Stomach Flu

Summary text
This article reviews the available literature on the factors contributing to the development of gastroesophageal reflux disease (GERD). The author concludes that the pathophysiology of GERD is multifactorial, and abnormalities in the gastroesophageal junction, the stomach, the esophagus and the nervous system may lead to development of the disease.

Key findings

The pathophysiology of GERD is multifactorial.The mechanisms contributing to the development of GERD include transient LES relaxations, reduced LES pressure, impaired esophageal mucosal defence, visceral hypersensitivity, hiatal hernia and delayed gastric emptying.Identification and understanding of the factors that cause GERD should help to improve management of the disease.Extended abstract
Background: Gastroesophageal reflux disease (GERD) is characterised by esophageal symptoms such as heartburn and acid regurgitation. Patients with GERD may also have chest pain in some cases or esophageal complications (e.g. reflux esophagitis, stricture and Barrett’s esophagus) and/or extra-esophageal syndromes (including reflux cough, reflux laryngitis, asthma and dental erosions). Several underlying factors are thought to contribute to the development of GERD.

Aim: To review the available literature on the pathophysiology of GERD, with particular emphasis on recently published research.

Methods: Literature searches in Medline and EMBASE were conducted. In order to ensure that up-to-date research was captured, abstracts from recent large congresses were also reviewed.

Discussion: The significance of the components of gastroesophageal refluxate (acid, weak acid, non-acid and bile) can be ascertained through combining pH monitoring with other techniques such as impedance and Bilitec monitoring. While acid reflux causes the majority of symptomatic reflux episodes, non-acid and weakly acidic refluxate can also cause symptoms. The further the refluxate travels up the esophagus, and the greater the volume, the longer acid is likely to be in contact with the esophageal mucosa. It is thought that individuals are more likely to perceive a reflux event if the refluxate has a high proximal extent and a large volume.
The gastroesophageal junction provides the first line of defence against refluxate, and comprises the lower esophageal sphincter (LES), crural diaphragm and the gastric sling. Both decreased LES resting pressure and shorter length of LES are associated with increased reflux. Transient LES relaxations, thought to be triggered by gastric distention, seem to play a key role in GERD. Sliding hiatal hernia and reduced gastric sling fibre pressure are also thought to be associated with GERD.
The esophagus acts as the second line of defence against reflux via two main mechanisms: esophageal clearance and mucosal defence. Impaired esophageal clearance is thought to lead to increased esophageal acid exposure in patients with reflux esophagitis. Pre-epithelial, epithelial and post-epithelial defences bring about resistance to refluxate, and breach of these defences is thought to lead to symptoms characteristic of GERD. Esophageal hypersensitivity, thought to be caused by impaired mucosal defence, dysfunction in the visceral neural pathway or sustained esophageal contractions, may also be responsible for GERD symptoms.
In terms of the stomach, there is some evidence to suggest that a correlation exists between duration of gastric emptying and esophageal acid exposure, which may give rise to GERD symptoms.

Conclusions: The factors contributing to GERD include abnormalities in the gastroesophageal junction, the stomach, the esophagus and the nervous system. The multifactorial pathophysiology of GERD may explain why a residual unmet need exists in management of the disease.

You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.