M. Barthet et al., EFFECTS OF TRIMEBUTINE ON SPHINCTER OF ODDI MOBILITY IN PATIENTS WITHPOSTCHOLECYSTECTOMY PAIN, Alimentary pharmacology & therapeutics, 12(7), 1998, pp. 647-652
Background: Trimebutine is an opiate modulator of the gastrointestinal
motility that interacts with enkephalinergic receptors. Aim: To evalu
ate the effects of trimebutine (50 mg intravenous injection) on the mo
tility of the sphincter of Oddi (SO) as assessed by endoscopic manomet
ry. Methods: Endoscopic manometry was performed on 15 cholecystectomiz
ed patients who presented with symptoms suggestive of SO dysfunction.
Prior to the endoscopic manometry, endoscopic ultrasonography was perf
ormed in order to rule out the possible presence of a bile duct stone.
Results: Injecting trimebutine resulted in a significant increase in
the SO antegrade phasic contraction rate (P = 0.02). Trimebutine decre
ased the basal pressure of the SO (32.5 vs. 27.5 mmHg), but the differ
ence is not statistically significant (P = 0.11). The effects of trime
butine differed depending on the basal SO motility anomalies involved,
but the period of latency was similar (mean 89 s; range 30-240 s). Th
e basal anomalies were an increased basal SO pressure of > 40 mmHg in
three patients, a tachyoddia (frequency of phasic contractions (PC)> 1
0/min) in six patients, prolonged PC (> 10 s) in two patients and an a
bsence of phasic contraction in one patient. The basal pressure of the
SO decreased in the three patients presenting with SO hyperpressure,
but returned to a normal value in one case. The frequency of the PC de
creased to normal in three out of the six patients with tachyoddia. Th
e duration of the PC returned to normal in the two patients with prolo
nged PC whereas their frequencies increased. Prolonged PC developed in
the patient without any detectable phasic contraction. Conclusions: T
rimebutine modulates SO motility in various ways depending on the basa
l SO motility anomaly observed after cholecystectomy. This regulatory
effect suggests the existence of encephalinergic control of SO motilit
y.