bluuebunny/crossref_metadata_2025_split huggingface dataset:
A comparison between enprostil and ranitidine in the management of gastric ulceration
Authors: MORGAN A. G. , PACSOO C. , TAYLOR P. , McADAM W. A. F. 
Published: July 2010

SUMMARYIn a randomly allocated, double‐blind, endoscopically controlled study, 98 patients with gastric ulcers were treated with either (a synthetic prostaglandin of E2‐like structure) enprostil 70 μg b.d. or 150 mg ranitidine b.d. The healing rates at 4, 8 and 12 weeks were enprostil 57, 91 and 94% and for ranitidine 55, 88 and 98%, respectively. Following ulcer healing, half the patients were followed for 1 year without treatment and the others were given 70 μg enprostil nocte. Endoscopy was repeated in both groups after 6 and 12 months or if dyspeptic symptoms returned. The recurrence rate without maintenance at 6 and 12 months, following ranitidine therapy, was 67 and 75%, and after enprostil therapy 50 and 61%, respectively. On maintenance enprostil, the recurrence rates were 28 and 40%. Forty‐seven per cent of patients who completed maintenance treatment had a proven ulcer recurrence within 6 months of stopping therapy. Diarrhoea was a common sideeffect of enprostil therapy. Seven patients were withdrawn because of diarrhoea or abdominal pain.
The effect of portal hypertension on indomethacin‐induced small intestinal ulceration in the rat
Authors: JONAS G. M. , ERICKSON R. A. , CHUNG K. 
Published: July 2010

SUMMARYThe purpose of this study was to determine whether portal hypertension potentiates intestinal ulceration induced by indomethacin. Portal hypertension was produced in male Sprague‐Dawley rats by two‐staged ligation of the portal vein. Sham‐operated rats were used as controls. The rats were given 20 mg/kg of indomethacin intragastrically, 7 and 14 days, respectively, after complete portal vein ligation. Forty‐eight and 72 h after indomethacin, portal pressures were measured and the whole small intestine removed for quantitative measurement of the percent of the mucosa ulcerated by computerized image analysis. There were no differences in the area of ulceration between the portal hypertensive and sham‐operated rats at either 7 or 14 days, despite the presence of significant portal hypertension. Portal hypertension does not appear to potentiate small intestinal ulceration induced by indomethacin in rats.
Colloidal bismuth subcitrate causes sustained release of gastric mucosal prostaglandin E2
Authors: MERTZ‐NIELSEN A. , STEENBERG P. , NEUMARK T. , BUKHAVE K. , RASK‐MADSEN J. 
Published: July 2010

SUMMARYGastric application of high doses of colloidal bismuth subcitrate (CBS) stimulates mucosal prostaglandin E2 (PGE2) production, which is considered part of the mechanism by which the drug accelerates peptic ulcer healing. Whether therapeutic, orally administered, doses of CBS cause a sustained stimulation of prostaglandin production is not known. We have, therefore, determined gastric luminal release of PGE2 during ‘steady‐state’perfusion of the stomach with CBS (10 mg/ml; isotonic mannitol 5 ml/min) and 4 h after the last oral dose of the drug (240 mg b.d.) for 2 weeks (isotonic mannitol 5 ml/min) in 8 healthy volunteers. A significant increase in PGE2 concentrations (712 (409–1076) vs. control 334 (252–655) pg/ml; medians with Q50 ranges; P < 0.02) and PGE2 output (12.5 (7.3–14.3) vs. control 4.8 (4.1–7.3) ng/15 min; P < 0.02) occurred during gastric perfusion with CBS. A similar increase in PGE2 concentrations (630 (297–1429) pg/ml; P < 0.02) and PGE2 output (12.6 (6.4–22.2) ng/15 min; P < 0.02) was observed following treatment with CBS for 2 weeks. These results suggest that therapeutic doses of CBS cause a sustained stimulation of gastric mucosal PGE2 formation.
Efficacy of misoprostol and ranitidine in the prevention of duodenal ulcer relapse and its correlation with endogenous gastric prostanoid synthesis
Authors: GOLDIN E. , KARMELI F. , RACHMILEWITZ D. 
Published: July 2010

SUMMARYWe determined endogenous gastric prostaglandin synthesis and its correlation with the prevention of duodenal ulcer relapse by misoprostol and ranitidine. Sixty‐one patients with recent endoscopically healed duodenal ulcer were randomly allocated in a double‐blind fashion for one year of treatment with misoprostol 400 μmUg nocte, ranitidine 150 mg nocte or placebo. Patients were followed every two months. Endoscopy was repeated at six and 12 months or beforehand, if relapse was suspected. Antral and fundic biopsies, 3–4 from each region, were obtained at each endoscopy for determination of prostaglandin synthesis. During the one year of treatment, 11 out of the 12 placebo treated patients flared up, as opposed to 10 out of 25 and four out of 24 misoprostol and ranitidine treated patients, respectively. The difference between all treatment groups was significant (P < 0.0001). In all subjects who flared up, pretrial endogenous antral and fundic prostaglandin E2 synthesis were not different from their respective synthesis in those who did not relapse. These results indicate that one year of treatment with both ranitidine and misoprostol prevents ulcer relapse better than placebo. However, ranitidine is significantly better than misoprostol. Both at six and 12 months there was no significant difference between the two treatment groups in the trend towards enhanced synthesis of gastric prostanoids.These results indicate that one year of treatment with both ranitidine and misoprostol prevents ulcer relapse better than placebo. However, ranitidine is significantly better than misoprostol. Both at six and 12 months there was no significant difference between the two treatment groups in the trend towards enhanced synthesis of gastric prostanoids.
Steady‐state pharmacokinetics of enteric coated 5‐amino‐salicylic acid tablets in healthy volunteers and in patients with Crohn's disease or ulcerative colitis
Authors: NORLANDER B. , GOTTHARD R. , STRÖM M. 
Published: July 2010

SUMMARYAn Eudragit‐L coated oral 5‐aminosalicylic acid (5‐ASA; mesalazine) product (Mesasal), has been formulated to deliver 5‐ASA to the distal small bowel and colon for the treatment of inflammatory bowel disease. The purpose of this study was to compare the pharmacokinetic profile of this product at steady‐state between healthy volunteers and two different patient groups with inflammation of either the small or the large bowel.Two carefully selected groups of patients, nine with Crohn's disease restricted to the small intestine and ten with total ulcerative colitis and one group of ten healthy volunteers received two 250 mg Mesasal tablets three times daily for 10 days to reach steady‐state. Plasma 5‐ASA and acetyl‐5‐ASA concentrations were followed for 48 h and urinary excretion for 72 h.There was a great variation in most pharmacokinetic parameters within each group and no significant differences were noticed between the groups. The location of the inflammatory process probably does not influence the pharmacokinetics of 5‐ASA in any significant way in patients with either Crohn's disease in the small bowel or total ulcerative colitis.
Omeprazole and Helicobacter Pylori: temporary suppression rather than true eradication
Authors: WEIL J. , BELL G. D. , POWELL K. , MORDEN A. , HARRISON G. , GANT P. W. , JONES P. H. , TROWELL J. E. 
Published: July 2010

SUMMARYTwenty‐four Helicobacter pylori (H. pylori)‐positive patients were treated for 28 days with either 20 mg omeprazole o.m. (n= 12) or 40 mg omeprazole o.m. (n= 12). Clearance (absence of H. pylori at the end of or shortly after treatment) and eradication (absence of H. pylori 1 month after cessation of treatment) were assessed using the 14C‐urea breath test. Observed clearance and eradication were: 20 mg omeprazole 3/12 and 0/12; 40 mg omeprazole 6/12 and 1/12 respectively. The effect on H. pylori is probably due to the change in gastric pH from acid to neutral, however it is insufficient to recommend the inclusion of omeprazole in regimens aimed at eradicating H. pylori.
Colchicine in primary biliary cirrhosis
Authors: WARNES T. W. 
Published: July 2010

SUMMARYColchicine, which has been used for hundreds of years in the treatment of gout, has found a new use in the treatment of cirrhosis. In the experimental animal, and in vitro, colchicine decreases inflammation, inhibits collagen synthesis and also increases collagen degradation by activating collagenase. Many of the putative beneficial actions of the drug in cirrhosis, as well as its toxic side effects, are due to the fact that it binds to tubulin and thereby disrupts microtubules; however, it is unclear which of these actions, mostly demonstrated in the experimental animal, are present in the doses currently used in man.There have been 4 controlled trials of colchicine in various forms of cirrhosis, three of which have concerned primary biliary cirrhosis. Data are currently available on 146 colchicine‐treated patients, of which 92 had primary biliary cirrhosis. Colchicine improves the conventional liver function tests in primary biliary cirrhosis and also reverses the basic defect in hepatic excretory capacity characteristic of this disease. The drug appears to have no significant effect on symptoms, clinical features or liver histology, but in 2 of the 3 primary biliary cirrhosis trials, as in the Mexican study of alcoholic and post‐hepatitic cirrhosis, colchicine treatment was associated with improved survival.
Somatostatin and octreotide in gastroenterology
Authors: BURROUGHS A. K. , McCORMICK P. A. 
Published: July 2010

SUMMARYSomatostatin and octreotide have a definitive role in the management of symptomatic gut neuroendocrine tumours, particularly VIPomas and carcinoid. They probably also have a role in variceal bleeding, but this needs further confirmatory randomized trials. At present there is a potential role in the management of short bowel syndrome, dumping syndrome and gastrointestinal fistulae, but randomized clinical studies are needed. Possibly there is a role in AIDS‐related diarrhoea and ‘idiopathic’ secretory diarrhoea, but more evidence is required. They have no role in acute pancreatitis and peptic ulcer bleeding. Irritable bowel syndrome remains unexplored but unlikely to benefit.
Fate of orally ingested enzymes in pancreatic insufficiency: comparison of two pancreatic enzyme preparations
Authors: DELCHIER J.‐C. , VIDON N. , GIRARDIN M.‐F. SAINT‐MARC , SOULE J.‐C. , MOULIN C. , HUCHET B. , ZYLBERBERG P. 
Published: July 2010

SUMMARYThe effect on steatorrhoea of a pH‐sensitive enteric‐coated pancreatic preparation (Eurobiol 25 000) was compared with a conventional pancreatic enzyme preparation (Eurobiol) in six adult patients with exocrine pancreatic insufficiency. In addition, the fate of orally ingested pancreatic enzymes in the upper digestive tract was evaluated by measuring gastric and duodenal pH, amount of enzymes in the stomach, duodenal enzyme output, and fat absorption at the angle of Treitz for the 4 hours following a standard meal. When compared with placebo, Eurobiol and Eurobiol 25 000 reduced daily faecal fat excretion by 24% (not significant) and 43% (P < 0.05), respectively. With the conventional preparation, enzyme output and fat absorption at the duodeno‐jejunal flexure were significantly improved (P < 0.05). Marked inter‐individual differences in duodenal enzyme recovery (lipase 3% to 80%; chymotrypsin 26% to 100%) and, consequently, in the reduction of steatorrhoea (0% to 67%) were observed, with the gastric emptying rate emerging as a key determinant factor. With the enteric‐coated preparation, enzyme output and fat absorption at the duodenojejunal flexure were not significantly improved. Discrepancy between the marked reduction of faecal fat excretion and the low duodenal enzyme recovery could indicate that enzyme delivery from microtablets occurs further down in the small bowel. Efficacy of enteric‐coated preparations could be enhanced by adding unprotected enzymes, especially in patients with rapid gastric emptying.
Pattern of breathing during upper gastrointestinal endoscopy: implications for administration of supplemental oxygen
Authors: BELL G. D. , ANTROBUS J. H. L. , LEE J. , COADY T. J. , MORDEN A. 
Published: July 2010

SUMMARYCardiopulmonary complications account for half the deaths associated with upper gastrointestinal endoscopy. The incidence of hypoxia at the time of upper gastrointestinal endoscopy can be greatly reduced by the administration of supplemental oxygen via nasal cannulae. Using dual thermistors in the mouth and nostrils of patients undergoing upper gastrointestinal endoscopy, the present study demonstrates that most patients breathe predominantly via the oral, rather than the nasal, route following intubation of the oesophagus. The implication from the study is that, if supplemental oxygen is to be used in ‘at risk’patients, it would be logical to employ an oral, rather than nasal, route of administration.
Influence of cisapride on antroduodenal motor function in healthy subjects and diabetics with autonomic neuropathy
Authors: WEHRMANN T. , LEMBCKE B. , CASPARY W. F. 
Published: July 2010

SUMMARYAntroduodenal manometry was used to assess motility in 10 healthy volunteers and 15 diabetics with cardiac autonomic neuropathy whilst they received 20 mg cisapride orally or an apparently identical placebo. Interdigestive motility was recorded after an overnight fast and for 2 hours following a 500 kcal liquid meal. Active treatment did not influence the number or duration of interdigestive motility cycles in either group although antroduodenal co‐ordination in both the fasting and the fed state was enhanced by cisapride (P < 0.05). In diabetics the postprandial antral motility index was increased by cisapride, whereas in healthy subjects antral and duodenal motility indices were increased both fasting and in the fed state (P < 0.05).These results suggest that impaired antroduodenal co‐ordination is of importance in delaying gastric emptying by diabetic subjects.
Effect of different doses of omeprazole on 24‐hour oesophageal acid exposure in patients with gastro‐oesophageal reflux
Authors: ROBINSON M. , MATON P. N. , ALLEN M. L. , HUMPHRIES T. J. , McINTOSH D. , CAGLIOLA A. J. , BRADSTREET T. E. 
Published: July 2010

SUMMARYTo define the optimum doses of omeprazole appropriate for acute and long‐term therapy of patients with gastro‐oesophageal reflux disease, 24‐h oesophageal pH was measured in 12 patients with symptomatic reflux and an abnormal 24‐h oesophageal acid exposure time (> 6%) in a randomized, double‐blind, four‐way crossover study comparing the effects of omeprazole 10, 20, or 40 mg/day and placebo. Total reflux time over 24 hours, number of reflux episodes per hour, and the number of reflux episodes lasting > 5 minutes were measured by ambulatory 24‐h oesophageal pH monitoring. All doses of omeprazole were superior to placebo in decreasing gastro‐oesophageal reflux as measured by each index.With placebo, oesophageal acid exposure was 16.3 % of the 24 hours, 10 mg omeprazole/day reduced that to 6.3 %, 20 mg/day lowered acid exposure to 0.9%, and 40 mg/day to 0.6%. Thus only the 20 and 40 mg doses reduced acid exposure to within the normal range. Similar results were obtained with the other indices of reflux. These data suggest that a rational dose regimen for reflux oesophagitis is 20 mg/day, a regimen that has proved effective in clinical trials. The present study indicates that 24‐hour oesophageal pH monitoring is a practical approach to the determination of drug dosage in patients with gastro‐oesophageal reflux.
Non‐steroidal anti‐inflammatory drug‐induced gastroduodenal injury: therapeutic recommendations
Authors: CURTIS W. D. , GRIFFIN J. W. 
Published: July 2010

SUMMARYNon‐steroidal anti‐inflammatory drug (NSAID) use is associated with gastro‐duodenal erosions and ulcers. Bleeding and perforation are reported complications in NSAID users. Therapeutic recommendations for NSAID‐induced gastroduodenal injury are necessary because of our rapidly growing geriatric population, a steady increase in prescriptions for NSAIDs, and the widespread use of over‐the‐counter NSAIDs. Studies seem to indicate that there is no relationship between acute NSAID‐induced mucosal injury and potential damage from chronic NSAID ingestion. Ranitidine (150 mg) b.d. effectively reduces the incidence of duodenal ulcer in NSAID users, but the same dose does not reduce the incidence of gastric ulcer. Misoprostol is effective in reducing the incidence of gastric ulcer in NSAID users, although confirmatory data on its effectiveness in preventing NSAID‐induced duodenal ulcer are lacking. In addition to anti‐ulcer therapy, treatment of NSAID‐induced ulcers includes discontinuing the drug, reducing the dose, or switching to a less potent NSAID. Longer courses of anti‐ulcer treatment may be required to achieve expected healing rates when NSAIDs are not discontinued. Results of treatment of NSAID‐related ulcers with currently available anti‐ulcer medications vary. Several studies have shown that 150 mg ranitidine b.d. heals both gastric and duodenal NSAID‐induced ulcers. Sucralfate has also been shown to heal NSAID‐induced duodenal ulcers. Misoprostol treatment of NSAID‐induced ulcers is not well documented, although there are placebo‐controlled data that substantiate its benefit in gastric ulcer patients not taking NSAIDs.
Review article: the treatment of Helicobacter pylori infection
Authors: HEATLEY R. V. 
Published: July 2010

SUMMARYThe discovery of Helicobacter pylori has stimulated great interest in its role in gastritis, non‐ulcer dyspepsia and peptic ulceration. Treatment regimens to eradicate this organism from gastric mucosa have also received considerable attention. Current recommendations limit the use of triple drug combinations only to specific patient groups.
Does a previous course of tripotassium dicitrato bismuthate afect the subsequent chances of successful Helicobacter pylori eradication?
Authors: BELL G. D. , POWELL K. , BURRIDGE S. M. , HARRISON G. , WEIL J. , GANT P. W. , JONES P. H. , TROWELL J. E. 
Published: July 2010

SUMMARYWe have performed a retrospective study of 103 patients with either peptic ulcer or non‐ulcer dyspepsia, infected with metronidazole‐sensitive strains of Helicobacter pylori (H. pylori), who were treated with a combination of tripotassium dicitrato bismuthate and metronidazole for a period of at least two weeks.Dual therapy with tripotassium dicitrato bismuthate plus metronidazole showed similarly high eradication rates (≥ 80%) of H. pylori from patients irrespective of age, gender or clinical diagnosis. Most importantly, dual therapy achieved a similar eradication rate of H. pylori infection in 41 patients who had previously been treated with tripotassium dicitrato bismuthate alone or in combination with an antibiotic other than metronidazole. It therefore appears that H. pylori does not become resistant to treatment with tripotassium dicitrato bismuthate.
Verapanzil inhibits in‐vitro leucotriene B4 release by rectal mucosa in active ulcerative colitis
Authors: GERTNER D. J. , RAMPTON D. S. , STEVENS T. R. J. , LENNARD‐JONES J. E. 
Published: July 2010

SUMMARYIncreased mucosal eicosanoid synthesis occurs in active ulcerative colitis; suppression of the synthesis of pro‐inflammatory leucotrienes could be therapeutically useful. Neutrophil 5‐lipoxygenase is calcium‐dependent. In this study, the effect of the calcium channel antagonist, verapamil, on the release of eicosanoids by colitic rectal mucosal biopsies has been examined. Verapamil in therapeutic concentration (5 μ g/ml, 10‐5 M) reduced leucotriene B4 release from actively inflamed rectal mucosa by 30% (from 60 (5.0 S.E.M.) ng/g wet weight/20 min without, to 42 (5.7 S.E.M.) with verapamil, P < 0.05), but had no effect on leucotriene B4 release by rectal biopsies taken from patients with quiescent ulcerative colitis (39 (2.8 S.E.M.) ng/g wet weight/20 min without, and 43 (5.0 S.E.M.) with verapamil). Verapamil did not affect mucosal prostaglandin E2 release. The results suggest that, in active ulcerative colitis, verapamil inhibits mucosal 5‐lipoxygenase activity and warrants therapeutic evaluation.
Cholestasis in transplant patients—what is the role of cyclosporin?
Authors: BLUHM R. E. , RODGERS W. H. , BLACK D. L. , WILKINSON G. R. , BRANCH R. 
Published: July 2010

SUMMARYThe use of the drug cyclosporin is limited by toxicity. It would be advantageous to develop therapeutic monitoring of cyclosporin which would predict the development of clinical toxicity. In the present study, alternative methods of measuring cyclosporin levels were evaluated in a heterogenous population of transplant patients, comparing a fluorescent polarization immunoassay using a non‐specific polyclonal antibody, which measures both cyclosporin and its main metabolites, and a specific high‐performance liquid chromatography assay for unchanged cyclosporin in blood.Neither measured variable alone correlated with laboratory evidence of renal toxicity (serum creatinine) or liver toxicity (serum glutamate transaminase, lactic dehydrogenase, alkaline phosphatase, or serum bilirubin). The relationship between metabolites and parent cyclosporin was quantitated using the ratio of cyclosporin levels determined by fluorescent polarization immunoassay over levels determined by high‐performance liquid chromatography. A cohort of patients with markedly elevated ratios of cyclosporin were identified. When patients’data were reviewed collectively and individually there was a correlation between an elevated ratio and the serum bilirubin (r= 0.41, P < 0.001). This association could be either due to cyclosporin as a cause of cholestasis or to cholestasis from any cause resulting in netaboite accumulation. Further studies are needed to clarify the role of cyclosportin in hepatic dysfunction and develop erly, specific markers for this cyclosporin‐associated toxicity.
β‐Galactosidase from Aspergillus niger in adult lactose malabsorption: a double‐blind crossover study
Authors: CORAZZA G. R. , BENATI G. , SORGE M. , STROCCHI A. , CALZA G. , GASBARRINI G. 
Published: July 2010

SUMMARYAn assessment was made of the efficacy of a β‐galactosidase, obtained from Aspergillus niger and added to intact milk, in decreasing lactose malabsorption and intolerance. Sixteen adult patients with malabsorption and intolerance to this sugar were studied in a double‐blind crossover study vs. placebo. A 5‐hour hydrogen breath test was used to assess malabsorption of lactose contained in 400 ml milk. When compared with placebo, the addition of exogenous lactase to intact milk caused a statistically significant reduction in the maximum breath H2 concentration (P < 0.01) and in the cumulative H2 excretion (P < 0.005). In the same way, the cumulative index for gastrointestinal intolerance was significantly lower (P < 0.005) after the ingestion of lactase‐added milk. This study demonstrates that enzyme replacement therapy, with β‐galactosidases obtained from Aspergillus niger, is effective in decreasing lactose malabsorption and its consequent intolerance in adult subjects with lactase deficiency.
Review article: metabolic consequences of long‐term inhibition of acid secretion by omeprazole
Authors: KOOP H. 
Published: July 2010

SUMMARYMetabolic sequelae of profound and long‐lasting inhibition of gastric acid secretion by omeprazole have largely been neglected. Data from long‐term studies suggest that vitamin B12 stores decrease slightly over several years, although this was not clinically relevant within the first 4 years of therapy. Additionally, it cannot be completely ruled out that patients with an increased iron demand may develop iron deficiency, but data available at present do not provide any evidence that iron malabsorption is to be expected under normal conditions. Protein homeostasis and calcium metabolism seem to be unaffected by long‐term omeprazole therapy. Based upon present experience, serum cobalamin concentration should be monitored in patients undergoing omeprazole therapy for several years.