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Biomedical subjects

B Velösy

Publications and source records attributed to B Velösy.

8 recordsLinked to original sources
PubMed2001

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.

Autonomic Nervous System↗
PubMed1998

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.

Animals↗
PubMed1997

[Gallbladder hypomotility in diabetic polyneuropathy].

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.

Diabetes Mellitus, Type 1↗
PubMed1997

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.

Aged↗
PubMed1995

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)

Adult↗
PubMed1994

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.

Adult↗
PubMed1993

[Diagnosis of Verner-Morrison syndrome (VDHA) and its treatment with sandostatin an streptozocitin].

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.

Humans↗