Although gastroesophageal reflux disease (GERD) is a common disorder in Western countries, with a significant impact on quality of life and healthcare costs, the mechanisms involved in the pathogenesis of symptoms remain to be fully elucidated. GERD symptoms and complications may result from a multifactorial mechanism, in which acid and acid-pepsin are the important noxious factors involved. Prolonged contact of the esophageal mucosa with the refluxed content, probably caused by a defective anti-reflux barrier and luminal clearance mechanisms, would appear to be responsible for macroscopically detectable injury to the esophageal squamous epithelium. Receptors on acid-sensitive nerve endings may play a role in nociception and esophageal sensitivity, as suggested in animal models of chronic acid exposure. Meanwhile, specific cytokine and chemokine profiles would appear to underlie the various esophageal phenotypes of GERD, explaining, in part, the genesis of esophagitis in a subset of patients. Despite these findings, which show a significant production of inflammatory mediators and neurotransmitters in the pathogenesis of GERD, the relationship between the hypersensitivity and esophageal inflammation is not clear. Moreover, the large majority of GERD patients (up to 70%) do not develop esophageal erosions, a variant of the condition called non-erosive reflux disease. This summary aims to explore the inflammatory pathway involved in GERD pathogenesis, to better understand the possible distinction between erosive and non-erosive reflux disease patients and to provide new therapeutic approaches.

Nonerosive reflux disease (NERD) is a distinct pattern of gastroesophageal reflux disease (GERD). It is defined as a subcategory of GERD characterized by troublesome reflux-related symptoms in the absence of esophageal mucosal erosions/breaks at conventional endoscopy. In clinical practice, patients with reflux symptoms and negative endoscopic findings are markedly heterogeneous. The potential explanations for the symptom generation in NERD include microscopic inflammation, visceral hypersensitivity (stress and sleep), and sustained esophageal contractions. The use of 24-hour esophageal impedance and pH monitoring gives further insight into reflux characteristics and symptom association relevant to NERD. The treatment choice of NERD still relies on acid-suppression therapy. Initially, patients can be treated by a proton pump inhibitor (PPI; standard dose, once daily) for 2-4 weeks. If initial treatment fails to elicit adequate symptom control, increasing the PPI dose (standard dose PPI twice daily) is recommended. In patients with poor response to appropriate PPI treatment, 24-hour esophageal impedance and pH monitoring is indicated to differentiate acid-reflux-related NERD, weakly acid-reflux-related NERD (hypersensitive esophagus), nonacid-reflux-related NERD, and functional heartburn. The response is less effective in NERD as compared with erosive esophagitis.

Gastro-oesophageal reflux disease (GERD) includes wide spectrum of symptoms caused by gastric acid regurgitation through the incompetent lower oesophageal sphincter in oesophagus. Etiopathogenesis of GERD is multifactorial.

to establish the relationship between Helicobacter pylori eradication and appearance or aggravating of present GERD. If this relationship exist, the aim is to estimate its level and clinical consequences.

50 Helicobacter pylori positive patients with different endoscopic findings (ulcer disease, gastritis and non-ulcer dyspepsia) to whom eradication of Helicobacter pylori was done, were following next 6 months. Questionnaire, uppear GI endoscopy with verification changes of oesophagus in accordance to LA classification, histopathological examination of gastric and oesophageal mucosal biopsy specimens, and oesophageal manometry have been done to all patients. These examinations have been done before Helicobacter pylori eradication and one, three. six and none months after that.

non statistical significant difference was found among the appearance or aggravating of present GERD in all patients during the following period (Cochran Q test; p=0,408). Non statistical significant difference was found among the endoscopic types of oesophagitis (LA classification) in all patients during the following 6 months (Friedman test; p=0,058). Non statistical significant difference was found among the changes of histopathological findings on distal oesophagus, too (Friedman test; p=0,217).

Eradication od Helicobacter pylori infection does not cause the appearance or aggravating of present GERD. The presence of mildly form of GERD, or aggravating of present GERD is transitory, and haven't the statistical signification.