Gastroesophageal Reflux Disease

Gastroesophageal Reflux Disease

Gastroesophageal reflux disease (GERD) is a complex, multi-factorial condition which is reported to affect 14-20% of the population of the US [1]. It arises when the epithelium of the oesophagus comes into contact with the acidic contents of the stomach, causing irritation and inflammation to the esophageal lining termed esophagitis. Excessive reflux of acid and pepsin results in necrosis of the mucosa of the esophagus causing erosins and ulcers. GERD is a chronic condition and although some relief is afforded to sufferers when the esophagus heals, the condition often resurfaces after a couple of months after treatment. Serious complications can arise from this disease therefore making

The pathophysiology of GERD is complicated and many physiological modifications take place. Under normal circumstances, the body executes a number of operations to prevent the reflux of acid from the stomach. Saliva containing bicarbonate is produced by the salivary glands of the mouth which neutralizes any remaining acid present in the oesophagus after swallowing. Another mechanism is the functioning of the lower oesophageal sphincter. This contains smooth muscle which is contracted at rest to close the junction between the esophagus and the stomach thereby preventing any back-flow of acid into the esophagus. Impairment of these protective mechanisms contributes to the manifestation of GERD. Two of the most accepted contributory factors in the onset of GERD are transient lower esophageal sphincter relaxations (tLESR) and hiatal hernias.

As previously mentioned, under normal conditions the lower esophageal sphinter is contracted and is only relaxed in response to swallowing. When relaxation occurs in the absence of swallowing, the event is termed transient lower esophageal relaxations. This occurrence is very common in GERD sufferers and accounts for between 63% and 74% of reflux events in patients [2]. It has also been demonstrated that an increased frequency of tLESR leads to the onset of GERD. Stimuli's that trigger or modulate tLESRs include gastric distension, posture and sleep [3].

The vast majority of patients with GERD also have hiatal hernias. A hiatal hernia occurs when a small portion of the stomach protrudes upwards through the diaphragm. This causes the lower esophageal sphincter to move from its positioning at the level of the diaphragm to lie in the chest along with the small portion of the stomach. It has been reported that patients with a hiatal hernia were more likely to suffer from episodes of acid reflux than those who had none and this was thought to be due the extended periods of reflux in patients with large hiatal hernias [5].

The predominant symptoms of GERD include heartburn due to the stimulation of nerve fibres in the esophagus; and nausea which can result in vomiting. Various complications can arise in patients that have this condition such as ulcers of the esophagus due to acid damage, stricture which is the narrowing of the lumen of the esophagus due to the development of scar tissue after ulcer healing and esophageal adenocarcinoma. Several studies have been performed which link symptomatic GERD with esophageal adenocarcinoma [6].

1. Kahrilas, P., Gastroesophageal reflux disease. N Engl J Med, 2008. 359: p. 1700-7.

2. Mittal, R. and R. McCallum, Characteristics of transient lower esophageal sphincter relaxation in humans. American Journal of Physiology- Gastrointestinal and Liver Physiology, 1987. 252(5): p. 636.

3. Mittal, R., et al., Transient lower esophageal sphincter relaxation. Gastroenterology, 1995. 109(2): p. 601-610.

4. Kahrilas, P., GERD pathogenesis, pathophysiology, and clinical manifestations. Cleveland Clinic journal of medicine, 2003. 70(5): p. 4.

5. Sloan, S., A. Rademaker, and P. Kahrilas, Determinants of gastroesophageal junction incompetence: hiatal hernia, lower esophageal sphincter, or both. Ann Intern Med, 1992. 117(12): p. 977-982.

6. Lagergren, J., et al., Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. The New England journal of medicine, 1999. 340(11): p. 825.

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