Ethiopathogenesis of Gastroesophageal Reflux Disease

Overview

The primary cause of the gastroesophageal reflux disease is the impairment of motility and not that of acidicsecretion. The reflux disease develops when the balance between aggressive and defensive factors becomesdisequilibriated. Among the aggressive factors the gastro-oesophageal (duodeno-gastro-oesophageal) reflux isclassified. In its pathogenesis, the major role has the concentration of the hydrochloric acid, presence of bile andof pancreatic enzymes. These factors may be potentiated by the hiatal hernia, gastric dysmotility, insufficientpyloric competency, and subsequent duodeno-gastric reflux. Key factor in the development of the gastroesopha-geal reflux disease is the length of esophageal exposition to the refluxed gastric content. The role of duodenalcontent is not yet clear. Mucosal impairment probably comes from the synergistic effects of hydrochloric acidand 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 thecompetence of the lower esophageal sphincter and by the contractile activity of the diaphragm. Transition ofepithels in the region of gastro-oesophageal junction is not yet fully understood. When inflammatory and reactivechanges are found in the cardiac mucosa, the case is classified as carditis. Three potential mechanisms ofincompetence in the region of gastro-oesophageal junction been described: Transient relaxation of the loweroesophageal sphincter, hypotension of the lower oesophageal sphincter, anatomical disruption of the gastro-oe-sophageal junction, which is frequently connected with hiatal hernia. Majority of papers indicates that theessential causes of the gastroesophageal reflux disease are transient relaxations of th e lower esophageal sphincterand diaphragm. In patients with massive reflux esophagitis, pressure of the lower esophageal sphincter is weak andamplitude of esophageal contractions is low. Gradient in the region of the lower esophageal sphincter is formed inthe vicinity of the functioning valve, which is formed by musculo-mucosal fold located in transition of esophagusand stomach. In healthy persons, refluxed fluid is quickly removed from the esophagus, which is the second lineof defence. Reduction of the frequency or the power of peristaltic contractions causes delayed esophagealclearance. Gravitation and neutralisation of acids by bicarbonates in saliva assist the clearance. Pathogenicprocesses can be augmented by the retardation of gastric emptying. Composition of the refluxed fluid reflectsthe seriousness of the disease. Two mechanisms of impaired esophageal emptying has been identified: Peristalticdysfunction and „re-reflux” related to some hiatal hernias. The third line of defence is the less known and it isrepresented by „tissue resistance”. The role of eicosanoids in the gastroesophageal reflux disease is not yetknown because their levels do not correlate with the seriousness of the symptoms. Increased prevalence of thereflux 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, deficientesophageal clearance and emptying of the stomach. Among the serious factors may belong the frequency andmagnitude of the gastro-oesophageal reflux, however, the key role probably plays the dysfunction of the loweresophageal sphincter.

Key words:
gastroesophageal reflux disease, lower esophageal sphincter, hiatal hernia, Heliobacter pylori, carditis,