Attempts have long been made to use the prostigmine-morphine provocation test for the selection of postcholecystectomy patients suffering from sphincter of Oddi (SO) dyskinesia. Since the whole procedure is based upon the evaluation of subjective complaints, this test has frequently been criticized. To improve the diagnostic value of this method, we have visualized SO spasms during prostigmine-morphine provocation by means of quantitative hepatobiliary scintigraphy (QHBS). Twenty-two cholecystectomized patients with typical postprandial biliary pain were included in this study. In the first series of studies, QHBS with technetium-99m 2,6-diethylphenylcarbamoylmethyl-diacetic acid was performed in each patient 2 days before prostigmine-morphine provocation. The time to peak activity (Tmax) and the half-time of excretion (T1/2) over the liver parenchyma (LP), hepatic hilum (HH) and common bile duct (CBD), and the duodenum appearance time (DAT), were determined and served as control values. In the second series of experiments, sphincter spasms were evoked by prostigmine-morphine administration and visualized by means of QHBS. The same parameters were evaluated and serum levels of aspartate aminotransferase (AST) were determined simultaneously at regular intervals. In 12 patients who responded to prostigmine-morphine provocation with typical biliary pain and a significant AST elevation (Nardi positive group) the hepatobiliary scintigram demonstrated a marked biliary obstruction. Tmax and T1/2 over the LP, HH and CBD were significantly increased, while DAT was significantly longer relative to the corresponding data obtained without provocation. Four of the remaining ten patients indicated atypical abdominal pain during prostigmine-morphine provocation, but the AST level remained unchanged in all ten (Nardi negative group).(ABSTRACT TRUNCATED AT 250 WORDS)

This study was performed to evaluate the gallbladder motility in long-standing diabetes mellitus. The gallbladder function of diabetic patients was measured by means of quantitative hepatobiliary scintigraphy, and the severity of the associated autonomic and sensory polyneuropathy was determined. The presence of a marked gallbladder hypomotility was established, and a positive correlation was observed between the severity of the autonomic disturbance and the contractile disorder. This study underlines the important role of the neuropathy in the development of gallbladder hypomotility accompanying long-term diabetes mellitus.

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Recurrent biliary pain after cholecystectomy is presumably due to sphincter of Oddi dysfunction (SOD). There is no ideal non-invasive test for SOD, and the diagnosis often relies on invasive procedures such as sphincter of Oddi (SO) manometry. Amyl nitrite-augmented quantitative hepatobiliary scintigraphy (QHBS) was performed on nine asymptomatic volunteers and 22 patients with SOD of biliary types I and II. Normal QHBS parameters were established in the asymptomatic volunteers. QHBS revealed a partial obstructive pattern in nine patients in whom SO stenosis was suspected and in 13 patients in whom SO dyskinesia was suspected. This obstructive pattern remained unchanged in the former group, but was completely relieved in the latter group of patients on amyl nitrite administration. In conclusion, amyl nitrite-augmented QHBS proved to be a useful non-invasive method in the diagnosis of SOD of biliary types I and II and permitted differentiation between organic stenosis and functional motor abnormalities of the SO.

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