Current understanding of Pathophysiology of GERD I DewaNyomanWibawa
Gastroentero-hepatologyDiv, Dept.of Internal Medicine, UdayanaUniv./ SanglahGeneralHospital, Denpasar, Bali.
According to the Montreal International Consensus Group, gastroesophageal reflux disease (GERD) is defined as a condition that develops when the reflux of stomach contents causes troublesome reflux-associated symptoms.1Gastroesophageal reflux is the reflux of gastric contents other than air into or through the esophagus.Gastroesophageal reflux results from several factors that lead to symptoms or injury of the mucosa of the esophagus or the airway by reflux of corrosive material from the stomach.2
GERD is a common disorder, affecting almost half of the US population, with varying severity. Forty percent of the US population experiences reflux symptoms about once per month, 20% complain of symptoms once per week, and 7–10% report daily symptoms (essential) GERD affects 10–20% of western populations. It is less common in Asian and African countries.3
GERD is believed to be caused by the effect of refluxed gastric acid on esophageal epithelial cells. Several factors have been proposed as important in the pathophysiology of GERD. They include dysfunction of the lower esophageal sphincter (LES), hiatal hernia, esophageal dysmotility, impaired esophageal defense mechanisms, gastric acid hypersecretion, duodeno-gastroesophageal reflux, esophageal hypersensitivity, delayed gastric emptying and genetic factors (tiberiu). Risk factors of GERD are advancing age (>65 years), obesity, genetic factors (essential), cigarette smoking, alcohol, coffee, obesity, high fat diet, food products such as chocolate, peppermint, and citrus juices; as well as a slew of medications (narcotics, calcium channel blockers etc).4
The etiology of GERD is multifactorial. Aberrant transient lower esophageal sphincter relaxations (TLESRs) are the major pathophysiologic factor in GERD. TLESR is defined as the relaxation of the lower esophageal sphincter in response to gastric distension. In healthy persons, TLESRs occur in the absence of a swallow, last 10–30 seconds, and result in physiologic gastroesophageal reflux. TLESRs are regulated by the neurotransmitter γ-aminobutyric acid (GABA) acting on GABA type B receptors located in the peripheral nervous system as well as in the brainstem. In many cases, GERD is thought to be caused by an increased number of or prolonged TLESRs.3,4
Increased gastric acid production as well as delayed gastric emptying with distention may trigger TLESRs. Poor esophageal clearance due to defects in primary or secondary esophageal peristalsis allows prolonged exposure of the esophageal mucosa to acid.3,4
to gastroesophageal reflux.3,4
Figure 1. Pathophysiology of GERD.5
A hiatal hernia usually occurs when there is a defect in the diaphragmatichiatus that allows the proximal stomach to herniate above thediaphragm and into the thorax. It is unclear how this predisposes togastroesophageal reflux; however, it is thought that the barrier functionof the LES to prevent the reflux of gastric contents into theesophagus is disrupted. Large hiatal hernias also lead to increasedacid dwell times in the distal esophagus.3,4
The association of GERD and Helicobacter pylori (H. pylori) is very controversial. While some argue that the infection might play a role in the prevention of GERD by altering the nature of the refluxate (gastritis leading to achlorhydria), others find no link between the infection and esophageal diseases Prevalence studies seem to suggest that H. pylori infection is inversely associated with reflux esophagitis in some populations. Eradication studies also suggest that
H. pylori infection is protective with respect to GERD.6
References
1. Vakil N, van Zanten SV, Kahrilas P, et al. The Montreal definition and classification of gastroesophageal reflux disease: a global evidence-based consensus. Am J Gastroenterol. 2006;101(8):1900-1920.
2. Murray JA. Gastroesophageal reflux disease. In: Hauser SC, ed. Mayo Clinical Gastroenterology and Hepatology Board Review. 4th ed. New York: Oxford University Press, Inc. 2011. pp: 3-17.
4. Hershcovici T, Fass R. Gastroesophageal reflux disease. In: Hawkey CJ, Bosch J, Richter JE, et al. Textbook of Clinical Gastroenterology and Hepatology. 2nd ed. West Sussex: Blackwell Publishing Ltd. 2012. pp:177-193.
5. Weinstein WM, Hawkey CJ, Bosch J. Gastroesophageal reflux disease. In: Weinstein WM, Hawkey CJ, Bosch J, eds. Clinical Gastroenterology and Hepatology. 1st ed.New York: Elsevier Mosby. 2005.p157-166.
