In Situ Nick End Labeling as a Molecular Immunopathological Indicator for the Severity of DNA Fragmentation and Gastroduodenal Tissue Damage among H. Pylori Cag A Positive Patients

摘要

Background and Objective: The aim is to determine the correlation between gastric Apoptotic Index (AI), inflammatory cells AI; H. pylori CagA; Gastric secretions; and other proposed factors that may induce apoptosis and subsequently induce different gastric lesions. Methodology: Gastroduodenal biopsies taken from 80 patients for histopathology and H. pylori diagnosis. Cag A and DNA fragmentation detected by in situ hybridization Serum samples used for evaluation of Serum pepsinogen I (PGI); II (PGII; Gastrin-17 (G-17) . Findings: Significant difference between gastric tissue (AI), inflammatory cells; inflammatory cells versus gastric tissue AI; CagA positivity among gastric disorders (p value = 0.022). Cag A correlated with gastric AI and inflammatory cells AI. Significant difference in Inflammatory Cells AI among Cag Apositive versus CagA negative cases (p value = 0.002). Significant difference in AI between gastric tissue and Inflammatory Cells among Cag A positive (p value = 0.000) with inverse correlation (p value = 0.014). Gastric AI and Inflammatory cells AI Inversely correlated with PGI/PGII level and CagA positivity. Marginal inverse correlation between gastric AI, Gastrin17 level and CagA positivity was reported (p value = 0.056). Inflammatory cells AI correlated with PMNs grade and CagA positivity (p = 0.044). Gastric cells AI correlated with PMNs grade (p = 0.001). Gastric AI and inflammatory cells AI correlated with age. Gastric AI and inflammatory cells AI inversely correlated with gender. Significant difference in gastric AI; inflammatory cells AI and usage of PPIs; NSAID usage; smoking, drinking of tap water. Marginal inverse correlation between NSAID usage and gastric AI (p = 0.000), inflammatory cells AI (p = 0.001). Conclusion: Cag A correlated with AI among different gastro duodenal nonmalignant disorders. Inverse correlation between AI and PGI/PGII level; gastric AI and Gastrin17 level. AI correlated with PMNs grade; age and Cag A positivity. AI not correlated with PPIs, smoking, tap water. Inflammatory cells AI Inversely correlated with Gender.