REPLY
Omeprazole Therapy in Resistant Reflux Disease
Elly Klinkenberg-Knol;
Stephan Meuwissen; and
Henk Festen
1 February 1995 | Volume 122 Issue 3 | Pages 236-237
IN RESPONSE:
Drs. Waldum and Brenna express their concerns regarding omeprazole-induced hypergastrinemia. We have recommended continued follow-up of patients receiving long-term therapy with proton-pump inhibitors, particularly patients with high serum gastrin levels that showed enhanced progression toward atrophic gastritis. The significance of this finding remains unclear and requires further study. This follow-up strategy also applies to the risk for progression from hyperplasia to dysplasia of ECL cells.
Concerning the potential cause of food retention in patients with high gastrin levels, we have postulated that omeprazole might be responsible for the food retention caused by the decreased emptying rate of solid food in healthy volunteers [1-3]. Another explanation might be decreased antral motility [4] and delayed gastric emptying caused by elevated serum gastrin levels. Vagal nerve damage might also be among the factors causing delayed gastric emptying in some of our patients.
Drs. Wright and Sarich suggest that the severe hypergastrinemia observed in 10 of 91 patients receiving long-term omeprazole therapy might be caused by a difference in metabolism of the drug. If their hypothesis is correct, a lower dose of omeprazole should be needed in these patients to achieve remission. However, we did not observe a decreased need for the drug. In contrast, these patients experienced frequent recurrences during maintenance treatment with omeprazole (20 mg/d or 40 mg/d). In our opinion, the main cause of this severe hypergastrinemia is delayed gastric emptying.
Profound acid inhibition may interfere with the absorption of certain nutrients such as iron and cobalamin [5]. However, although the resorption of protein-bound cobalamin was found to decrease during omeprazole treatment, no changes in serum cobalamin levels were detected during continuous maintenance therapy that lasted as long as 4 years [5]. Similarly, no changes in several other metabolic measurements were found during long-term treatment.
We agree that conscientious behavior by physicians in prescribing proton-pump inhibitors, particularly in young patients, is still required.
1. Klinkenberg-Knol EC. Recent Advances in the Diagnosis and Management of Gastro-oesophageal Reflux Disease. Amsterdam: VU University Press; 1990.
2. Hongo M, Lin YF, Ugiie H, Okumo Y, Yamada M, Satake K, et al. Acid suppression by omeprazole inhibits gastric emptying in normal subjects (Abstract). Gastroenterology. 1989; 96:A218.
3. Rasmussen L, ster-Jorgensen E, Qvist N, Kvaglund K, Houendal C, Pederson SA. A double-blind placebo-controlled trial of omeprazole on characteristics of gastric emptying in healthy subjects. Aliment Pharmacol Therap. 1991; 5:85-9.
4. Dooley CP, Miranda M, Valenzuela JE. Comparative effect of gastrin on hydrogen ion secretion, antroduodenal motility and the interdigestive motility complex in man. Dig Dis Sci. 1984; 29:714-20.
5. Festen H, Klinkenberg-Knol EC, Kuipers E, Lamers C, Jansen J, Biemond I, et al. Cobalamin absorption during omeprazole treatment: short and long-term studies (Abstract). Gastroenterology. 1993; 104:A77.
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