Peptic Ulcer
Conditions
Keywords
peptic ulcer, gastritis, sTREM-1, cytokines, Changes of inflammatory status in gastric mucosa, sTREM-1 as a disease marker
Brief summary
Although all PPIs are effective, there are some differences in their clinical performance, particularly in terms of the degree and speed of gastric acid suppression. Few data are also available about their effect of the pathophysiological mechanisms of gastritis and peptic ulcer disease. Aim of the present study is to investigate the effect of therapy with esomeprazole or rabeprazole on the mechanism of pathogenesis of gastritis and particularly on the pattern of release of pro- and anti- inflammatory cytokines associated to peptic ulcerative process by the gastric mucosa.
Detailed description
Although all PPIs are effective, there are some differences in their clinical performance, particularly in terms of the degree and speed of gastric acid suppression. Few data are also available about their effect of the pathophysiological mechanisms of gastritis and peptic ulcer disease. Triggering receptor expressed on myeloid cells (TREM)-1 is a recently discovered receptor expressed on the surface of neutrophils and monocytes. Engagement of TREM-1 has been reported to trigger the synthesis of proinflammatory cytokines. A soluble form of TREM-1, named sTREM-1, was observed and identified at significant levels in serum samples from patients with disease of the gastrointestinal tract inflammatory bowel disease. rendering interest about the implication of sTREM-1 in their pathogenesis. sTREM-1 was also found elevated in the gastric juice of patients with peptic ulcer disease being correlated to the degree of the infiltration of the gastric mucosa by neutrophils. Published data of our group elicit that sTREM-1 secretion is a crucial parameter for evolution from chronic gastritis to peptic ulcer disease. Samples of biopsies of gastric mucosa were cultured in the absence/presence of endotoxins showing that the inflamed mucosa was a potent secretor of sTREM-1 whatever ceased to exist post-antisecretory treatment. Aim of the present study is to investigate the effect of therapy with esomeprazole or rabeprazole on the mechanism of pathogenesis of gastritis and particularly on the pattern of release of pro- and anti- inflammatory cytokines associated to peptic ulcerative process by the gastric mucosa.
Interventions
Upper GI endoscopy, one time on diagnosis and a second time 15 days after the end of the treatment. Gastric juice will be aspirated immediately after the entrance of the endoscope into the gastric lumen. Four biopsy specimens will be obtained from adjacent areas of the gastric antrum. Each biopsy will be used for in vitro culture. Blood will be sampled from one antecubital vein under aseptic conditions. Each patient will be given antisecretory treatment and - if necessary- eradication treatment of H. pylori according to international guidelines.
Sponsors
Study design
Eligibility
Inclusion criteria
* Written informed consent. * Abdominal pain or discomfort and/or * Epigastric pain with nausea and vomiting and/or * Dyspepsia.
Exclusion criteria
* Recent upper GI bleeding * Gastric carcinoma * Diabetes mellitus * Liver cirrhosis * Acute or chronic renal failure * The ingestion of any antimicrobial or antisecretory medication for at least 15 days prior to endoscopy.
Design outcomes
Primary
| Measure | Time frame |
|---|---|
| Effect of treatment on changes of cytokines levels in serum of patients | Baseline and 8 weeks |
Secondary
| Measure | Time frame |
|---|---|
| Effect of treatment on changes of cytokines levels in supernatants of cultures of gastric mucosa | Baseline and 8 weeks |
Countries
Greece