Gastric ulcer: a double blind comparison of 800 mcg misoprostol versus 300 mg ranitidine.

Seventy-nine patients with endoscopically confirmed gastric ulcers received either ranitidine (37 patients) or misoprostol (42 patients) in a randomized double-blind manner. Fifty-six percent of the patients treated with ranitidine, and 38% of those treated with misoprostol presented with endoscopically healed ulcers after four weeks of treatment. After eight weeks complete healing had occurred in 86% of the patients receiving ranitidine, and 74% of those on misoprostol. These differences were not statistically significant. In smokers, ranitidine was superior to misoprostol, leading to a higher healing rate at four weeks (73% versus 20%). Thus there was no evidence that in patients with gastric ulcer misoprostol overcomes the negative effect of cigarette smoking.

[Fever and liver cirrhosis]. / Etats fébriles et cirrhose.

Occurrence of fever in a patient with liver cirrhosis should suggest the following: 1. Endotoxemia. Endotoxins are normally present in portal blood; in hepatic cirrhosis they are insufficiently cleared by the liver and their presence can be demonstrated in the systemic circulation by the "limulus test". Fever is one of the many consequences ascribed to the presence of endotoxins in the blood. 2. Infections. Cirrhosis and alcoholism (which often accompanies it) impair host defenses against bacteria and other organisms. Thus, infections are actually more frequent in hepatic cirrhosis as is shown by the example of bacterial endocarditis. Spontaneous bacterial peritonitis must be searched for carefully when ascites is present. 3. Alcoholic hepatitis. This diagnosis is established histologically. The usual symptoms, occurring with variable incidence, include anorexia, nausea and vomiting, abdominal pain, fever and jaundice in the presence of hepatomegaly, leukocytosis and an elevated SGOT. Differential diagnosis from obstructive jaundice and a severe prognosis without alcohol abstinence make early diagnosis mandatory. Its evolution in cirrhosis can be astonishingly rapid. In the absence of hepatic encephalopathy, corticosteroids do not appear to be recommended. 4. Hepatoma.

Ruptured pancreatic pseudocysts: diagnosis by endoscopy. Report of 3 cases.

Report on 3 cases of spontaneous perforation of a pancreatic pseudocyst into the stomach; presenting symptom was in each case an acute upper GI-bleeding. The pseudocyst was endoscopically seen as a well delineated, hemorrhagic protrusion into the stomach. After full perforation the spontaneous ostium had the appearance of a surgical anastomosis. High amylase concentration in the aspirate ave further diagnostic evidence. All 3 patients survived, 2 of them without surgery.

[Pseudocysts and retention cysts in acute and chronic pancreatitis (author's transl)]. / Pseudozysten und Retentionszysten bie akuter und chronischer Pankreatitis. Eine vergleichende Analyse anhand von 42 Fällen.

42 cases of pancreatic cyst in acute (22 cases) pr chronic (20 cases) pancreatitis were seen between 1962 and 1976. Analysis of the case data revealed the following: (1) exact assignment of the cyst to acute or chronic pancreatitis is often possible only by long-term observation; (2) the cysts of chronic pancreatitis are not a uniform group: some (8 cases) apparently occurred in acute pancreatitis through necrotic episodes (pseudocysts), others (12 cases) by a retention mechanism; these "retention cysts" develop later in the course of chronic pancreatitis than the pseudocysts and produce a different clinical picture with better prognosis; (3) barium meal and retrograde cholangiopancreatography proved of diagnostic value' (4) if the cysts persist for more than six weeks operation is indicated because of the high incidence of complications.

Increased gastrin release in chronic calcifying pancreatitis and in chronic alcoholism.

Plasma gastrin levels were measured by radioimmunoassay before and after a test meal associated with 40 ml ethanol in 21 patients presenting with chronic calcifying pancreatitis, in 10 apparently normal subjects drinking since at least 5 years 100 g alcohol a day, in 14 subjects presenting hepatic alcoholic cirrhosis and in 18 apparently normal non alcoholic controls. Post-stimulation gastrin concentration were higher in chronic pancreatitis patients or in normal alcoholics (peak post-stimulation value: 74 +/- 41 and 74 +/- 43 pg/ml respectively) than in cirrhotics or non alcoholic controls (45 +/- 26 and 41 +/- 15 pg/ml respectively) (m +/- SD).

Impaired secretin release in chronic alcoholic dogs.

Plasma immunoreactive secretin has been compared before and after stimulation by intraduodenal infusion of HCl in 3 dogs who had received 2 g-kg-1-day-1 alcohol for 3 years and 4 non-alcoholic control dogs. After HCl infusion, blood secretin was lower in chronic alcoholic animals than in controls. This decreased post-stimulation concentration of secretin in chronic alcoholic dogs was in contrast to the increased release of gastrin after a meal which has been previously described.

Atropine-induced inhibition of the enhanced CCK release observed in alcoholic dogs.

As it has been previously shown, the pancreatic secretory response to an intraduodenal infusion of oleic acid is increased in animals accustomed to daily ethanol consumption compared to matched controls. This action has been verified in dogs provided with a Thomas cannula and consuming 2 g kg-1 ethanol or not, daily since 3 years. An intravenous infusion of 0.75 mg kg-1 h-1 of atropine suppresses the difference between alcoholic and non-alcoholic animals. Therefore, the increased release of CCK-PZ in response to meal, which is characteristic of chronic alcoholic animals, is under cholinergic control.

Canine exocrine pancreatic secretory changes induced by calcium or ethanol plus calcium intraduodenal infusion.

In dogs provided with chronic gastric and pancreatic fistulas (Thomas cannula), an 80-minute intraduodenal CaCl2 (0.6 mM/kg.) infusion against a background of secretin perfusion (GIH, 1.0 CU/kg./hr.) elicits a complex "pancreon" response consisting of both excitatory and inhibitory effects on the protein and alkaline components, respectively, of pancreatic secretion. It is postulated that these pancreatic secretion changes are the result of the interplay of released CCK and calcitonin. The lack of pancreatic secretion modifications when ethanol (0.7 mg./kg.) was added to the intraduodenal CaCl2 infusion suggests that the former counteracts the effects of the latter on the nerves and/or the endocrine cells of the gut. Ca++ concentration and output in pancreatic secretion did not change significantly either with the intraduodenal CaCl2 alone or associated with ethanol. Fasting blood Ca++ levels were not modified either by the secretin perfusion or by the intraduodenal CaCl2 infusion, either given alone or associated with ethanol.

Reserpine-induced dissociation of canine pancreatic secretion.

In five dogs, provided with chronic pancreatic and gastric fistulas (Thomas' cannula), the effects on exocrine pancreatic secretion of an intravenous continuous perfusion of gastrin (Eurorga, hog gastrin I-II, 6 mug./kg./hr.) and secretin (GIH, 0.5 C.U./kg.hr.) was studied before and after 48 hours of reserpine treatment (0.1 mg./kg./24 hr.). When compared with the pretreated plateau levels, reserpine induced a significant pancreatic secretion dissociation, a depressive of the alkaline and a rising of the protein component. The former phenomenon suggests a participation of a catecholamines in the secretin-elicited pancreatic electrolyte secretion. The latter, an enhanced sensitivity of intranpancreatic and/or acinar cells of the "pancreon" to gastrin stimulation.

[Treatment of stomach ulcers with cimetidine and pirenzepine]. / Traitement de l'ulcère gastrique par la cimétidine et la pirenzépine.

37 patients with endoscopically confirmed gastric ulcers received either cimetidine (19 patients) or pirenzepine (18 patients) in a double-blind trial. At 4 weeks, 53% of the patients treated with cimetidine and 44% of those treated with pirenzepine had endoscopically healed ulcers. At 8 weeks, complete healing had occurred in 83% of the patients taking cimetidine and 71% of those taking pirenzepine. These differences are not statistically significant.

Healing and relapse of reflux esophagitis during treatment with ranitidine.

In 108 patients the healing and relapse of reflux esophagitis, defined endoscopically by the presence of epithelial defects (erosions and ulcerations) of the esophageal mucosa, were studied. In the first study, with open treatment of ranitidine, the healing rate after 6 wk was 50%. The most important factor that negatively influenced healing was the extent of esophageal erosions. Patients with isolated erosions had a 6-wk healing rate of 78%; the healing rate was 38% in patients with longitudinally confluent lesions and 23% in those with circumferential erosions of the distal esophagus. Smoking also had an unfavorable effect. Age, sex, duration of history, body weight, and alcohol consumption were not related to outcome. Symptoms improved during treatment with ranitidine, but the correlation between symptoms and endoscopic findings at 6 wk was weak. In the second study, relapse was investigated in 61 patients with healed esophagitis in a randomized, double-blind trial comparing placebo and ranitidine (150 mg at bedtime for 6 mo). In both groups, relapse occurred in more than one-third of the patients, with no significant difference between ranitidine and placebo treatment. Patients with worse daytime symptoms at the time of previous healing had a higher relapse rate. The initial severity of esophagitis and smoking did not influence recurrence. Thus, the initial endoscopic findings are of prognostic value in reflux esophagitis. Smoking retards healing. Low-dose maintenance treatment with ranitidine does not prevent relapse.

Gastric ulcer: a double-blind comparison of 100 mg pirenzepine plus antacid versus 800 mg cimetidine plus antacid.

Fifty-five patients with endoscopically confirmed gastric ulcers received either cimetidine (28 patients) or pirenzepine (27 patients) in a randomized double-blind manner. Fifty-seven per cent of the patients treated with cimetidine and 48% of those treated with pirenzepine presented with endoscopically healed ulcers after 4 weeks of treatment. By 8 weeks complete healing had occurred in 83% of the patients taking cimetidine and 76% of those taking pirenzepine. These differences were not statistically significant. Severity of pain on entering the study was correlated with slower healing of the ulcer. Side effects occurred in 5 of 27 patients in the pirenzepine group and 3 of 28 in the cimetidine group. They were mostly mild and did not differ from side effects observed in other studies.

[Dissolution of gallstones based on 6 months treatment with a single daily dose of ursodeoxycholic acid]. / Dissolution de lithiase vésiculaire après 6 mois de traitement par dose journalière unique d'acide ursodésoxycholique.

51 patients with radiolucent gallstones of diameter less than or equal to 15 mm were treated for 6 months with a new form of ursodeoxycholic acid (UDCA) in a single dose of 450 mg at bedtime. This new form has 3 components with fractionate liberation. The rate of partial and complete dissolution after 6 months was 63.4%, reaching 85% for gallstones of less than 5 mm diameter. The results show that a single dose of 450 mg UDCA at bedtime is as effective as UDCA at mealtimes in the dissolution of radiolucent gallstones. Administration of the drug once a day should be more acceptable to patients.

Canine exocrine pancreatic secretory changes induced by an intragastric ethanol test meal.

In five dogs with chronic gastric fistulas (Thomas cannula) and a new type of chronic pancreatic fistula which permits collection of pure nonactivated pancreatic juice after ingestion of a test meal, the following series of experiments were performed: In the first series, a test meal (400 gm. canned dog meat) was given with 200 ml. saline simultaneously infused through the gastric cannula. In response to this stimulus, the 20-minute peak pancreatic flow rate and bicarbonate output were respectively 33% and 34%, of the maximal secretion of the pancreatic gland obtained with secretin in six control dogs provided with gastric and the classical Thomas duodenal fistula. The 20-minute peak protein output represented 84% of the maximal secretory capacity attained with dose-response curves to CCK in the same group of control animals. In the second series either 1.5 or 2.0 gm./kg. ethanol were given instead of saline. Intragastric ethanol induced a dissociation of pancreatic secretion: a significant inhibition of flow rate, of bicarbonate concentration and output and a significant rise of protein concentration; protein output remaining unchanged. It is postulated that ethanol, acting on the stomach and duodenojejunum, evokes, independently of its gastrin-releasing capacity, and unknown humoral or nervous mechanism that counteracts the ethanol-elicited cholinergic-mediated inhibition of pancreatic protein secretion which has been previously described.

Evidences for duodenopancreatic reflexes and an anti-CCK factor with lidocaine infused intravenously and sprayed topically on pancreatic papilla in nonalcoholic and alcohol-fed dogs.

In 14 duodenal Thomas fistula dogs, four of them alcohol-fed for two years, lidocaine, applied topically to the duodenal pancreatic papilla, inhibited secretin-induced pancreatic secretion probably by interrupting duodenopancreatic reflexes that contribute to the "pancreon's" cholinergic tone. Opposite effects were observed with lidocaine administered against a CCK plus secretin background stimulation of the pancreas. The significant rising of volume and protein output above plateau levels were enhanced by chronic alcohol feeding. Lidocaine infused intravenously did not change secretin-induced pancreatic secretion but raised CCK and secretin evoked plateau secretion levels. Chronic alcoholism enhanced these latter effects. Atropine perfusion superimposed on CCK and secretin stimulation did not prevent but raised the intravenous lidocaine-induced pancreatic secretion changes. It is postulated that the modifications elicited by lidocaine sprayed topically and infused intravenously on CCK plus secretin evoked pancreatic secretion plateau levels are due to depression of an anti-CCK factor secreted by the small intestine mucosa.