MODIFICÃRILE HISTOPATOLOGICE ȘI IMUNOHISTOCHIMICE DIN MUCOASA GASTRICÃ COLONIZATÃ DE HELICOBACTER PYLORI

  • Gabriela PARLOG Universitatea de Medicină și Farmacie ”Gr. T. Popa” Iași
  • Doina MURARESCU Universitatea de Medicină și Farmacie ”Gr. T. Popa” Iași
  • Carmen UNGUREANU Universitatea de Medicină și Farmacie ”Gr. T. Popa” Iași
  • M. DANCIU Universitatea de Medicină și Farmacie ”Gr. T. Popa” Iași
  • Maria - Sultana MIHAILOVICI Universitatea de Medicină și Farmacie ”Gr. T. Popa” Iași
Keywords: HELICOBACTER PYLORI, CHRONIC GASTRITIS, PROLIFERATION, Ki-67, CARCINOGENESIS

Abstract

Helicobacter pylori (H. pylori)
colonize gastric mucosa causing both inflammatory changes, premalignant lesions and malignant
tumors, including gastric lymphoma and carcinoma. In this study, our propose was to
evaluate the histopatological changes corellated with immunohistochemical results demonstrating
the types of cellular infiltration and proliferative activity of gastric mucosa infected with H.
pylori. Material and method: Gastric endoscopic examinations was performed in 468 patients
with anti-H. pylori antibodies and dispeptic phenomena. Snippets harvested endobiopsic
stomach were fixed in formalin and processed by paraffine inclusion. Histological sections
were stained with hematoxylin-eosine and Giemsa. In 65 cases of endobiopsic fragments (36
deep chronic gastritis with intestinal metaplasia, glandular atrophy and intraepithelial neoplasia
and 29 carcinomas) immunohistochemical reactions were performed by applying reagents for
evidence of H. pylori colonies, of T lymphocytes (CD3) and macrophages (CD68) and Ki-67
reagent for proliferating nuclear antigen labelling. Results: Endobiopsic specimen found in all
H. pylori or by Giemsa staining or by anti-H. pylori antibodies when they were in small
numbers. Histologically, were diagnosed: 463 superficial and deep chronic gastritis associated
with premalignant lesions, 29 carcinomas, 2 non-Hodgkins lymphoma and an adematous
polyp. Immunohistochemically, inflammatory infiltrate consisted of numerous T lymphocytes,
macrophages and lymphoid follicles. Foveolar cell nuclei, in areas of intraepithelial neoplasia
and carcinomatous cells were intensely stained with Ki-67, demonstranting increased proliferation.
Conclusions: In gastric infection with H. pylori, inflammatory infiltrat is composed of
abundant macrophages and T lymphocytes. Ki-67 was absent or minimal in chronic gastritis,
while in areas of intraepithelial neoplasia was positive in both foveolar and coating epithelium.
Anti-H. pylori antibodies in human serum remains one of the simplest methods to detect H.
pylori, therefore it plays an important role in practice. Medical eradication of bacteria may
cancel inflammatory changes, metaplasia and proliferation of gastric mucosa and thus it
prevents the cascade of carcinogenesis.

Author Biographies

Gabriela PARLOG, Universitatea de Medicină și Farmacie ”Gr. T. Popa” Iași

Doctorand

Spitalul Județean de Urgențã Bacãu

Doina MURARESCU, Universitatea de Medicină și Farmacie ”Gr. T. Popa” Iași

Facultatea de Medicinã
Disciplina de Morfopatologie

Carmen UNGUREANU, Universitatea de Medicină și Farmacie ”Gr. T. Popa” Iași

Facultatea de Medicinã
Disciplina de Morfopatologie

M. DANCIU, Universitatea de Medicină și Farmacie ”Gr. T. Popa” Iași

Facultatea de Medicinã
Disciplina de Morfopatologie

Maria - Sultana MIHAILOVICI, Universitatea de Medicină și Farmacie ”Gr. T. Popa” Iași

Facultatea de Medicinã
Disciplina de Morfopatologie

References

1. Marshall BJ, Warren JR. Unidentified curved bacili on gastric epithelium in active chronic gastritis.
Lancet 1983; 1: 1273-1275.
2. Wotherspoon AC, Doglioni C, Diss TC et al. Regression of primary low-grade B-cell gastric
lymphoma of mucosa-associated lymphoid tissue type after eradication of Helicobacter pylori.
Lancet 1993; 342: 575 - 577 
3. Uemura N, Okamoto S, Yamamoto S. H. pylori infection and the development of gastric cancer. N
Engl J Med 2001; 345: 784-789.
4. Graham DY, Sung JJY, Helicobacter pylori In: Feldman M, Friedman LS, Brandt LJ editors.
Sleisenger & Fordtran’s Gastrointestinal and Liver Disease Pathophisiology/ Diagnosis/ Management.
Philadelphia: WB Saunders, 2006, 1049-1056.
5. Misiewicz G, Harris A. Clinician’s Manual on Helicobacter pylori. Science Press Ltd, 1995.
6. Mégraud F. Epidemiology of Helicobacter pylori infection. In: Rathbone BJ, Heatley RV editors.
Helicobacter pylori and Gastroduodenal Disease. Blackwell Scientific Publications, 1992.
7. *** Schistosomes, Liver Flukes and Helicobacter pylori. In: IARC Monographs on the Evaluation
of Carcinogenic Risks to Humans 61. Lyon: International Agency for Research on Cancer, 1994.
8. Kuipers EJ. Exploring the link between Helicobacter pylori and gastric cancer. Aliment Pharmacol
Ther 1999; 13 (Suppl 1): 3–11.
9. Yuasa H, Tanaka S, Sawa H et al. Transgenic expression of Helicobacter pylori CagA induces
gastrointestinal and hematopoietic neoplasms in mouse. PNAS 2008; 105 (3): 1003–1008.
10. Correa P. A human model of gastric carcinogenesis. Cancer Res 1988; 48: 3554.
11. Fujioka T, Kodama R, Honda S, Guei-Hua G, Nishizono A, Nasu M. Long-term sequelae of
experimental gastritis with Helicobacter pylori: a 5-year follow-up study. J Clin Gastroenterol
1997; 25: S8 - S12.
12. Kodama M, Murakami K, Okimoto T, Sato R, Watanabe K, Fujioka T. Expression of mutant type-p53
products in H. pylori-associated chronic gastritis. World J Gastroenterol 2007; 13 (10): 1541-1546.
13. Lee YC, Lee KH, Han JH et al. Effects of nonsteroidal anti-inflammatory drugs on Helicobacter
pylori-infected gastric mucosae of mice: apoptosis, cell proliferation, and inflammatory activity.
Infection Immunity 2001; 69 (8): 5056–5061.
14. Zavros Y, Rieder G, Ferguson A, Merchant JL. Gastritis and hypergastrinemia due to Acinetobacter
lwoffii in mice. Infection Immunity 2002; 70 (5): 2630–2639.
15. Wang L, Zheng L, Wang SY, Zhui TF, Zhu HG. Clonal analysis of gastric carcinoma and
precancerous lesions and its relation to Ki-67 protein expression. Neoplasma 2009; 56: 48-58.
16. Oguma1 K, Oshima1 H, Aoki M et al. Activated macrophages promote Wnt signalling through
tumour necrosis factor-a in gastric tumour cell. EMBO J 2008; 27: 1671–1681.
Published
2019-11-12