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Background: Persistent infection with Helicobacter pylori is associated with the recurrence of duodenal ulcer. Whether the efficacy of bismuth therapy in reducing the rate of recurrence of duodenal ulcer is due to its antimicrobial effects on H. pylori or to a direct protective action on the mucosa is still a matter of debate., Methods: To study the effect of the eradication of H. pylori on the recurrence of duodenal ulcer, we treated 104 patients with H. pylori infection and recurrent duodenal ulcer with either amoxicillin (750 mg three times daily) plus metronidazole (500 mg three times daily) or identical-appearing placebos, given orally for 12 days. All patients also received ranitidine (300 mg each night) for 6 or 10 weeks. Endoscopy was performed before treatment and periodically during follow-up for up to 12 months after healing., Results: Among the 52 patients given antibiotics, H. pylori was eradicated in 46, as compared with 1 of the 52 given placebo (89 percent vs. 2 percent, P < 0.001). After six weeks, the ulcers were healed in 48 patients given antibiotics and 39 given placebo (92 percent vs. 75 percent, P = 0.011). Side effects, mainly diarrhea, occurred in 15 percent of the patients given antibiotics. Among the patients followed up for 12 months, duodenal ulcers recurred in 4 of 50 patients given antibiotics and 42 of 49 given placebo (8 percent vs. 86 percent, P < 0.001). Ulcers recurred in 1 of 46 patients in whom H. pylori had been eradicated, as compared with 45 of 53 in whom H. pylori persisted (2 percent vs. 85 percent, P < 0.001)., Conclusions: In patients with recurrent duodenal ulcer, eradication of H. pylori by a regimen that does not have any direct action on the mucosa is followed by a marked reduction in the rate of recurrence, suggesting a causal role for H. pylori in recurrent duodenal ulcer.

Organelle transport along microtubules is believed to be mediated by organelle-associated force-generating molecules. Two classes of microtubule-based organelle motors have been identified: kinesin and cytoplasmic dynein. To correlate the mechanochemical basis of force generation with the in vivo behaviour of organelles, it is important to quantify the force needed to propel an organelle along microtubules and to determine the force generated by a single motor molecule. Measurements of force generation are possible under selected conditions in vitro, but are much more difficult using intact or reactivated cells. Here we combine a useful model system for the study of organelle transport, the giant amoeba Reticulomyxa, with a novel technique for the non-invasive manipulation of and force application to subcellular components, which is based on a gradient-force optical trap, also referred to as 'optical tweezers'. We demonstrate the feasibility of using controlled manipulation of actively translocating organelles to measure direct force. We have determined the force driving a single organelle along microtubules, allowing us to estimate the force generated by a single motor to be 2.6 x 10(-7) dynes.

The effect of treatment of rats with the liver monooxygenase inducer phenobarbital on the formation of reactive oxygen in neoplastic liver nodules and the surrounding normal tissue was investigated. Liver nodules were induced by treatment of rats with diethylnitrosamine (single i.p. injection of 0.15 mumol/kg body weight on day 1 after birth) followed by chronic administration of phenobarbital-sodium (PB; 0.05% in diet) after weaning. Groups of rats were kept on PB until sacrifice or were withdrawn from the promoter 3-6 weeks prior to killing. Emission of chemiluminescence was used as a sensitive means to detect the formation of reactive oxygen in microsomal preparations from the various tissues incubated with NADPH and the chemiluminigenic detector lucigenin. In addition, a 2-dimensional photon counting system has been developed that permits the analysis of the spatial distribution of lucigenin-chemiluminigenic signals over liver tissue sections incubated with reduced phosphopyridine dinucleotides. In general, we observed increased levels of reactive oxygen formation in liver nodules when compared with the normal liver tissue. Highest levels were seen in nodules that stemmed from PB-induced rats. Studies on the expression and activity of cytochrome P-450 in liver nodules as well as experiments with specific inhibitors point towards a participation of the liver monooxygenase system in reactive oxygen formation, although additional metabolic pathways seem to be involved as well. The observed increases in reactive oxygen in liver nodules of PB-treated rats might be related to the promoting activity of this drug.

15,300 endoscopies of the upper and lower gastrointestinal tract were done during the years 1974-1982. During this time 915 polyps were excised. 3.2% of the polyps excised from the stomach, as contrasted to 64.8% of the ones taken from the colorectal part of the gastrointestinal tract were classified as precancerous lesions. These results show, that endoscopic polypectomy is a very efficient procedure in regard to prophylaxis of colon carcinoma, however almost without significance in this regard for prophylaxis of gastric carcinoma.

Seventy-two outpatients with endoscopically diagnosed duodenal ulcer were studied in a 4-6 week randomised, single-blind trial comparing sucralfate (1 g tds 2 h after each meal and 1 g nocte) with cimetidine (200 mg tds and 400 mg nocte). Endoscopy was performed after 4 weeks and was repeated at 6 weeks if healing was not achieved at 4 weeks. Ulcer pain and antacid consumption were recorded in a diary by patients. Twenty-three of 35 (65.7%) sucralfate-treated patients and 27 of 37 (73.0%) cimetidine-treated patients had complete ulcer healing after 4 weeks. The overall healing rates after 6 weeks for the sucralfate and cimetidine groups were 91.4% (32 of 35 patients) and 83.8% (31 of 37 patients), respectively. Neither difference was statistically significant. Pain relief and antacid consumption were similar in both groups. Nausea was reported by 4 patients in the sucralfate group and two requested withdrawal because of this complaint. Hematological and biochemical parameters were not affected by treatment with either sucralfate or cimetidine. We conclude that sucralfate is safe and as effective as cimetidine in the treatment of duodenal ulcer.

The efficacy of various antimicrobial and anti-ulcer agents on the elimination of Campylobacter pylori in duodenal ulcer patients was investigated. Ranitidine, cimetidine, pirenzepine, aluminium phosphate gel as well as combinations of H2-receptor antagonists or pirenzepine + penicillin V, ciprofloxacin, ofloxacin, phenyl-mercuryborate or rifampicin had no influence on C. pylori in vivo. Short term elimination of C. pylori was achieved in 3/15 patients treated with ranitidine + bacampicillin and in 1/5 treated with cimetidine + metronidazole. This elimination was accompanied by a significant reduction of polymorphonuclear infiltration of the antral mucosa. Development of bacterial resistance was observed in patients with additional quinolones, metronidazole and rifampicin but not in patients treated with betalactam antibiotics.

Recurrence rates of chronic duodenal ulcer after initial therapy with pirenzepine or cimetidine were investigated in a prospective, randomized trial with a total of 80 patients. After 12 weeks of therapy with pirenzepine (50 mg b.i.d) or cimetidine (200 mg t.i.d. + 400 mg nocte) 68,7% and 88,5% respectively were healed (chi 2 = 3,97; p less than 0,05). These patients showed recurrences in 73,6% after pirenzepine and in 84,6% after cimetidine during a six months observation period. This difference is not statistically significant, nor was life table analysis capable to show any difference in the relapse pattern between the two groups.

One hundred and forty six gastric ulcer patients were given open treatment using 1 g cimetidine daily to heal their ulcers. Of 130 who completed the acute treatment period of eight weeks, 112 (86%) had healed ulcers. Of these 112 patients with healed ulcers, 108 entered a one year double blind study to compare the effect of cimetidine maintenance therapy (400 mg at night) with placebo. Of the 84 patients available for assessment at the end of one year, 86% in the cimetidine treated group were in remission compared with 45% in the placebo treated group (chi 2 = 15.03; p less than 0.001). There were similar losses from non-compliance and drop out in both groups. The incidence of untoward effects and significant drug related laboratory abnormalities was low. The results indicate that cimetidine heals nearly 90% of acute gastric ulcers within eight weeks and that subsequent low dose maintenance treatment at night offers a considerable benefit over placebo therapy.

Radioimmunoassayable basal serum levels of luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin (hPRL), 17 beta-estradiol (E2) and testosterone (T) were estimated in a total of 68 patients, who were treated because of peptic ulcer with 1 g cimetidine per day. 37 patients were male and 31 were female subjects, respectively. Hormone serum levels were assayed before and 4 to 6 weeks after start of therapy. A significant increase of LH serum levels (p less than 0.025) and a significant decrease of hPRL (p less than 0.025) was noted in the male subjects during therapy. Similarly, a decrease of hPRL serum levels (p less than 0.001) was registered in the female subjects during treatment with 1 g cimetidine per day. All other hormone serum levels in both female and male subjects remained unchanged. The present data combine to suggest that 1 g cimetidine per day does not provoke hyperprolactinemia. In addition, cimetidine at the dose used does not interfere with other hormones of the hypothalamus-pituitary-gonadal axis and therefore, cannot be considered, responsible for endocrine disorders during treatment with cimetidine.

The efficacy of cimetidine 400 mg b.i.d. as compared with a single evening dose 800 mg was evaluated in a single-blind multicentre trial involving 86 patients with endoscopically proven duodenal or pyloric ulcer. After four weeks of treatment the healing rates were 64.4% (29/45) with 400 mg cimetidine twice daily and 78% (32/41) with 800 mg nocte; after eight weeks the corresponding rates were 77.7% (35/45) and 85.3% (35/41). Administration of 800 mg cimetidine every evening is, consequently, at least as effective as a twice-daily regimen. In the second half of the treatment period it was significantly more effective in reducing pain and antacid consumption. The single noctural dose takes the pathogenetic importance of overnight gastric acidity into consideration, entails a simplification of therapy and may improve patient compliance. It should, therefore, take preference over the conventional twice-daily regimen.

Nizatidine, a new H2-receptor antagonist, was compared with ranitidine in a double-blind, randomized, multicentre trial for the prevention of duodenal ulcer relapse. This is the interim analysis of 197 patients admitted to the study by 1 September 1985, having finished a 6-month treatment period by 1 March 1986. At night, 96 and 101 patients received 150 mg nizatidine and 150 mg ranitidine, respectively. Both groups were well matched for demographic data, duration and severity of ulcer disease. Calculating cumulative relapse rates by the life-table method of Cutler and Ederer, 18% on nizatidine and 13% on ranitidine had experienced a symptomatic or asymptomatic recurrence. The difference is not statistically significant. The symptomatic response was identical in both groups, 3/4 of the patients in both groups being free of any symptom over all 6 months. During maintenance treatment, 24% of the patients on nizatidine and 32% of those on ranitidine reported new symptoms, listed as 'adverse events'. However, none of these events was likely to be drug related. There was no difference between the two groups concerning the percentage change of laboratory variables from baseline to endpoint.

In a double-blind randomized trial 91 patients with endoscopically confirmed duodenal and/or prepyloric ulcers received either 1000 mg cimetidine daily (44 patients) or placebo (47 patients) for 4 weeks. At 2 weeks complete ulcer healing was significantly increased in patients receiving cimetidine (45%) in comparison with those treated with placebo (15%) (p less than 0.01). At 4 weeks 73% of the patients on cimetidine and 32% of those on placebo showed complete healing (p less than 0.001). Ulcer size decreased more rapidly with cimetidine than placebo (p less than 0.05). With respect to the number of pain-free days and nights cimetidine was significantly superior to placebo during the days of the second week only (p less than 0.05). Cimetidine patients consumed significantly less antacids than those receiving placebo (p less than 0.01). There was no significant correlations between ulcer healing and freedom from pain at the end of either cimetidine or placebo treatment in this study. No specific side effects referable to cimetidine were observed.

Luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin (hPRL) and testosterone (T) were assayed in a total of 131 patients with peptic ulcer. Initial oral treatment was performed with 1000 mg cimetidine per day for 6 to 12 weeks. After healing was confirmed endoscopically, the patients were switched to a maintenance dose of 400 mg per day cimetidine for 3 years. Serum hormone levels before and during the two regimens were estimated in 48 male, 22 postmenopausal and 5 premenopausal subjects. Comparison between the two cimetidine doses was possible in 76 male, 44 postmenopausal and 6 premenopausal patients. In all patients hormone parameters assayed before therapy were within the normal ranges. FSH was noted to increase significantly in all but the premenopausal group but remained within the normal range. In contrast, hPRL declined significantly in all groups of subjects except for premenopausal females during cimetidine treatment. LH and T did not change during treatment and no differences of hormone serum levels were noted between the two regimens. Present data combine to suggest that an initial treatment with 1000 mg of cimetidine per day did not provoke hyperprolactinemia, and a switch from an initial high dose to a maintenance dose of 400 mg per day did not cause further changes in hormone serum levels. Changes of LH, FSH, hPRL and T recorded in the present study are too small to be considered responsible for possible endocrine disorders observed during cimetidine therapy.

The aim of the present investigation was to compare the efficacy of a low-dose antacid (Maalox 70, 280 mmol/day) with that of the H2-receptor antagonist cimetidine (Tagamet, 200 mg three times daily and 400 mg/day) after 14 and 28 days in the treatment of duodenal ulcer. The prospective multicentre study included 171 patients with endoscopically confirmed duodenal ulcers. The patients were randomly assigned to the treatment groups with antacid containing Mg and Al hydroxide (M)(4 X 70 mmol/day; n = 86) or to the group receiving cimetidine (T) (1000 mg/day; n = 85). The two treatment groups were matched for age, sex, drinking and smoking habits, and drug use. Endoscopic examinations were carried out before the start of treatment and 14 days later. If the ulcer was still present at this time, the second endoscopic examination was done after a further 14 days. Endoscopically, the ulcer had healed at 14 days in 38.8% (M) and in 34.9% (T) and at 28 days in 80.0% (M) and 74.7% (T), respectively. The healing rate did not differ significantly between the two treatment groups. Complaints, measured as percentage of days per week with upper abdominal pain, were significantly reduced in both groups. No significant differences were found between the two treatment groups with regard to pain relief or side effects. Treatment had to be abandoned in one patient receiving antacid because of diarrhoea and in one patient receiving cimetidine because of the absence of any response.(ABSTRACT TRUNCATED AT 250 WORDS)

In a prospective double blind study the efficacy and safety of the new H2-receptor antagonist famotidine was compared with ranitidine. 48 patients with endoscopically proven duodenal ulcer were randomly allocated to receive famotidine 40 mg once at night, 20 mg bid, 40 mg bid or ranitidine 150 mg bid. After 4 weeks of treatment the ulcers of 7/12, 10/12, 9/12 and 6/12 patients were healed; the corresponding rates after 8 weeks were 9/12, 12/12, 11/12 and 10/12. Statistically there was no significant difference between the various groups. Adverse events of any clinical importance were not observed. These data indicate, that famotidine is as effective and as safe as ranitidine for the treatment of acute duodenal ulcer.

Relapse rates of duodenal ulcer after treatment with sucralfate or cimetidine were investigated in a one-year follow-up study. During this period 23 out of 27 patients (85.1%) initially treated with sucralfate relapsed, in comparison with 17 out of 21 patients (80.9%) after cimetidine therapy. Recurrence after cimetidine was more often asymptomatic than after sucralfate. These results suggest that recurrence rates of duodenal ulcer are not essentially influenced by the mode of action of the initially used drug. Cytoprotection by sucralfate did not result in fewer or later relapses than reduction of acidity by cimetidine.

A randomised multicentre, double-blind study of the efficacy and safety of roxatidine acetate 150 mg at bedtime or 75 mg twice a day was conducted in 300 outpatients with endoscopically confirmed duodenal ulcers. After 14 days' treatment with roxatidine acetate substantial reductions in ulcer sizes had been obtained, in addition to healing rates of 87 to 89%, with no significant differences between the dosage regimens. There were graded reductions in day and night-time assessment of epigastric pain for both treatment groups and no differences in the mean numbers of antacid tablets consumed. In addition, cigarette smoking did not influence the healing rates produced by either treatment schedule. 11 patients reported 12 mild adverse reactions, with gastrointestinal symptoms the most frequent, and no clinically significant alterations in laboratory values. The present data suggests that a single bedtime dose of roxatidine acetate 150 mg produces effective duodenal ulcer healing and pain relief equivalent to that produced by a twice daily dosage regimen.

253 patients were treated for 3 years with 400 mg cimetidine at night to prevent relapses of recently healed duodenal ulcers. The efficacy of maintenance treatment was evaluated on a life table basis. In contrast to previous studies not the first but the third symptomatic relapse was taken as the major criterium of treatment failure, an assumption, that better represents the everyday practical situation. Further endpoints for the life table calculation were: the wish of the patient to stop treatment after the first or second recurrence, the failure of a first or second recurrence to heal within 12 weeks and side effects. At 1, 2 and 3 years 5 +/- 2.4%, 16 +/- 4.6% and 20 +/- 5.2% respectively had to be considered as treatment failures. 4 patients presented with a bleeding relapse, none of which necessitated emergency operation. There were no irreversible side effects. This study demonstrates that treatment of recurrent duodenal ulcers with 400 mg cimetidine at night for 3 years is safe and improves considerably the quality of life of the majority of patients. The authors suggest that drug maintenance treatment should be offered before surgery is recommended.

Concrements in the prepapillary portion of the Wirsungian duct result in secretion with simultaneous obstruction and, thus, represent a potential cause of pancreatitis. The removal of these concrements is indicated and rendered possible by endoscopic incision of the pancreatic duct. This procedure has been performed only very rarely up to the present. Its efficacy is demonstrated by a case report.

In the course of routine gastroduodenoscopic examination of 218 patients bioptic mucosal specimens were examined bacteriologically for the presence of Campylobacter (C.) pylori. The organism was isolated from 52 out of 53 patients (98%) with duodenal ulcer, 7 out of 9 with gastric ulcer (78%), 24 out of 31 with mucosal erosions (77%), 10 out of 10 with duodenitis (100%), 16 out of 16 with chronic active gastritis (100%) and from 40 out of 73 patients (55%) with inactive chronic gastritis. By contrast, all specimens from 26 patients with endoscopically and histologically normal mucosa were negative for this bacterium. The rate of elimination of C. pylori from mucosal specimens was investigated as a first step towards studying the influence of antibiotic therapy upon healing of gastric and duodenal ulcers. For this purpose 30 patients with duodenal ulcers were treated either with ranitidine alone (15) or together with bacampicillin (15), which was shown to be highly active in studies with ampicillin in vitro. After 4 weeks the organism was still found in specimens from all patients treated with ranitidine alone, but also in 12 out of 15 patients given combined therapy. This result demonstrates that systemic antimicrobial chemotherapy with bacampicillin is insufficient to eradicate C. pylori from the stomach and the duodenum.

Nonspecific ulcerative proctitis is a variant of diffuse ulcerative colitis with a markedly different clinical course and prognosis. Therapy of choice today consists in salicylazosulphapyridin enemas. Preparation and application as well as results of treatment are discussed.