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In prospective trials in patients with malignant biliary obstruction, it has been reported that Wallstents prolong stent patency, but this does not translate into a significant survival benefit. Compared with prospective trials, however, survival may be different in clinical practice because of differences in patient compliance. We report on a retrospective, long term analysis comparing Wallstents versus plastic stents.Plastic endoprostheses (70 patients) and endoscopic Wallstents (95 patients) were placed in 165 consecutive patients with irresectable, malignant biliary obstruction in a first (1990-91) and second (1992-93) time period. Stent occlusion was treated by plastic stent placement.Patient characteristics were quite comparable in both stent groups. Initial placement of a Wallstent resulted in an increase of median stent patency of the first (10 vs 4 months, p0.001) and second (8 vs 3 months, p0.05) stent, a decrease of additional endoscopic procedures (20 vs 58%, p0.005), an increase of patient compliance reflected by a decrease of patients dying with untreated stent occlusion (9 vs 30%, p0.001), and an increase of survival time (6.5 vs 4 months, p0.05).Initial placement of a Wallstent results in an increase of stent patency of the first and second stent. Duration of stent patency appears to have a determinant effect on patient compliance. Increased stent patency and patient compliance seem to improve survival in clinical practice.

Background: Cholylsarcosine, the synthetic conjugate of cholic acid and sarcosine, is resistant to deconjugation-dehydroxylation during enterohepatic cycling in rodents and improves lipid absorption in a canine model of intestinal bile acid deficiency caused by distal intestinal resection. Experiments were performed to define its metabolism and effect on biliary secretion in humans. Methods: The circulating bile acid pool was labeled with [ 14 C]cholylsarcosine, and its turnover rate and biotransformation were determined by sampling bile daily. Cholylsarcosine (or cholyltaurine) was infused into the duodenum for 8 hours to define its effect on bile flow and biliary lipid secretion. Results: Cholylsarcosine was lost rapidly from the enterohepatic circulation with a t12 of 0.5 days. The compound was not biotransformed by hepatic or bacterial enzymes. Cholylsarcosine had choleretic activity similar to that of cholyltaurine but induced more phospholipid and cholesterol secretion than cholyltaurine in four of five subjects. Infusion of cholylsarcosine (or cholyltaurine) at a rate averaging 0.6 μmol · min −1 · kg −1 gave a biliary recovery of 0.2 μmol · min −1 · kg −1 ; this value is the T max for active ileal transport of conjugated bile acids in humans. Laboratory tests for liver injury remained within normal limits. Conclusions: In humans, cholylsarcosine is not metabolized, is nontoxic, and has similar effects on biliary secretion as cholyltaurine. It appears safe to test in long-term studies the effect of cholylsarcosine on bile acid-deficiency states in humans.

In a 28-day non-blinded study of 1071 patients with functional dyspeptic symptoms in a general practice setting, 666 presented with mainly typical symptoms of functional dyspepsia and received 5 mg cisapride three times daily, while 405 with predominating symptoms indicative of gastroesophageal reflux received 10 mg cisapride three times daily. On the basis of an anamnestic risk factor analysis for organic lesions, 'low-risk' patients were to be treated directly with cisapride, while for 'high-risk' patients a more thorough gastrointestinal examination was recommended before starting cisapride. Of patients in the dyspepsia group 75% reported a good or excellent response; the corresponding rate was 80% in the reflux group. Low-risk patients in both groups tended to respond better than high-risk patients (mean difference, 11%). Patients and investigators reached identical assessments of response. Concomitant antacids, calcium antagonists, beta-blockers and sedatives did not affect the results, but concomitant NSAIDs reduced the mean improvement rate by 14% (p0.01). Adverse effects such as abdominal cramps and loose stools were uncommon (or = 3.4%).

Risk assessment of recurrent variceal bleeding is essential for therapeutic decisions and is usually performed by endoscopy of the upper gastrointestinal tract. We studied the value of portal venous duplex sonography in predicting subsequent variceal bleeding in patients with cirrhosis.Thirty patients with cirrhosis who received sclerotherapy because of acute variceal hemorrhage for the first time (hemorrhage group), 30 patients with cirrhosis who had no previous hemorrhage (nonhemorrhage group), and 30 control subjects were examined prospectively. With the use of portal duplex and color Doppler sonography, flow direction, flow velocity, vein diameter, and response to respiration of portal vein vessels were measured and portosystemic collaterals and thrombosis of portal vessels were visualized. The results of these measurements and imaging findings were combined into a Doppler sonoscore. At entry into the study, all patients were classified on the basis of a sonoscore as having a low (sonoscore,4) or a high (sonoscore,or = 4) risk for subsequent hemorrhage. During a mean follow-up period of 2 years (range, 15-36 months), the predictive value of this Doppler sonoscore was studied.In the hemorrhage group, the prevalence of recurrent hemorrhage was 40%, despite sclerotherapy, and the mortality rate was 60%. In patients with a Doppler sonoscore of 4 or more, the prevalence of recurrent hemorrhage was 67%, whereas in patients with a score less than 4, the prevalence was only 22% (p.02). After sclerotherapy, endoscopic criteria showed no significant correlation with the prevalence of bleeding. In the nonhemorrhage group, the prevalence of variceal hemorrhage occurring was 13%, and Doppler sonographic criteria showed no significant correlation with the prevalence of subsequent hemorrhage.We conclude that Doppler sonography, performed after the first occurrence of variceal hemorrhage, provides useful prognostic information regarding the risk of recurrent hemorrhage. If these results are confirmed, Doppler sonography may be used to select the best method of treatment.

Controlled studies showed that cisapride is effective in non-ulcer dyspepsia. Its prokinetic properties are not complicated by dopamine inhibition. In our study the dose of 5 mg t.i.d. was adequate for the treatment of patients with gastric symptoms, while for patients with reflux symptoms the preferred dose is 10 mg t.i.d. cisapride. The average improvement after 1 month of treatment was 68%. Additional medication with antacids was not of benefit. Side effects such as abdominal cramps or diarrhea were minimal (less than 4%). 1071 patients were selected according to the principles described by Talley et al. in 1987. This method was well accepted by investigators and patients and is recommended for similar studies.

Aneurysms of the hepatic artery are rare and may present multiform clinical pictures. Prompt diagnosis is important because life threatening complications can be treated by relatively simple measures. A case of posttraumatic intrahepatic aneurysm of the hepatic artery with arterioportal fistula and successful transcatheter embolisation is reported. The present state of the art is outlined and indications for diagnosis and therapy are presented.

The stress ulcer formation is enhanced significantly in rats operated with pyloro-jejunostomy and Roux-en-Y anastomosis by taurocholic acid or a mixture of taurocholic and glycocholic acid. However, the incidence of stress ulcers is significantly reduced by adding lysolecithin to the drinking solution containing these bile acids in the same concentration, though lysolecithin alone induces significantly more stress ulcers than tap water in rats with the same operation submitted to immobilisation stress.

A case of chronic, lethal vitamin A intoxication is reported, the diagnosis of which was not established intra vitam. The patient presented with chronic mixed prehepatic and hepatic icterus and hypersplenism with hemolytic anemia. On post mortem histological examination, abundant deposits of neutral lipids in the reticuloendothelial cells of liver, spleen and bone marrow were found. Chemical analysis of the lipids extracted from these organs revealed esterified fatty acids. Triglycerides could be ruled out since the triglyceride content of the patient's liver was significantly lower than that of a normal control. By means of thinlayer chromatographic analysis it was possible to identify retinol, i.e. retinylester (vitamin A) in the deposits. Vitamin A was determined photometrically and found to be very elevated in the liver and, to a lesser degree, in the spleen of the patient. These findings lead to a definite diagnosis of chronic hypervitaminosis A. Unique features of the case presented are both hemolytic anemia and the lethal outcome of the chronic hypervitaminosis A.

We present an operation model in rats, which according to our opinion prevents duodenogastric reflux effectively. The duodenum is divided distally from the pylorus and a pyloro-jejunostomy performed combined with a Roux-en-Y anastomosis. Rats operated this way and submitted to restraint stress developed significantly less stress lesions than operated control under same conditions. However, operated rats submitted to the operation and offered a 5 mMol/l drinking solution of crude taurocholic acid during 20 days before submitted to stress had significantly more stress lesions than operated animals with tap water before restraint stress.

Cysteamine induces duodenal ulcers in rats, but bile diversion inhibits ulcer formation. Since lysolecithin inhibits stress ulceration in rats, it is assessed now whether lysolecithin inhibits cysteamine-induced ulcers, too. Male rats were operated: division of the duodenum distally to the pylorus, duodenojejunostomy. Roux-en-Y duodenojejunostomy. 4 groups comprising 10 animals. Drinking solution for group 1, 3 and 4: Na taurocholate and glycocholic acid (5 mmol/l). For group 2 addition of 0.2 mmol/l lysolecithin. Cysteamine-HCl (10%) twice subcutaneously on the 19th day in group 1, 3 and 4, isotonic NaCl in group 2. In group four 1 ml lysolecithin per gastric tube 1 h before cysteamine.Group 1: 8 animals with 16 ulcers, group 2: 7 with 10 ulcers, group 3: no ulcers, group 4: 3 with 5 ulcers (p less than 0.05/p less than 0.02).Lysolecithin, a substance produced during fat digestion, exerted an ulceroprotective property (lyso-protection) under experimental conditions, as shown here for the first time, to the author's knowledge. The enhancement of cysteamine-induced duodenal ulcer development by bile salts is again documented.

The study was undertaken to establish whole blood mercury levels in the Saskatchewan population and to identify characteristics of individuals with higher blood levels. The mean blood mercury level was 6.7 ng/ml, the median level 5 ng/ml and the range 1 to 42 ng/ml. Native persons living in northern Saskatchewan who had recently eaten local fresh-water fish had the higher levels. A greater consumption of fish and higher blood mercury levels were recorded during the fresh-water fishing season.

Prognostic and therapeutic implications of acute severe gastrointestinal bleeding were retrospectively analyzed, on the basis of history, clinical and endoscopic findings, in a group of 50 consecutive patients with endoscopically documented ulcer of the stomach or duodenum. In patients with hemorrhagic shock and a history of melena and/or hematemesis represents the most important indication for urgent action. In this setting the surgical approach remains the therapy of choice if other measures (endoscopic coagulation, somatostatin application) are unable to prevent further bleeding. Except in situations with acute arterial bleeding, the endoscopic finding itself is not decisive in selecting the therapeutic procedure.

In this investigation we assess whether diversion of bile and pancreatic secretion protects rats from ulceration under maximal acid secretion as it does in cysteamine-induced ulcers. The rats were divided into a cysteamine-group (Cy) comprising 16 rats and a secretagogue group (PC) with 18 white male rats. Half of the animals of each group were submitted to the diversion-operation (division of the duodenum distally from the pylorus, jejuno-duodenostomy and entero-y-anastomosis), Cy2 and PC2 respectively. The other animals were not operated (Cy1 and PC1). In the cysteamine group the rats were given twice cysteamine-HC1 injections subcutaneously and the PC group were given a 24 h infusion with pentagastrin and carbachol. All animals of the Cy1 group had duodenal ulcers, 3 perforated. However, only 2 rats had one ulcer each in the Cy2 group (p less than 0.01). The PC1 group totalled 30 duodenal ulcers in the 9 animals with 10 perforations, 13 ulcers in 6 animals with 3 perforations in PC2. Furthermore in PC1 group 34 gastric ulcers were found in 7 rats and only 4 ulcers in the PC2 group. It is therefore concluded, that the diversion operation provided protection against cysteamine-induced duodenal ulcers (p less than 0.01) and ulcer formation under maximal acid stimulation in the duodenum (p less than 0.02) as well as in the rat stomachs (p less than 0.05). In the PC group the restraint haltering of the animals promoted presumably a stress situation with bile reflux in the non-operated whereas in the operated animals (PC2) reflux did not occur.