Special Health Section • Beyond Heartburn: Reflux Disease
The Science of Gastroesophageal Reflux Disease (GERD)
April 2008
By Roy C. Orlando, M.D.
Gastroesophageal reflux is, by definition, the effortless movement of acidic gastric contents from stomach to esophagus. It occurs in everyone, multiple times every day, and usually without producing symptoms or signs of damage to the esophagus or other organs.
This lack of damage reflects the ability of the body to protect itself by: a) limiting the frequency and extent of reflux events by contraction of the lower esophageal sphincter and diaphragm, b) limiting the duration that the acidic gastric contents stay in the esophagus by volume clearance via gravity and esophageal contractions and acid dilution and neutralization by swallowing saliva and secretions from esophageal glands, and c) limiting the penetration of acid and other substances into the esophageal wall by the barrier function of its epithelial lining.
In about 20% of the adult U.S. population (approximately 60 million people) the reflux of acidic gastric contents into the esophagus produces symptoms and signs of tissue damage to the esophagus, oropharynx, larynx and airway. These individuals are designated as having Gastroesophageal Reflux Disease (GERD). For the vast majority of subjects with GERD, the disease is a nuisance, reducing the quality of life, but not affecting lifespan. The latter is apparent in that the most common form of GERD involves damage to the esophagus - damage that is typically reflected by the development of heartburn, a substernal burning discomfort worse after meals and on reclining and relieved relatively promptly by ingestion of antacids. In approximately 50% of those with heartburn there are visible breaks (erosions) in the lining of the esophagus on endoscopy. The other roughly 50% with heartburn have no obvious lesions on endoscopy and so are designated as having 'non-erosive' reflux disease (NERD). Like those with erosions, those with NERD also have breaks in the esophageal lining but these are only detected microscopically and require an esophageal biopsy. In either case, the breaks in the esophageal lining enable acid to penetrate the esophageal wall, and by so doing to stimulate the (nerve) pain fibers within it - giving rise to the symptom of heartburn. Since acid penetration of the wall is critical to the generation of heartburn, it explains why antacid ingestion typically relieves the symptom and why agents that block acid secretion by the stomach (histamine-2 receptor antagonists, e.g. ranitidine, or proton pump inhibitors, e.g. omeprazole), typically block heartburn's re-occurrence.
What causes acid reflux to transition from benign occurrence in every adult to damaging in some can be viewed like a football game - where acid plays offense and the esophageal lining (epithelium) plays defense. Disease occurs when the offense beats down the defense and this is a function of: a) the total time that acid is in contact with the epithelium, and b) the basic health and integrity of the epithelium. Consequently, GERD occurs in some because of prolonged contact of acid with the epithelium, usually more than 1.2 hrs/day (this is determined by a clinical test known as esophageal pH monitoring). In those with prolonged contact of acid with epithelium, the major problem is typically a defect in the function of the lower esophageal sphincter (LES). When not swallowing, the LES stays contracted (closed) which serves to keep gastric contents from entering the esophagus; however contraction can be impaired by frequent, spontaneous relaxations, poor intrinsic muscle strength, or lacking extrinsic support from the neighboring diaphragm - the latter a common occurrence in those with a hiatal hernia. Alternatively GERD occurs in others despite apparently normal total time of acid contact with the epithelium (less than 1.2 hrs/day). This occurs because of the existence of an already weakened epithelial defense, and so one requiring less time for acid to produce its damage. The causes for this are as yet unclear but are probably multiple, including poor diet, bad habits (alcohol, tobacco products), and stress.
Dr. Roy C. Orlando is a Bozymski and Heizer Distinguished Professor in Gastroenterology & Adjunct Professor of Cell and Molecular Physiology at UNC.
Treatment of GERD: Does A-N-T-A-C-I-D Spell Relief?
By Ryan D. Madanick, MD
 Gastroesophageal reflux disease (GERD) affects 20% of Americans, which equals approximately 60 million Americans, a staggering number considering the economic impact that GERD has. For centuries, antacids were the primary agents used to deal with reflux symptoms. Improvements in the understanding about the underlying causes of the disease and its symptoms have led to remarkable progress in the treatment of this common illness.
Antacids work by buffering the gastric contents, which decreases their acidity. Early antacids were composed of sodium bicarbonate. Most over-the-counter antacids today use other types of alkali salts, such as magnesium hydroxide, aluminum hydroxide, and calcium carbonate, to achieve their effects. Because many reflux symptoms are related to acid, many people with intermittent symptoms obtain relief by using antacids on an "as-needed" basis.
 However, some individuals have more chronic or continual symptoms, or complications such as strictures or Barrett's esophagus, that require more potent suppression of acid production. In 1973 the first of a novel class of medications, the histamine-2-receptor antagonists, was introduced. These medications work by blocking one of the three receptors on the parietal cell (the cell that produces acid in the stomach), the histamine-2-receptor.
Unfortunately, these medications, which include cimetidine, famotidine, ranitidine, and nizatidine, leave 2 types of receptors unblocked and acid is incompletely suppressed. Thus in the 1980s another more potent type of medication, the proton pump inhibitor, was developed.
In the last 20 years, this class of drugs, which includes omeprazole, lansoprazole, rabeprazole, pantoprazole and esomeprazole, has revolutionized the
management of GERD. After one of three types of receptors on the parietal cell is stimulated, acid is produced by a pump that exchanges hydrogen (the "proton") for potassium. These drugs work by blocking this final step in the production of acid within the stomach. Because they block acid production regardless of the type of stimulus, these drugs are the most potent acid-suppressing medications available to date.
Ryan D. Madanick, MD, is Assistant Professor of Medicine, UNC School of Medicine, Center for Esophageal Diseases and Swallowing.
Complications of GERD: Scopes and Surgery
By Nick Shaheen, MD
 "I can't believe I ate the whole thing!" "Plop Plop Fizz Fizz, Oh what a relief it is!" The verbiage of reflux and indigestion is everywhere in our society. For most patients with gastroesophageal reflux disease (GERD), the condition is primarily a nuisance - "I have to watch what I eat and when I eat it, or I will pay." Many others control their symptoms with either over-the-counter medications or a doctor's prescription.
However, a small number of people with reflux will go on to develop more severe forms of the disease. It is these people who doctors most want to detect and treat, however, like most things in life, it just isn't that simple.
For most people, reflux means heartburn. Although this is not the only manifestation of reflux disease, it is the most common. It would stand to reason that the people who have the worst heartburn are also those with the worst inflammation in their esophagus, but it turns out that this is not necessarily the case. The severity of heartburn is actually a poor predictor of how much inflammation there is in the esophagus. You really can't tell unless you look.
And what does "looking" entail? To find out the condition of the lining of the food tube, or esophagus, we need to place a tube through the mouth and down the throat. This procedure is called an upper endoscopy, although it is informally referred to as a "scope." By scoping the patient, the doctor can tell how bad the disease is, and therefore, how aggressive the therapy should be.
Inflammation of the esophagus from the acid reflux is called esophagitis. Repeated insults to the esophagus can result in a narrowing of the esophagus, or a stricture. Patients who develop a stricture may chronically have trouble eating, but sometimes they may not know about it until they gulp a big piece of hot dog without chewing it well. If the hot dog (or anything else) gets caught in the stricture, the patient may require an endoscopy to get it out. A stricture sounds serious, and it is, but like plumbers, the gastroenterologists can generally open up the esophagus with a series of endoscopic maneuvers.
The most feared complication of reflux is esophagealcancer. It is important to know, however, that this is one of the rarest complications as well. With chronic acid exposure, the lining of the esophagus can change to a different cell type, called Barrett's esophagus. The good news is that Barrett's is more resistant to acid. The bad news is that, on rare occasion, the Barrett's will degenerate into cancer. If we look inside you and find the Barrett's, we will likely ask you to come back for scheduled endoscopies to keep an eye on the tissue and make sure it does not progress to cancer.
Although all this sounds scary, for almost all patients with heartburn, their life will not be shortened by the disease, and controlling the symptoms is the most important part. Newer acid suppressive medicines are highly effective, meaning that for most people, a pill a day should do it.
Take your medicine like your doctor tells you, avoid too much alcohol and fatty foods, and for heaven's sake, don't "eat the whole thing!"
Nick Shaheen, MD, is a Ray Haywood '63 Medical Alumni Teaching Professor of Medicine and Director of the Center for Esophageal Diseases and Swallowing at the University of North Carolina.
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