter pylori kronik aktif gastrit etiyolojisinde en sık ve en önemli faktör olup, peptik ülser, adenokarsinoma ve MALT Lenfoma gibi çeşitli hastalıklara da zemin hazırlayabilmektedir.Helikobakter pylori gastriti olgularında inflamatuar hücre profilinin ortaya konması Helikobakter pylorinin neden olabileceği hastalıkların patogenezine ışık tutabilmek için önemlidir. Bu çalışmada Helikobakter pylori gastritli olgulardaki inflamatuar hücre profili araştırıldı. Yöntem ve Gereçler: Çalışmaya 100 adet Helikobakter pylori pozitif kronik gastrit ve 20 adet Helikobakter pylori negatif gastrit vakası dahil edildi. Tüm guruplarda H&E ve giemsa boyaması yanında ayrıca immünohistokimyasal olarak CD3, CD4, CD5, CD8, CD10, CD20, CD68, CD79α ve CD138 boyamaları uygulandı ve detaylı inflamatuar hücre analizi yapıldı. Bulgular: İmmünohistokimyasal incelemede, Helikobacter pylori negatif ve pozitif olgular arasında CD3, CD20, CD68 ve CD79α pozitiflikleri açısından anlamlı bir farklılık saptanmadı. Helikobakter pylori miktarı arttıkça CD10 ile ve CD138 ile pozitif reaksiyon veren inflamatuar hücre sayısı anlamlı derecede artarken, CD4, CD5 ve CD8 pozitif olanların sayılarının ise anlamlı derecede azaldığı tesbit edildi. Ayrıca CD138 pozitif plazma hücreleri tüm olgularda en yüksek yoğunluktaki hücre tipiydi. Tartışma ve Sonuç: HP gastritlerinde HP’nin en yoğun olduğu grupta plazma hücrelerinin belirgin biçimde artması ve CD5 pozitif lenfositlerin azalmasının HP ilişkili mide hastalıklarının patogenezinde rol oynuyor olabileceği düşünülmüştür.

🔖

Cite This Article

ALABALIK, U., BÜYÜKBAYRAM, H., KELEŞ, A. N., FIRAT, U. (2016). Analysis Of Inflammatory Cell Profile In Helicobacter Pylori Positive Gastrit Cases. Dokuz Eylül Üniversitesi Tıp Fakültesi Dergisi, Cilt: 30 - Sayı: 1, 9–17. https://ajindex.com/articles/160665

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (1)

  1. Referans1 Marshall BJ, Warren JR. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet, 1984;1:1311-1315. Referans2 Dunn BE, Cohen B, Blaser MJ. Helicobacter pylori. Clin Microbiol Rev, 1997; 10:720-741. Referans3 Forman D. The prevalence of Helicobacter pylori infection in gastric cancer. Aliment Pharmacol Ther, 1995; 9:71-76. Referans4 Chuan X, Nonghua L. Kyoto global consensus report for treatment of Helicobacter pylori and its implications for China. Zhejiang Da Xue Xue Bao Yi Xue Ban. 2016; 45:1-4. Referans5 Dixon MF, Genta RM, Yardley JH, et al: Classification and grading of gastritis. The updates Sydney system Am J Surg Pathol. 1996;20:1161-1181. Referans6 Owen DA: Gastritis and carditis. Mod. Pathol, 2003; 16:325. Referans7 Kumar V, Abbas K, Fausto N, Aster C, Robbins and Cotran Pathologic Basis of Disease, 8.ed, Philedelphia: Elsevier, 2010; p.774,775. Referans8 Cecilia MF-Preiser et al: The non-neoplastic Stomach in Gastrointestinal Pathology Plus: An atlas and text. 3.ed, Philedelphia:Lippincott William Wilkins, 2008; p. 190-192. Referans9 Genta R, Segura AM; Will Curing Helicobacter Pylori Eliminate Gastric Cancer? Adv Anat Pathol1999; 3: 228-232. Referans10 Hoshi T, Sasano H, Kato K: Cell Damage and Proliferation in Human Gastric Mucosa Infected by Helicobacter pylori-A Comparison Before and After H. Pylori Eradication in Non-Atrophic Gastritis; Hum Pathol 1999; 30: 1412-1417. Referans11 Hatz RA, Meimarakis G, Bayerdörffer E, et al. Characterization of Lymphocytic Infiltrates in Helicobacter pylori-Associated Gastritis. Scand J Gastroenterol 1996; 31:222-228. Referans12 Broide E, Sandbank J, Scapa E, et al. The Immunohistochemistry Profile of Lymphocytic Gastritis in Celiac Disease and Helicobacter Pylori Infection: Interplay between Infection and Inflammation. Mediators Inflamm 2007;2007:81838. Referans13 Rossi G, Fortuna D, Pancotto L, et al. Immunohistochemical Study of Lymphocyte Populations Infiltrating the Gastric Mucosa of Beagle Dogs Experimentally Infected with Helicobacter pylori. Infect Immun 2000; 68: 4769-4772. Referans14 Oksanen A, Sankila A, Boguslawski K, et al. Inflammation and cytokeratin 7/20 staining of cardiac mucosa in young patients with and without Helicobacter pylori infection. J Clin Pathol 2005;58:376–381. Referans15 Soo Won Hong, Mee Yon Cho, Chanil Park. Expression of eosinophil chemotactic factors in stomach cancer. Yonsei Medical Journal, 1999; 40: 131-136. Referans1