The changing epidemiology of GERD: geography and Helicobacter pylori.
BACKGROUND
Issues have arisen regarding H. pylori infection and GERD that have caused unnecessary confusion among practicing physicians. In the last century GERD became increasingly recognized in the West and it has become evident that the prevalence of GERD is now occurring in many previously underdeveloped countries.


METHODS
This review article fosters understanding of the issues by focusing on the esophageal acid load and the factors that control it. In particular, we discuss the effects of the change in the patterns of gastritis that have occurred naturally as well as after H. pylori eradication and correlate those changes with their effects on the esophageal acid load. We show how it is possible to separate gastroesophageal reflux from gastroesophageal reflux disease based on differences in esophageal acid load. We also describe how the practice of assessing gastroesophageal reflux based on the time the intraesophageal pH is less than 4 resulted in investigators systematically discarding data critical to understanding of the effect of their interventions on esophageal acid load. Testable hypotheses are presented to explain the interactions between H. pylori and GERD and between H. pylori and the changing epidemiology of GERD.


CONCLUSIONS
We propose that the confusion regarding H. pylori and the changing epidemiology of GERD is based on the failure to critically examine the historical evidence in relation to the other H. pylori-related diseases as well as reliance on techniques that are either unable to measure, or systematically discard data critical for understanding effects of various interventions on the esophageal acid load. This has resulted in propagation of erroneous concepts regarding H. pylori and adenocarcinoma of the esophagus and has resulted in some patients being denied appropriate therapy.
Graham
David Y
DY
Department of Medicine, Veterans Affairs Medical Center and Baylor College of Medicine, Houston, Texas 77030, USA.
D000143:Acids / Q000378:metabolism; D000942:Antigens, Bacterial / Q000378:metabolism; D001426:Bacterial Proteins / Q000378:metabolism; D003906:Developing Countries / Q000706:statistics & numerical data*; D004381:Duodenal Ulcer / Q000150:complications; D004947:Esophagus / Q000378:metabolism; D005756:Gastritis / Q000382:microbiology; D005764:Gastroesophageal Reflux / Q000453:epidemiology* / Q000378:metabolism / Q000382:microbiology*; D005843:Geography; D016481:Helicobacter Infections / Q000453:epidemiology* / Q000378:metabolism; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D015994:Incidence; D015995:Prevalence; D014481:United States / Q000453:epidemiology
D000143:Acids; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori