Gallbladder hypomotility in diabetic polyneuropathy.

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.

The effects of somatostatin and octreotide on the human sphincter of Oddi.

OBJECTIVE: Somatostatin acts at different sites in the human gastrointestinal tract and generally inhibits the release and effects of many gastrointestinal hormones and neuropeptides. Together with its long-acting analogue octreotide, somatostatin is widely used in the treatment of hormone-producing tumours, variceal bleeding, etc., but multi-centre trials have failed to prove a beneficial effect in the treatment of acute pancreatitis or in the prevention of post-ERCP pancreatitis (pancreatitis following endoscopic retrograde cholangiopancreatography). The aim of the present work was to study the effects of somatostatin and octreotide on the human sphincter of Oddi by means of quantitative hepatobiliary scintigraphy (QHBS). METHOD: Fifteen cholecystectomized patients were enrolled in the study, six in the somatostatin group and nine in the octreotide group. QHBS was performed initially with a standard protocol (baseline data), then repeated after 0.1 mg octreotide or a 250 microg bolus + 250 microg/h somatostatin administration. In the 60th min of QHBS, 0.5 mg glyceryl trinitrate (GTN) was administered sublingually. RESULTS: QHBS demonstrated that both somatostatin and octreotide caused a marked impairment in the bile flow: the half-time of excretion (T1/2) over the common bile duct was significantly prolonged compared with baseline data (somatostatin group: common bile duct T1/2 180 min versus 59.7+/-31 min; octreotide group: common bile duct T1/2 140.9+/-60.5 min versus 30.7+/-11.7 min). Glyceryl trinitrate administration accelerated the transpapillary bile flow, with significant decreases in the elevated T1/2 in both groups. CONCLUSION: Increased transpapillary flow induced by glyceryl trinitrate may be beneficial in the treatment of acute or post-ERCP pancreatitis.

Humoral mechanisms and clinical aspects of biliary tract motility.

This review is intended to summarize current information on neurohumoral regulation of the gallbladder and sphincter of Oddi motility under both physiological and pathological circumstances with emphasis on Hungarian contributions to today's knowledge. The mechanism of action of neurohumoral agents that interact on these segments of the biliary tract, and the explored details of the stimulation-contraction/relaxation coupling process of these substances, will be discussed. A modified classification of biliary tract motility disorders with new diagnostic and therapeutic approaches will also be provided. This information will aid understanding of the pathogenesis of motor disorders of the gallbladder and sphincter of Oddi, and will indicate possibilities for pharmacological exploitation in the treatment of diseases resulting from biliary tract motility abnormalities.

[Gallbladder hypomotility in diabetic polyneuropathy]. / Epehólyag-hypomotilitas diabeteses polyneuropathiában.

A study was made of the pathogenic role of gallbladder hypomotility, which is presumably responsible for the high incidence of gallstone disease in long-standing diabetes mellitus. The gallbladder motility of diabetic patients (n = 10) was measured by means of quantitative hepatobiliary scintigraphy, and the severity of concomitant autonomic and sensory polyneuropathy was determined. The presence of marked gallbladder hypomotility was proven, and a positive correlation was observed between the severity of autonomic neuropathy and the contractile disorder. In this group of diabetic patients, a hypaesthetic sensory polyneuropathy too was recognized, the degree of which exhibited a positive correlation with the autonomic neuropathy score. This study underlines the important role of the autonomic neural dysfunction in the development of gallbladder hypomotility accompanying long-term diabetes mellitus.

Beneficial effect of lovastatin on sphincter of Oddi dyskinesia in hypercholesterolemia and hypertriglyceridemia.

This report describes an impaired sphincter of Oddi relaxation function in relation to hypercholesterolemia and hypertriglyceridemia. As indicated by repetitive amyl nitrite-augmented quantitative hepatobiliary scintgraphy, normalization of serum lipids by means of diet and a 3-month treatment period with 20 mg of lovastatin per day resulted in an improvement of sphincter of Oddi relaxation.

Effect of glyceryl trinitrate on the sphincter of Oddi spasm evoked by prostigmine-morphine administration.

OBJECTIVE: In this study the effect of glyceryl trinitrate on the prostigmine-morphine-induced sphincter of Oddi spasm was evaluated in nine female patients with sphincter of Oddi dyskinesia. METHOD: Sphincter of Oddi spasm was induced by prostigmine-morphine administration (0.5 mg prostigmine intramuscularly and 10 mg morphine subcutaneously) and visualized by quantitative hepatobiliary scintigraphy. The entire procedure was repeated during glyceryl trinitrate infusion (Nitrolingual 1 microg/kg/min for 120 min). RESULTS: Prostigmine-morphine provocation caused significant increases in the time to peak activity (Tmax) over the hepatic hilum (HH: 34.33 +/- 5.05 vs. 22.77 +/- 3.26) and the common bile duct (CBD: 60.44 +/- 5.99 vs. 40.0 +/- 2.88) and in the half-time of excretion (T1/2) over the liver parenchyma (LP: 120.04 +/- 16.01 vs. 27.37 +/- 2.19), HH (117.61 +/- 14.71 vs. 31.85 +/- 3.99) and CBD (158.11 +/- 9.18 vs. 40.1 +/- 6.24), indicating a complete spasm at the level of the sphincter of Oddi. Glyceryl trinitrate infusion completely normalized the prostigmine-morphine-induced alterations in these quantitative parameters (TmaX over the LP: 11.33 +/- 1.13; over the HH: 18.88 +/- 1.48; and over the CBD: 36.22 +/- 1.92; and T1/2 over the LP: 28.21 +/- 1.83; over the HH: 33.42 +/- 3.10; and over the CBD: 41.66 +/- 6.33), suggesting an effective sphincter-relaxing effect of glyceryl trinitrate. CONCLUSION: These results provide the first evidence of the effectiveness of glyceryl trinitrate on the morphine-induced sphincter of Oddi spasm in humans. Since glyceryl trinitrate is able to overcome even the drastic effect of morphine, it might be of relevance in the treatment of sphincter of Oddi dyskinesia.

Evaluation of results of the prostigmine-morphine test with quantitative hepatobiliary scintigraphy: a new method for the diagnosis of sphincter of Oddi dyskinesia.

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)

Differentiation between organic stenosis and functional dyskinesia of the sphincter of Oddi with amyl nitrite-augmented quantitative hepatobiliary scintigraphy.

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.

[Diagnosis of Verner-Morrison syndrome (VDHA) and its treatment with sandostatin an streptozocitin]. / Verner-Morrison (WDHA) szindróma diagnózisa és kezelése Sandostatin és streptozotocin adagolással.

A case report is presented of a man with Verner-Morrison syndrome of extreme severity, caused by an unresectable pancreatic VIPoma. The pathological role of vasoactive intestinal polypeptide (VIP) is discussed in the pathogenesis of Watery Diarrhoea, Hypokalaemia, Achlorhydria (WDHA) syndrome. The authors describe the typical symptoms of the syndrome and provide a diagnostic and therapeutic strategy. Plasma level of VIP was determined by the authors' own VIP RIA method. Administration of a long acting somatostatin analogue, octreotide (Sandostatin, Sandoz) at a dose of 100 micrograms daily, decreased the plasma level of VIP from about 55 to 38 fmol/ml, which was associated with complete regression of the diarrhoea. Due to the 'escape phenomenon' the dose of Sandostatin was gradually increased and finally completed with streptozotocin (Zanosar, Upjohn) administration, which was repeated every 8 weeks. The combination of Sandostatin and streptozotocin resulted in complete regression of diarrhoea and substantial diminution of the tumour mass. The patient displayed a weight gain and returned to normal life.