Pattern of gastritis as manipulated by current state of Helicobacter pylori infection

نویسندگان

  • MOHAMED M. ELSEWEIDY
  • MONA M. TAHA
  • NAHLA N. YOUNIS
  • KHADIGA S. IBRAHIM
  • HAMDI A. HAMOUDA
  • MOHAMED A. ELDOSOUKY
  • HALA SOLIMAN
چکیده

Helicobacter pylori (H. pylori) infection prevails from 60-80% in patients with gastric ulcer and 90100% in those having duodenal ulcer. Patients with such type of chronic infection are at increased risk to develop peptic ulcers or gastric adenocarcinomas. The present work aims mainly to identify the pattern of chronic gastritis and potential effect of H. pylori infection using certain biomarkers, histological and immunochemical tests. Fifty eight individuals, clinically diagnosed as having chronic gastritis, were participated in the present study. They were categorized into 2 groups, the first one (31%) demonstrated positive reaction to IgM antibodies of Helicobacter pylori (H. pylori) (>40u/ml) and the second group (69%) demonstrated negative reaction. Blood and antral biopsy samples were collected, directed to determination of serum gastrin, pepsinogen I (PgI), pepsinogen II (PgII), prostaglandin E2 (PGE2) and interlukin-6 (IL-6). Immunohistochemistry technique was also done in antral biopsy to demonstrate the expression of inducible nitric oxide synthase (iNOS), nitrotyrosine, DNA fragmentation, myeloperoxidase and histopathological examination. Serum gastrin, PgI, PgII, PGE2, IL-6 demonstrated significant increase in gastritis patients as compared to normal group. PgI, PgII showed significant increase joined with slight increase of IL-6 in IgM positive group as compared to negative one. Immunostaining testes in antral biopsy showed strong positive reactions for the above mentioned markers as compared to IgM negative group (mild positive reaction). In conclusion, gastritis patients who express IgM antibodies for H. pylori infection showed higher gastrinaemia and more pronounced atrophic, inflammatory and apoptotic damage than those not expressing IgM antibodies. Key-Words: H. pylori gastritis; gastrin; pepsinogen; prostaglandin E2; iNOS; DNA fragmentation; myeloperoxidase; IgM

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تاریخ انتشار 2010