Citric acid-enhanced Helicobacter pylori urease activity in vivo is unrelated to gastric emptying

Authors


Dr D. Y. Graham, Veterans Affairs Medical Center (111D), 2002 Holcombe Blvd., Houston, TX 77030, USA. E-mail: dgraham@bcm.tmc.edu

Abstract

Background:

In a previous study, the use of a citric acid test meal produced a rapid dose-dependent increase in urease activity that was significantly greater than that resulting from a pudding meal, ascorbic acid or sodium citrate. The mechanism was hypothesized to be related to the ability of citric acid to delay gastric emptying and possibly to enhance intragastric distribution of the urea.

Objective:

To compare the effects of sodium citrate, two doses of citric acid and a pudding meal on gastric motor function.

Method:

Eleven normal healthy volunteers were investigated using non-invasive techniques to measure gastric emptying and gastric motility. We evaluated gastric emptying using the Meretek 13Ceebiscuit solid phase gastric emptying breath test, which employs a 340-calorie biscuit containing 200 mg of the edible 13C-blue–green alga Spirulina platensis, after the administration of test meals of pudding, 2 g and 4 g of citric acid and 2 g of sodium citrate. Electrogastrograms (Digitrapper EGG) were also recorded for 30 min before and 180 min after the test meal.

Results:

Gastric emptying, as assessed by the half-time (T1/2), was delayed similarly with the pudding (136.8 ± 9 min) and with 4 g of citric acid (144.5 ± 7 min) (> 0.7). Sodium citrate (108.7 ± 6 min) and 2 g of citric acid (110.1 ± 6 min) had similar effects on gastric emptying (P=0.986), and were significantly less effective in delaying gastric emptying (< 0.01) compared to pudding or 4 g of citric acid. The electrogastrograms remained normal and there were no differences among meals and no relation with the gastric emptying results.

Conclusions:

The increased intragastric urea hydrolysis associated with citric acid test meals cannot be attributed to delayed gastric emptying. Changes in the intragastric distribution of urea or a direct effect of citric acid on the bacteria (e.g. via the cytoplasmic protein, UreI) are more likely to be responsible.

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