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LETTER

Omeprazole, Serum Gastrin, and Gastric Acid Suppression

right arrow R. Matthew Gideon; Vera Paoletti; and Donald O. Castell

1 February 1995 | Volume 122 Issue 3 | Pages 237-238


TO THE EDITOR:

It is well known that the decrease in gastric activity caused by omeprazole results in increased serum gastrin levels. We asked whether a precise relation exists between fasting serum gastrin levels and gastric acid suppression in patients receiving omeprazole. If such a relation exists, physicians could obtain fasting serum gastrin levels from their patients receiving omeprazole as a simple measure of the degree of gastric acid suppression. We used ambulatory intragastric pH monitoring to assess gastric acid suppression in 45 patients with gastroesophageal reflux who were receiving different doses of omeprazole. The pH probe was placed with the antimony electrode in the gastric fundus, 10 cm below the manometrically located lower esophageal sphincter. Monitoring was accomplished using a battery-powered Mark 3 Digitrapper (Synetics Medical, Inc., Irving, Texas). Serum gastrin was drawn after an overnight fast, immediately after placement of the pH probe, and at the start of 24-hour monitoring.

Figure 1 shows the relation between the total percentage of the time intragastric pH remained less than 4.0 over the entire 24-hour period and fasting serum gastrin levels, obtained on the testing day and expressed in pg/mL for patients receiving daily omeprazole doses of 20, 40, and 80 mg. Regression analysis shows a poor correlation (r = 0.04) when the collective fasting serum gastrin levels are compared with the total percentage of time the intragastric pH remained less than 4.0 in the 45 patients receiving omeprazole therapy. Many patients receiving various omeprazole doses had fasting gastrin values in the normal range (<100 pg/mL).



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Figure 1. Relation between the percentage of time intragastric pH remained below 4.0 compared with fasting serum gastrin levels during a 24-hour period in patients receiving various doses of omeprazole. {square} = 20 mg; {triangleup} = 40 mg; {circ} = 80 mg.

 

To determine whether this relation was affected by the omeprazole dose, we also compared the fasting serum gastrin level with the total percentage of time the intragastric pH remained less than 4.0 on individual doses. A poor correlation was consistently found at all dose levels.

We conclude that serum gastrin levels do not reliably predict the degree of gastric acid suppression in patients receiving omeprazole.


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The Graduate Hospital, Philadelphia, PA 19146.

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