TY - JOUR
T1 - Gradual cessation of proton pump inhibitor (PPI) treatment may prevent rebound acid secretion, measured by the alkaline tide method, in dyspepsia and reflux patients
AU - Niv, Yaron
PY - 2011/9
Y1 - 2011/9
N2 - 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. We 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. min and these changes parallel peak acid output measured in gastric aspirate. We hypothesize that gradual step down cessation of PPI will prevent this clinical relevant event. By measuring alkaline tide after PPI cessation we may prove this hypothesis.
AB - 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. We 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. min and these changes parallel peak acid output measured in gastric aspirate. We hypothesize that gradual step down cessation of PPI will prevent this clinical relevant event. By measuring alkaline tide after PPI cessation we may prove this hypothesis.
UR - http://www.scopus.com/inward/record.url?scp=80051817299&partnerID=8YFLogxK
U2 - 10.1016/j.mehy.2011.06.007
DO - 10.1016/j.mehy.2011.06.007
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C2 - 21723045
AN - SCOPUS:80051817299
SN - 0306-9877
VL - 77
SP - 451
EP - 452
JO - Medical Hypotheses
JF - Medical Hypotheses
IS - 3
ER -