About 1 in 5 adults in the United States have gastroesophageal reflux disease (GERD), a painful, heartburn-triggering condition thought to be caused by stomach acid splashing up into the esophagus. A study in the Journal of the American Medical Association suggests that it's the body's inflammatory response—more than the stomach acid itself—that's causing the damage.
Acid Suppressing Medications
Billions of dollars are spent every year on stomach acid-suppressing drugs like proton pump inhibitors (think Prilosec, Prevacid, and Zegerid). For example, in a New York Times article, a 2015 analysis showed Medicare spent $2.5 billion in 2013 on one acid reflux drug alone, Nexium. In general, they help many people, but not all. These new findings suggest there may be other ways to fight the condition, the researchers say.
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"Although this radical change in the concept of how acid reflux damages the esophagus of GERD patients will not change our approach to its treatment with acid-suppressing medications in the near future, it could have substantial long-term implications," said senior author Stuart Spechler, M.D., said in a statement. Dr. Spechler is a former professor of Internal Medicine at UT Southwestern and chief of the Department of Gastroenterology at the Dallas VA Medical Center.
Impact of Inflamation
In the study, Kerry Dunbar, M.D., Ph.D., and her colleagues looked at 12 patients who had esophagitis (when the esophagus becomes irritated and swollen), a complication that isn't seen in every GERD patient. Each of the patients stopped taking their proton pump inhibitors for 12 weeks. The doctors took biopsies and closely observed what happened both before as well as 1 and 2 weeks after the patients stopped taking their medication.
The patients did end up developing more damage, as the researchers thought they would. But the tissue didn't show a chemical-like burn that might be expected from stomach acid splashing into the esophagus. Instead, they found white blood cells, inflammatory proteins, and signaling molecules (known as cytokines), which are more consistent with what you would find when the body reacts to an injury.
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The patients may only represent 1 to 5 percent of people with GERD, so more research is needed, noted Peter J. Kahrilas, M.D., of Northwestern University in Chicago, in an editorial accompanying the study. But targeting this inflammation could help those who don't respond to conventional treatments.
"The therapeutic puzzle will only be solved piece by piece," writes Dr. Kahrilas. "Dunbar et al may have just placed a very important piece."