MARKED REBOUND ACID HYPERSECRETION AFTER TREATMENT WITH RANITIDINE

Objectives: Dyspeptic symptoms frequently recur rapidly after withdraw al of H2 antagonists, and this might be related to rebound acid hypers ecretion. We have studied this phenomenon in healthy volunteers with a nd without Helicobacter pylori infection. Methods: Basal and gastrin-r eleasing peptide (GRP) (40 pmol/kg/h) stimulated acid output, and gast rin concentration were measured in 18 healthy volunteers (nine were H. pylori positive). Studies were performed before and at 60 h and 10 da ys after completion of a 60-day course of ranitidine 300 mg nocte. Res ults: In the H. pylori-negative healthy volunteers, basal acid output increased by a median of 137% 2 days after stopping ranitidine therapy compared with pretreatment values (p < 0.01) and returned to pretreat ment values by day 10 posttreatment. Their GRP-stimulated acid output increased by a median of 108% 2 days post ranitidine (p < 0.01) and re mained slightly increased at day 10. In H. pylori-positive healthy vol unteers, basal acid output increased by a median of 96% 2 days after r anitidine therapy ceased (p < 0.01) and returned to pretreatment value s by day 10 posttreatment. Their GRP-stimulated acid output also incre ased by a median of 56% 2 days posttreatment and returned to pretreatm ent values by day 10. The increase in acid output both basally and in response to GRP was not accompanied by any rise in gastrin concentrati on in either the N. pylori-positive or -negative subjects. Conclusion: Ranitidine therapy is associated with marked rebound hypersecretion o f acid, and this may contribute to rapid resurgence of symptoms after therapy has been discontinued.