[Chronic pancreatitis: natural history and development in relation to alcoholism]. / Pancréatite chronique: histoire naturelle et évolution en relation avec l'alcoolisme.

42 cases of chronic pancreatitis treated between 1976 and 1986, presenting 0.2% of all patients seen at the surgical clinic in the same period, have been reviewed. 37 patients (88%) were alcoholics and the prevalence of males was 83%. -Study of dietary habits showed a very high alcohol intake of 135.3 g alcohol per day, contrasting with the control group's alcohol consumption of 44.9 g per day. Alcohol intake calculated per life of patient with chronic pancreatitis represented 850.4 kg, whereas the control group consumed 344.1 kg (beer and wine). -Patients with chronic pancreatitis had started excessive alcohol consumption at an average age of 18 +/- 2 years and continued for an average of 18.0 +/- 1 years. These data correspond to zone A, i.e. Southern Europe. The evolution was analyzed with regard to persistence or cessation of alcoholism. Repeated attacks of chronic pancreatitis were seen in both groups. Patients abstaining from alcohol had only one attack during an average period of 10 years. Painful recurrences after surgery seem to be more frequent with persistent alcoholism (4 out of 5 patients), whereas in 15 patients without alcoholism they were observed only 3 times. -This shows that alcoholism remains the main factor in the natural history and evolution of chronic pancreatitis.

[Effects of chronic pancreatitis on salivary secretion]. / Effets de la pancréatite chronique sur la sécrétion salivaire.

In chronic pancreatitis, increased concentrations of Na+ and Cl- in sweat have been attributed to increased parasympathetic drive. It was postulated that similar changes might occur in saliva. To avoid masking increased parasympathetic drive, saliva was collected without stimulation. In patients with chronic pancreatitis, there were significant increases of concentrations of Na+ and Cl- in basal salivary concentrations. These differences disappeared when salivary secretion was stimulated with citric acid. Anatomic or neurologic modification of the salivary glands seemed unlikely as stimulated concentrations did not differ from those in the control subjects. Perfusion of cholecystokinin (CCK) did not modify concentrations of Na+ or Cl-. Parasympathetic blockade reduced salivary secretion in both patients and controls (p less than 0.001). As tubular absorption of Na+ and Cl- was constant and the volume of saliva was diminished, it followed that there was a reduction in Na+ and Cl- salivary output. As amylase secretion is under sympathetic control, atropine had little effect other than increasing the salivary amylase concentration. The secretory modifications observed with atropine were the same in both patients and control subjects, as the increased parasympathetic drive of the patients was blocked.

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.

[Ranitidine therapy of duodenal ulcer: comparison of once-a-day and twice-a-day administration. A Swiss multicenter double-blind study]. / Ranitidintherapie des Ulcus duodeni: Vergleich der zweimaligen und der einmaligen Applikation. Eine multizentrische Schweizer Doppeltblindstudie.

In a Swiss multicenter double-blind trial ranitidine was given in doses of 300 mg nocte and 150 mg b.d. for the treatment of duodenal ulcer. Ninety-seven patients with endoscopically proven ulcer were treated for four, and in cases of non-healing for eight, weeks. Cumulative healing rates with 300 mg and 2 X 150 mg were 77% and 78% after four weeks and 90% and 94% after eight weeks respectively. 60 and 65% of the patients were asymptomatic after four weeks. Smoking did not adversely affect healing. Thus, ranitidine in a dose of 300 mg nocte is as effective as ranitidine in a dose of 150 mg b.d. in the treatment of duodenal ulcer.

[Acute complications caused by a mucilaginous laxative]. / Complication aiguë d'un traitement par laxatif mucilagineux.

Prescription of so inoffensive-seeming and common a treatment as mucilaginous laxative may have major (if rare) side effects, such as sudden esophageal obstruction. This usually occurs in old people who do not take enough water with the laxative and who may have minor esophageal pathology such as motility disorders or epibronchic diverticulum. The usually typical symptoms are sudden onset, with retrosternal pain, dysphagia or total aphagia, alimentary vomiting and pseudohypersialorrhea. Diagnosis is always by radiography and endoscopy. Radiography must be performed with gastrografin, due to the risk of bronchoaspiration or esophageal fissure. Endoscopy may demonstrate the mucilagenous mass responsible for the obstruction and in most cases restore patency of the esophagus. This technique should always be attempted, if necessary several times, before resorting to surgery. The authors stress that in patients with a risk of esophageal obstruction, such as old people with esophageal disorders, it is essential to explain clearly to the patient that the laxative must be taken with a sufficient quantity of liquid.

[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.

[Intravenous sedation for gastroscopy: comparison between midazolam and diazepam]. / Sédation par voie intraveineuse pour gastroscopie: comparaison midazolam-diazépam.

Benzodiazepines are often used as premedication or intravenous sedative agents for endoscopies. The present study included 74 patients. It compared the sedative and amnestic properties of midazolam and diazepam, their relative potencies as well as the comfort of both the patient and the endoscopist during gastroscopy. The comparison has shown some statistically significant differences, allowing the following conclusions: amnesia was more frequent with midazolam; the dose requirement (in mg X kg-1) for adequate sedation was more important with diazepam, confirming the greater potency of midazolam; generally speaking, sedation was excellent with both drugs.

[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.

[Disturbance of exocrine secretion by the human pancreas in hyperlipoproteinemia]. / Perturbation de la sécrétion exocrine du pancréas humaine lors d'hyperlipoprotéinémie.

Basal and stimulated (secretin/CCK pancreozymin) duodenal aspirates were analyzed for flow rate and the protein and bicarbonate concentrations in 7 non-alcoholic controls and in 7 subjects with type IV hyperlipoproteinemia. Basal volume and bicarbonate concentration did not differ in the two groups. In the hyperlipoproteinemia patients, basal protein concentration and flow rates were significantly different from controls (p = 0.0143 and p = 0.0182 respectively). The bicarbonate flow rate is also increased in hyperlipoproteinemia. The data obtained after stimulation were similar for protein and HCO3 in both groups. These findings are identical to those observed by SARLES in alcoholic and hypercalcemic animals and in man. It is possible, but not yet proven, that hyperlipoproteinemia pancreatitis is due to protein precipitates in the pancreatic canaliculi.