Alkaline gastroesophageal reflux (GER) is a controversial concept for
the pathogenesis of non-infectious esophagitis in the absence of measu
rable acid GER. Excessive duodenogastric reflux, as it can be seen in
antroduodenal motility disorders, seems to be prerequisite. Yet, bile
acids, a marker for duodenal secretions, are more frequently found dur
ing acid than during alkaline GER. Moreover: it has not been possible
to show mucosal toxicity by bile acids ol trypsin when tested at conce
ntrations similar to those measured in esophageal refluxate. It remain
s therefore questionable as to whether alkaline pH measured in the eso
phagus results from reflux of duodenal contents or if it is a sign of
increased salivary or esophageal secretions, and if the analogy of gas
tritis and esophagitis secondary to biliary reflux is allowed. Alkalin
e GER more probably is an erroneus pathogenic concept for esophagitis
which requires intensified antacid therapy.