In patients with clinically uncertain herniations, MRI is a valid diagnostic tool with a high positive predictive value.

A study was performed to find and test quantitative methods of analysing echographic signals for the differentiation of diffuse liver diseases. An on-line data acquisition system was used to acquire radiofrequency (RF) echo signals from volunteers and patients. Several methods to estimate the frequency-dependent attenuation coefficient were evaluated, in which a correction for the frequency and depth-dependent diffraction and focusing effects caused by the sound beam was applied. Using the estimated value of the attenuation coefficient the RF signals themselves were corrected to remove the depth dependencies caused by the sound beam and by the frequency-dependent attenuation. After this preprocessing the envelope of the corrected RF signals was calculated and B-mode images were reconstructed. The texture was analysed in the axial direction by first- and second-order statistical methods. The accuracy and precision of the attenuation methods were assessed by using computer simulated RF signals and RF data obtained from a tissue-mimicking phantom. The phantom measurements were also used to test the performance of the methods to correct for the depth dependencies. The echograms of 163 persons, both volunteers and patients suffering from a diffuse liver disease (cirrhosis, hepatitis, haemochromatosis), were recorded. The mutual correlations between the estimated parameters were used to preselect parameters contributing independent information, and which can subsequently be used in a discriminant analysis to differentiate between the various diseased conditions.

The present study was undertaken to compare the effects of equimolar amounts of long-chain triglycerides (LCT) and medium-chain triglycerides (MCT) on plasma cholecystokinin (CCK) concentrations and gallbladder contraction in man. On separate mornings and in random order six healthy volunteers ingested either 60 mmol LCT or 60 mmol MCT. Plasma CCK concentrations were measured by a sensitive and specific radioimmunoassay and gallbladder contraction by ultrasonography. Ingestion of LCT induced significant increases in plasma CCK from 2.8 +/- 0.5 to 6.5 +/- 0.7 pmol/l (p less than 0.005) and decreases in gallbladder volume from 33.4 +/- 5.9 to 13.2 +/- 4.2 cm3 (p less than 0.005). On the other hand, no significant changes in plasma CCK and gallbladder volume were found after MCT. Ingestion of MCT was followed by abdominal cramps and diarrhea, while LCT were without side effects. It is concluded that, in contrast to LCT, MCT do not induce CCK release and gallbladder contraction.

A computerized method that requires only 1-2 minutes to quantify gallbladder volume from real-time sonograms is described. This time is considerably shorter than that required using the hand-calculation method. There was a highly significant correlation between gallbladder volumes calculated by computer and hand (r = 0.97; P less than .001).

The diagnostic accuracy of Doppler ultrasound in the detection of renal arterial disease has been assessed in a prospective study of 61 hypertensive patients. The findings of Doppler ultrasound were compared with the results of renal angiography. In 15 patients (24.5%) no accurate Doppler signs could be obtained and the Doppler ultrasound examination was considered a technical failure. Of the remaining 46 patients, 24 had renal artery stenosis. Nine of the stenoses were not detected by Doppler ultrasound and in three patients a false positive diagnosis of renal artery stenosis was made. The sensitivity of Doppler ultrasound was 62.5%, the specificity 86.4% and the overall diagnostic accuracy was 73.9%. By comparing the 15 patients in whom Doppler ultrasound failed with the 46 in whom it was successful, age appeared to be higher and creatinine clearance lower in the failure group. By comparing the 34 patients with true positive and true negative results with the 12 patients with false results, no significant differences were found. In a multivariate analysis, higher age showed a significant relation to failure of Doppler ultrasound. Doppler ultrasound has limited value in the screening of hypertensive patients for renal artery stenosis.

To determine the role of cholecystokinin and the cholinergic system in cephalic stimulation of gallbladder contraction and to compare the degree of gallbladder contraction by cephalic stimulation with postprandial gallbladder contraction, 8 healthy volunteers (4 males, 4 females, 20–65 years) underwent the following studies: sham feeding of an appetizing meal, sham feeding with intravenous atropine, and ingestion of the same meal. Gallbladder volume was measured by real-time ultrasonography and plasma cholecystokinin by a sensitive and specific radioimmunoassay using antibody T204. Gallbladder contraction in response to sham feeding, 30 ± 4% (p = 0.0001 vs. basal), amounted to half of that seen after real feeding, 69 ± 5% (p < 0.0001 vs. basal). Significant dissociation between gallbladder response to sham feeding and real feeding was seen from 40 min (p < 0.005-p = 0.0001). Atropine did not affect basal gallbladder volume but completely abolished gallbladder contraction in response to sham feeding. Neither sham feeding without nor sham feeding with atropine significantly affected plasma cholecystokinin levels. On the other hand, real feeding induced significant increases in plasma cholecystokinin from a basal level of 2.3 ± 0.1 pM to a peak value of 5.9 ± 0.4 pM at 40 min. It is concluded that an important cephalic phase of postprandial gallbladder contraction exists which is cholecystokinin-independent but dependent on a cholinergic mechanism.

The effects on gallbladder motility of long term treatment with the somatostatin analog SMS 201-995 (SMS) were studied in five patients with acromegaly treated for 6-32 months with 200-300 micrograms SMS daily. SMS (100 micrograms) or placebo was injected sc 45 min before a standard breakfast. Gallbladder volume (ultrasonography), plasma cholecystokinin (CCK), and pancreatic polypeptide (PP) were measured until 120 min after the meal. SMS completely suppressed the postprandial gallbladder contraction, despite a blunted, though still statistically significant, increase in plasma CCK from 1.6 +/- 0.2 pmol/L to an average of 3.7 +/- 1.7 pmol/L (P less than 0.01). The postprandial plasma PP peak after placebo was replaced by a slight but statistically significant decrease after SMS (P less than 0.05). A statistically significant correlation between the plasma CCK values and corresponding gallbladder volumes was seen only after placebo injection, not in the SMS study. We conclude that during long term treatment of acromegalics with SMS, an injection of 100 micrograms, sc, completely abolishes gallbladder contraction for at least 2 h after a standard breakfast, despite blunted, but still significant, CCK release. The data suggest a decreased sensitivity of the gallbladder to endogenous CCK during long term treatment with SMS. Careful control of patients with respect to the formation of gallstones is recommended.

effects of loperamide on pancreaticobiliary functions are Loperamide, a peripherally acting opiate receptor agonist poorly investigated. Inhibition of gallbladder emptying or with antidiarrheal action, inhibits ileal and colonic motor pancreatic enzyme secretion by loperamide may have imfunction. It was determined whether loperamide also affects portant clinical implications because stasis of bile is a major gallbladder emptying and pancreatic enzyme secretion in hufactor contributing to the formation of gallstones 6-10 and bemans. Plasma cholecystokinin (radioimmunoassay), gallbladcause impairment of pancreatic enzyme secretion may induce der volume (ultrasonography), and intraduodenal bilirubin or aggravate maldigestion. 11-13 and amylase output (spot sampling) were measured at regularThe aim of this study, therefore, was to determine the intervals before and during intraduodenal perfusion of an effect of loperamide on basal and meal-stimulated gallbladder amino acid meal in 8 healthy subjects: once without and once motility and pancreatic enzyme secretion in healthy volunwith pretreatment of 8 mg loperamide, ingested 13 and 4 teers. Gallbladder emptying and pancreatic enzyme secretion hours before the start of the meal. Loperamide decreased were studied in response to an intraduodenal amino acid basal amylase output from 3.2 { 0.5 to 1.0 { 0.5 kU/h meal to circumvent possible influences of loperamide on gas-(P õ .005) and abolished basal bilirubin output (21 { 5 vs.tric emptying or on the digestion of nutrients. 14 0 { 0 mmol/h; P õ .005) into the duodenum. Loperamide increased basal gallbladder volume from 28 { 4 to 39 { 4 PATIENTS AND METHODS mL (P õ .0001) but was without effect on basal plasma cholecystokinin (2.7 { 0.3 vs. 3.0 { 0.3 pmol/L). During Subjects. Eight healthy volunteers (3 women and 5 men; age the amino acid meal, pretreatment with loperamide inhibited range, 19-27 years) participated in the studies. None of the volunamylase output from 5.1 { 0.8 to 1.6 { 0.4 kU/h (P õ .001), teers was taking any medication or had a history of gastrointestinal bilirubin output from 39 { 6 to 18 { 6 mmol/h (P õ .0005) symptoms or surgery. The study protocol was approved by the and gallbladder contraction from 47% { 3% to 26% { 6% ethical committee of the University Hospital Nijmegen, and all sub-(P õ .05), whereas loperamide enhanced amino acid-stimu-jects gave their written informed consent before entering the study.