Presenter: Michael Vaezi, MD, PhD, MSc, Clinical Director, Division of Gastroenterology, Director of the Center for Swallowing and Esophageal Disorders, Professor of Medicine, Vanderbilt University Medical Center, Nashville
Following on the heels of the obesity epidemic, a second epidemic has become apparent—sleep-disordered breathing and its effect on esophageal conditions, primarily gastroesophageal reflux disease (GERD). Many, many primary care providers have heard the following complaint:
“I gained 10 pounds and now I have heartburn/cough/worsening asthma” (take your pick). What’s going on?
Weight gain is associated with increased intra-abdominal pressure; when patients lie down for sleep, that increased pressure can exceed the pressure of the lower esophageal sphincter (LES), and reflux is the result. In addition to the pressure-related effect, obesity may also impair gastric emptying, decrease LES pressure, and increase transient LES relaxation—all of which lead to increased esophageal acid exposure.
While proton pump inhibitors (PPIs) are the mainstay of treatment, Dr. Vaezi stresses that patients must understand that these do not cure reflux—they simply lower the acidity (pH) of the fluid that surges into the esophagus during sleep. While this protects the esophagus, the only long-term solution is weight loss. In the face of the obesity epidemic, the incidence of esophagitis, Barrett’s esophagus, and adenocarcinoma of the esophagus have been steadily rising in the U.S. and Western Europe. And the effect is dose-dependent—the risk progressively increases with increasing weight.
Obesity, reflux, and respiratory problems form a complex inter-relationship. Extraesophageal symptoms include chronic cough, laryngitis, asthma, and sleep disorders including apnea. Two mechanisms are proposed to explain extraesophageal symptoms of GERD:
1. Microaspiration (reflux): gastroduodenal contents enter the larynx or airways. Contents can include acid, pepsin, bile, and pancreatic enzymes. Chronic irritation of respiratory tissues can cause laryngitis, chronic cough, or asthma.
2. Vagal stimulation (reflex): Acid in the distal esophagus stimulates acid-sensitive receptors innervated by the vagus. Since the esophagus and the bronchial tree share vagal innervation, this stimulation can cause cough or exacerbate asthma. It can also result in non-cardiac chest pain for the same reason.
Asthma can also increase acid reflex, when more active breathing causes negative intrathoracic pressure, which encourages further proximal flow of gastric contents. Thus asthma and acid reflux can co-exist in a positive feedback loop with each other.
What to do? Dr. Vaezi provided the usual list of lifestyle modifications for treating GERD (smoking cessation, reducing alcohol(Drug information on alcohol) and caffeine(Drug information on caffeine), eating smaller meals, avoiding reflux-promoting drugs, elevating, the head of bed, and weight loss). But, he stressed that only weight loss is an evidence-based recommendation—the others are time-honored anecdote-based recommendations. GERD incidence increases with weight gain, and good studies show it resolves with weight loss. This is a reversible syndrome.
Many therapeutic trials of treatment for extra-esophageal syndromes have used twice-daily dosing of PPIs for 3 to 4 months. This is an un-approved dosing derived from pH monitoring studies that demonstrated the likelihood of normalizing esophageal acid exposure with twice-daily PPIs is 93% to 99%. Note that there are no controlled trials investigating the optimal dose or duration of PPI therapy for extra-esophageal GERD syndromes. Lack of response suggests non-GERD causes—if a patient with GERD and extra-esophageal symptoms does not improve, consider another diagnosis!