INTRODUCTIONThe causes of post-cholecystectomy pain are still a matter of debate. Some authors have attributed this pain to sphincter of Oddi (SO) dysfunction, which is also called biliary dyskinesia. 1±3 The frequency of SO dysfunction associated with post-cholecystectomy pain widely ranges from 14 to 79%. 4,5 Endoscopic biliary sphincterotomy is currently performed as part of the management of biliary dyskinesia 2, 6±8 despite an initial management involving surgical sphincterotomy. 9 In a prospective blind study, Geenen et al. obtained either an improvement or complete relief of post-cholecystectomy pain in 91% of patients presenting with SO dysfunction diagnosed on the basis of an increased basal SO pressure as determined manometrically.8 However, morbidity and mortality after endoscopic biliary sphincterotomy are not negligible and have been reported as high as 9.8% and 2.3%, respectively, in a recent large study. 10 SUMMARYBackground: Trimebutine is an opiate modulator of the gastrointestinal motility that interacts with enkephalinergic receptors. Aim: To evaluate the effects of trimebutine (50 mg intravenous injection) on the motility of the sphincter of Oddi (SO) as assessed by endoscopic manometry. Methods: Endoscopic manometry was performed on 15 cholecystectomized patients who presented with symptoms suggestive of SO dysfunction. Prior to the endoscopic manometry, endoscopic ultrasonography was performed in order to rule out the possible presence of a bile duct stone. Results: Injecting trimebutine resulted in a signi®cant increase in the SO antegrade phasic contraction rate (P 0.02). Trimebutine decreased the basal pressure of the SO (32.5 vs. 27.5 mmHg), but the difference is not statistically signi®cant (P 0.11). The effects of trimebutine differed depending on the basal SO motility

No abstract