ABSTRACT
OBJECTIVES: As our understanding of the pathophysiology of sphincter of Oddi dysfunction (SOD) expands, new avenues arise for pharmacological intervention. Recent evidence suggests that SOD results from a loss of myenteric plexus inhibitory neurons resulting in unopposed cholinergic tone. Octreotide inhibits postganglionic cholinergic neurons, and thus we hypothesize that administration of octreotide will decrease sphincteric pressure in individuals with SOD. METHODS: Thirty-eight patients presenting with recurrent abdominal pain and SOD (basal pressure > 40 mm Hg) were studied. The study was prospective, placebo controlled, and blinded. Patient allocation was consecutive. Sphincter of Oddi manometry was performed in standard fashion. The test group (n = 19) received octreotide acetate (100 microg i.v.), and the control group (n = 19) received i.v. saline. Basal, phasic, and duct pressures as well as phasic amplitude and frequency were recorded before and 3 min after the i.v. infusion. Changes in these parameters before and after i.v. infusions were compared. RESULTS: Octreotide caused a statistically significant reduction in peak and basal sphincter of Oddi pressures relative to saline (p < 0.01 and p < 0.001). Octreotide did not significantly affect wave amplitude, wave frequency, or duct pressure. CONCLUSIONS: Octreotide has the potential to be a valuable addition to the armamentarium for the medical management of SOD.
