Gastric Acid Rebound Secretion Measured by Alkaline Tide
Status:
Withdrawn
Trial end date:
2016-12-01
Target enrollment:
Participant gender:
Summary
Gastro esophageal reflux disease and ulcer related or non-ulcer dyspepsia, attacks 20% of the
Western population. These millions of patients are treated continuously with PPI for
different periods, many for many years. Recently, rebound acid hypersecretion was recognized
as a major clinical event after cessation of PPI therapy. Sustained hypergastrinemia due to
daily PPI therapy causes increased acid-secretory capacity that appears when the drug is
stopped. The transient increase in blood and urinary pH following gastric secretion has been
termed the alkaline tide phenomenon. Carbonic acid, formed in the presence of the enzyme
carbonic anhydrase, neutralizes intracellular hydroxyl ions produced as a result of luminal
acid secretion. The bicarbonate generated is removed from the cell via the baso-lateral
chloride bicarbonate exchanger. The investigators have shown in several studies that this
phenomenon parallels acid secretion. Thus, stimulation of acid secretion with test meal
increased base excess maximally after 45 minutes and these changes parallel peak acid output
measured in gastric aspirate. The investigators hypothesize that gradual step down cessation
of PPI will prevent this clinical relevant event. By measuring alkaline tide after PPI
cessation the investigators may prove this hypothesis.