Gastric Acid Rebound Secretion Measured by Alkaline Tide
Status and phase
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Details and patient eligibility
About
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.
Sex
Ages
Volunteers
Inclusion criteria
- Dyspepsia and reflux patients older than 18
Exclusion criteria
- patients on PPI, patients with severe diseases, younger than 18 y, older than 80 y, un-cooperative, COPD, uncompensated IHD, CRF
Trial design
Primary purpose
Allocation
Interventional model
Masking
0 participants in 2 patient groups
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Data sourced from clinicaltrials.gov
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