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The control of gastric acid and Helicobacter pylori eradication
Author(s) -
Sachs G.,
Shin J. M.,
Munson K.,
Vagin O.,
Lambrecht N.,
Scott D. R.,
Weeks D. L.,
Melchers K.
Publication year - 2000
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.2000.00837.x
Subject(s) - urease , helicobacter pylori , urea , gastric acid , periplasmic space , proton pump inhibitor , secretion , peptic ulcer , peptic , gastroenterology , medicine , biochemistry , pathogen , urea breath test , microbiology and biotechnology , helicobacter infections , rapid urease test , chemistry , gastritis , biology , gene , helicobacter pylori infection , escherichia coli
This review focuses on the gastric acid pump as a therapeutic target for the control of acid secretion in peptic ulcer and gastro‐oesophageal reflux disease. The mechanism of the proton pump inhibitors is discussed as well as their clinical use. The biology of Helicobacter pylori as a gastric denizen is then discussed, with special regard to its mechanisms of acid resistance. Here the properties of the products of the urease gene clusters, ureA, B and ureI, E, F, G and H are explored in order to explain the unique location of this pathogen. The dominant requirement for acid resistance is the presence of a proton gated urea transporter, UreI, which increases access of gastric juice urea to the intrabacterial urease 300‐fold. This enables rapid and continuous buffering of the bacterial periplasm to ≈ pH 6.0, allowing acid resistance and growth at acidic pH in the presence of 1 m M urea. A hypothesis for the basis of combination therapy for eradication is also presented.