Gastroesophageal reflux disease (GERD): is there more to the story?
Gastroesophageal reflux disease (GERD) affects both men and women worldwide, with the most common symptom of GERD being frequent heartburn. If left untreated, more serious diseases including esophagitis and/or esophageal cancer may result. GERD has been commonly held to be the result of gastric acid refluxing into the esophagus. Recent work, however, has shown that there are acid-producing cells in the upper aerodigestive tract. In addition, acid-producing bacteria located within the upper gastrointestinal tract and oral cavity may also be a contributing factor in the onset of GERD. Proton pump inhibitors (PPIs) are commonly prescribed for treating GERD; these drugs are designed to stop the production of gastric acid by shutting down the H(+)/K(+)-ATPase enzyme located in parietal cells. PPI treatment is systemic and therefore significantly different than traditional antacids. Although a popular treatment choice, PPIs exhibit substantial interpatient variability and commonly fail to provide a complete cure to the disease. Recent studies have shown that H(+)/K(+)-ATPases are expressed in tissues outside the stomach, and the effects of PPIs in these nongastric tissues have not been fully explored. Likewise, acid-producing bacteria containing proton pumps are present in both the oral cavity and esophagus, and PPI use may also adversely affect these bacteria. The use of PPI therapy is further complicated by the two philosophical approaches to treating this disease: to treat only symptoms or to treat continuously. The latter approach frequently results in unwanted side effects which may be due to the PPIs acting on nongastric tissues or the microbes which colonize the upper aerodigestive tract.
Vesper
Benjamin J
BJ
Center of Molecular Biology of Oral Diseases, College of Dentistry/Jesse Brown VAMC, University of Illinois at Chicago, Chicago, IL 60612, USA.
Altman
Kenneth W
KW
Elseth
Kim M
KM
Haines
G Kenneth
GK
Pavlova
Sylvia I
SI
Tao
Lin
L
Tarjan
Gabor
G
Radosevich
James A
JA
D000863:Antacids / Q000627:therapeutic use; D005744:Gastric Acid / Q000378:metabolism; D005764:Gastroesophageal Reflux / Q000188:drug therapy*; D017506:H(+)-K(+)-Exchanging ATPase / Q000737:chemistry / Q000378:metabolism; D006635:Histamine H2 Antagonists / Q000627:therapeutic use; D006801:Humans; D054328:Proton Pump Inhibitors / Q000627:therapeutic use; D043887:Receptor, Cholecystokinin B / Q000037:antagonists & inhibitors
D000863:Antacids; D006635:Histamine H2 Antagonists; D054328:Proton Pump Inhibitors; D043887:Receptor, Cholecystokinin B; D017506:H(+)-K(+)-Exchanging ATPase