ABSTRACT
Coeliac disease is the permanent intolerance to dietary gluten, the major protein component of wheat. Recent epidemiological studies have provided evidence showing that this disorder is common in various parts of the world. The counting and the immunoprofile of intraepithelial lymphocytes of the small bowel have been proposed as methods to measure mucosal infiltration in gluten-sensitive patients. The aim of the present study was to quantify and define the immunohistochemical profile of intraepithelial lymphocytes in the duodenal mucosa of patients suffering non-ulcer dyspepsia, and compare them with known cases of coeliac disease. Archival paraffin wax embedded duodenal sections from 50 endoscopic biopsies were stained using CD3, CD4, and CDS antibodies. Sections were obtained from 24 patients with confirmed coeliac disease, 20 patients with non-ulcer dyspepsia, and 6 patients with functional dyspepsia as control. Patients with non-ulcer dyspepsia were on gluten containing diets. The number of intraepithelial lymphocytes was quantified in five different villi by counting the number of lymphocytes/100 epithelial cells in each villus, and calculating the mean. Endomysial antibodies and testing for Helicobacter pylori were done in all cases. A positive correlation was observed between the degree of villous atrophy and CD3, CD4, and CD8+ intraepithelial lymphocytes. A positive correlation was also observed with the lamina propria lymphoid aggregates. H. pylori infection had a positive correlation with the degree of lymphoid aggregation in the lamina propria. Although the difference between potential coeliac disease and non-coeliac controls was significant, these lesions overlapped considerably. Clinicians as well as pathologists should increase the index of suspicion of coeliac disease. The frequent occurrence of duodenal intraepithelial lymphocyte expansions in other diseases may justify the use of immunohistochemical examination of duodenal biopsy specimens from patients suffering from dyspepsia
Subject(s)
Humans , Male , Female , Dyspepsia/diagnosis , Dyspepsia/etiology , Biopsy , Endoscopy, Digestive System , LymphocytesABSTRACT
Although it is fairly well accepted that Helicobacter pylori infection [H. pylori] plays a significant role in causing gastric cancer, the exact mechanisms involved in its pathogenesis are unclear and there is controversial data about the state of chronic gastritis and the precancerous lesion after treatment of H. pylori. This study was designed to investigate the relationship between H. pylori infection, the activity of chronic gastritis and oncogenes before and after treatment of H. pylori. Fifty-five of chronic gastritis cases were studied for H. pylori, activity of chronic gastritis, p53 and c-Myc expression. Positive H. pylori cases were re-evaluated again for the activity of gastritis, expression of p53 and c-Myc after treatment [6 months later]. Forty-five cases were positive for H. pylori. The activity of chronic gastritis correlated with H. pylori infection. p53 and c-Myc expression correlated positively with the grade of chronic gastritis. After treatment of H. pylori, the activity of gastritis decreased and the expression of both p53 and c-Myc decreased. H. pylori infection in the gastric mucosa may be implicated in the pathway of gastric carcinogenesis. It seems that H. pylori infection is responsible for early genomic instability even before any neoplastic changes and its eradication can reverse the sequence of inflammation and related atrophy, metaplasia, and genomic instability and, thus, may prevent gastric cancer development