[Ethiopathogenesis of gastroesophageal reflux disease].
The primary cause of the gastroesophageal reflux disease is the impairment of motility and not that of acidic secretion. The reflux disease develops when the balance between aggressive and defensive factors becomes disequilibriated. Among the aggressive factors the gastro-oesophageal (duodeno-gastro-oesophageal) reflux is classified. In its pathogenesis, the major role has the concentration of the hydrochloric acid, presence of bile and of pancreatic enzymes. These factors may be potentiated by the hiatal hernia, gastric dysmotility, insufficient pyloric competency, and subsequent duodeno-gastric reflux. Key factor in the development of the gastroesophageal reflux disease is the length of esophageal exposition to the refluxed gastric content. The role of duodenal content is not yet clear. Mucosal impairment probably comes from the synergistic effects of hydrochloric acid and the bile. The antireflux barrier, luminal clearance, and the tissue resistance may serve as protective factors. The first line of defence is the antireflux barrier--the retrograde flow of the gastric content is blocked by the competence of the lower esophageal sphincter and by the contractile activity of the diaphragm. Transition of epithels in the region of gastro-oesophageal junction is not yet fully understood. When inflammatory and reactive changes are found in the cardiac mucosa, the case is classified as carditis. Three potential mechanisms of incompetence in the region of gastro-oesophageal junction been described: Transient relaxation of the lower oesophageal sphincter, hypotension of the lower oesophageal sphincter, anatomical disruption of the gastro-oesophageal junction, which is frequently connected with hiatal hernia. Majority of papers indicates that the essential causes of the gastroesophageal reflux disease are transient relaxations of the lower esophageal sphincter and diaphragm. In patients with massive reflux esophagitis, pressure of the lower esophageal sphincter is weak and amplitude of esophageal contractions is low. Gradient in the region of the lower esophageal sphincter is formed in the vicinity of the functioning valve, which is formed by musculo-mucosal fold located in transition of esophagus and stomach. In healthy persons, refluxed fluid is quickly removed from the esophagus, which is the second line of defence. Reduction of the frequency or the power of peristaltic contractions causes delayed esophageal clearance. Gravitation and neutralisation of acids by bicarbonates in saliva assist the clearance. Pathogenic processes can be augmented by the retardation of gastric emptying. Composition of the refluxed fluid reflects the seriousness of the disease. Two mechanisms of impaired esophageal emptying has been identified: Peristaltic dysfunction and "re-reflux" related to some hiatal hernias. The third line of defence is the less known and it is represented by "tissue resistance". The role of eicosanoids in the gastroesophageal reflux disease is not yet known because their levels do not correlate with the seriousness of the symptoms. Increased prevalence of the reflux disease during the last years is often correlated with decreased incidence of Helicobacter pylori infections. Ethiopathogenesis of the reflux disease is multifactorial and can include deficient antireflux mechanisms, frequency of reflux episodes, volume and effectiveness of the refluxed fluid, mucosal resistance, deficient esophageal clearance and emptying of the stomach. Among the serious factors may belong the frequency and magnitude of the gastro-oesophageal reflux, however, the key role probably plays the dysfunction of the lower esophageal sphincter.
IV. interní klinika 1. LF UK a VFN, Praha.
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Lukás
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Marecek
D005764:Gastroesophageal Reflux / Q000209:etiology / Q000503:physiopathology*; D006801:Humans