OBJECTIVES: Dyspeptic symptoms frequently recur rapidly after withdrawal of H2 antagonists, and this might be related to rebound acid hypersecretion. We have studied this phenomenon in healthy volunteers with and without Helicobacter pylori infection. METHODS: Basal and gastrin-releasing peptide (GRP) (40 pmol/kg/h) stimulated acid output, and gastrin concentration were measured in 18 healthy volunteers (nine were H. pylori positive). Studies were performed before and at 60 h and 10 days after completion of a 60-day course of ranitidine 300 mg nocte. RESULTS: 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 pretreatment values by day 10 posttreatment. Their GRP-stimulated acid output increased by a median of 108% 2 days post ranitidine (p < 0.01) and remained slightly increased at day 10. In H. pylori-positive healthy volunteers, basal acid output increased by a median of 96% 2 days after ranitidine therapy ceased (p < 0.01) and returned to pretreatment values by day 10 posttreatment. Their GRP-stimulated acid output also increased by a median of 56% 2 days posttreatment and returned to pretreatment values by day 10. The increase in acid output both basal and in response to GRP was not accompanied by any rise in gastrin concentration in either the H. pylori-positive or -negative subjects. CONCLUSIONS: Ranitidine therapy is associated with marked rebound hypersecretion of acid, and this may contribute to rapid resurgence of symptoms after therapy has been discontinued.
OBJECTIVES: Dyspeptic symptoms frequently recur rapidly after withdrawal of H2 antagonists, and this might be related to rebound acid hypersecretion. We have studied this phenomenon in healthy volunteers with and without Helicobacter pylori infection. METHODS: Basal and gastrin-releasing peptide (GRP) (40 pmol/kg/h) stimulated acid output, and gastrin concentration were measured in 18 healthy volunteers (nine were H. pylori positive). Studies were performed before and at 60 h and 10 days after completion of a 60-day course of ranitidine 300 mg nocte. RESULTS: 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 pretreatment values by day 10 posttreatment. Their GRP-stimulated acid output increased by a median of 108% 2 days post ranitidine (p < 0.01) and remained slightly increased at day 10. In H. pylori-positive healthy volunteers, basal acid output increased by a median of 96% 2 days after ranitidine therapy ceased (p < 0.01) and returned to pretreatment values by day 10 posttreatment. Their GRP-stimulated acid output also increased by a median of 56% 2 days posttreatment and returned to pretreatment values by day 10. The increase in acid output both basal and in response to GRP was not accompanied by any rise in gastrin concentration in either the H. pylori-positive or -negative subjects. CONCLUSIONS:Ranitidine therapy is associated with marked rebound hypersecretion of acid, and this may contribute to rapid resurgence of symptoms after therapy has been discontinued.