bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of oral cisapride on colonic transit
Authors: KREVSKY B. , MALMUD L. S. , MAURER A. H. , SOMERS M. B. , SIEGEL J. A. , FISHER R. S. 
Published: July 2010

SUMMARYA prospective double‐blind cross‐over trial of oral cisapride 10 mg and placebo was performed to determine the effects of cisapride on the transit of colonic contents in normal humans. Six male volunteers were studied twice using Colonic transit scintigraphy. After passing a tube to the caecum, 50 μCi of 111Indium diethylene triamine pentaacetic acid were instilled into the bowel lumen. The movement of radiolabelled material was followed using a gamma camera interfaced to a digital computer. Cisapride decreased the half‐emptying of the caecum and ascending colon from 1.68 ± 0±4 hours to 0.72 ± 0.15 hours (P < 0.05). The total colon half‐emptying time was reduced from 38.5 ± 7.2 hours to 11.1 ± 2.9 hours on cisapride (P < 0.05). Cisapride accelerated transit through the transverse colon, but not the descending colon. The progression of the geometric centre was faster during cisapride administration than with placebo (P < 0.05). The number of bowel movements 48‐hours−1 increased after cisapride from 2.5 ± 0.8 to 5.0 ± 0.4 (P < 0.05). This study demonstrates that cisapride has a marked prokinetic effect on Colonic transit in normal subjects. Cisapride may be a useful agent in the treatment of constipation.
Marked suppression of stimulated gastric acid and pepsin secretion by enisoprost, a new PGE1 analogue
Authors: HOWDEN G W. , BURGET D. W. , SILLETTI C. , VAN EEDEN A. , TOMKINS K. B. , HUNT R. H. 
Published: July 2010

SUMMARYThe gastric antisecretory effects of three different doses of enisoprost, a new synthetic PGE1 analogue, were compared with placebo and misoprostol in 20 healthy male volunteers. Enisoprost 100, 200 and 400 μg all significantly (P < 0.0001; ANOVA) suppressed histamine‐stimulated acid and pepsin output when compared with placebo or misoprostol 200 μg. Misoprostol produced a significant decrease of stimulated acid output when compared with placebo (P= 0.0012). The concentration of pepsin in gastric juice was significantly (P < 0.0001) decreased by enisoprost at the commencement of histamine stimulation. This effect was short‐lived, and was maximal with enisoprost 400 μg. There was a significant dose‐response relationship for enisoprost for inhibition of stimulated acid output (P= 0.0065). Enisoprost was well tolerated, and no consistent drug‐related adverse effects were detected. The profile of antisecretory effect of enisoprost, producing marked suppersion of both acid and pepsin secretion independently, is unusual. This combination of activity along with any mucosal protective properties might be particular effective in the treatment of peptic ulcer disease.
Idiopathic slow‐transit constipation: whole gut transit times, measured by a new simplified method, are not shortened by opioid antagonists
Authors: FOTHERBY K. J. , HUNTER J. O. 
Published: July 2010

SUMMARYA simplified method for measuring mean whole gut transit time has been validated which avoids stool collection and is suitable for out‐patients. Radio‐opaque markers are swallowed daily for 14 days and the mean whole gut transit time is derived directly from an abdominal X‐ray. Using this new technique, neither nalmefene (in a double‐blind study of six patients) nor naloxone (in an open study of four patients) shortened mean whole gut transit time in idiopathic slow‐transit constipation.
Review: first‐pass metabolism by the gastrointestinal mucosa
Authors: BACK D. J. , ROGERS S. M. 
Published: July 2010

SUMMARYThe bioavailability of orally administered drugs may be reduced due to presystemic elimination. The first‐pass effect can occur in the gastrointestinal tract, the liver and lung. Although the liver is the main drug metabolizing organ in the body, the gut wall can play an important role in the first‐pass metabolism of certain drugs. Both phase I (preconjugation) and phase II (conjugation) reactions have been described. However, while the oxidative metabolic capacity of the intestinal mucosa is considerably smaller than that of the liver, the activity of conjugation reactions in the gut may be close to that of the liver, and in some cases may exceed it. Sulphate conjugation is particularly important for steriod hormones such as ethinyloestradiol, and for the β‐adrenoceptor stimulants isoprenaline and isoetharine. Glucuronidation has been demonstrated to occur in man for morphine, paracetamol and oestrogens. Significant drug—drug interactions have been described involving drugs undergoing sulphate conjugation. The study of intestinal metabolismin vivois difficult in man since direct methods (for example, hepatic portal vein catheterization) is justified in only a small number of patients. Therefore, much of our present understanding has been derived from various in‐vitro studies involving intestinal sheets, mucosal biopsies, isolated enterocytes and microsomal preparations.
Review: gut sterilization in inflammatory bowel disease
Authors: HODGSON H. J. F. 
Published: July 2010

SUMMARYAchieving a substantial reduction in the bacterial flora of the gut is a theoretically attractive means of treating inflammatory bowel disease, particularly colonic disease. There are practical difficulties in obtaining a sustained reduction of the colonic bacterial count, and the potential role of such a treatment regimen is therefore the initiation of remission. The data in the literature supporting such a suggestion are anecdotal, and a controlled study is indicated.
Ranitidine and cimetidine in the healing of duodenal ulcer: meta‐analysis of comparative clinical trials
Authors: McISAAC R. L. , McCANLESS I. , SUMMERS K. , WOOD J. R. 
Published: July 2010

SUMMARYAll available ranitidine and cimetidine comparative trials in acute duodenal ulcer disease were examined: of the 44 trials, 36 favoured ranitidine, and there was an overall difference in ulcer healing of 7%. Further stratification enabled examination of trials with common attributes: the most frequent endoscopic assessment was at 4 weeks to compare ranitidine 150 mg twice daily with cimetidine 1 g day−1 or 400 mg b.d. Twenty of these trials had sufficient data to permit pooling. Ranitidine was favoured in 18/20 trials and in three the differences achieved statistical significance. Results of the trials were combined using meta‐analysis to calculate differences in ulcer healing. Most studies had sample sizes that were insufficient to detect clinically‐important differences; the power to detect a 20% difference was less than 80% in 15/20 trials, and for a 10% difference was less than 80% in all but one trial. Fifteen trials compared ranitidine 150 mg b.d. with cimetidine 1 g day−1: healing after 4 weeks therapy was overall 6% greater for ranitidine. This was statistically significant (P < 0.05) and the combined total number of patients had a power of 83% to detect this difference. In five trials the dose of cimetidine used was 400 mg b.d.: the 12% difference in healing in favour of ranitidine 150 mg b.d. was statistically significant, and the combined trials had a power of 95% to detect this difference. Ranitidine 150 mg twice daily heals significantly more duodenal ulcers after 4 weeks of therapy than either cimetidine 400 mg b.d. or cimetidine 1 g day−1.
Comparison of the effectiveness of midazolam and diazepam in lipid emulsion as sedation during upper gastrointestinal endoscopy
Authors: BULLIMORE D. W. , MULLEY B. A. , COOKE P. , MILOSZEWSKI K. J. A. 
Published: July 2010

SUMMARYIn a study of 101 patients undergoing upper gastrointestinal endoscopy, 90% of patients had complete amnesia for the procedure after intravenous midazolam (average dose 10 mg), but only 61% had complete amnesia after intravenous diazepam in lipid emulsion (average dose 18.4 mg) (P= 0.0006). However, when assessed by two different tests, recovery within the first hour was significantly more rapid after diazepam (P < 0.0001). Prolonged sedation (over 20 hours after injection) was reported occasionally by patients who had received either drug. Thus, as with patients who have been sedated with diazepam, those who have been sedated with midazolam should also be advised to avoid driving or operating machinery for at least 24 hours after injection.
Contractility of human gallbladder muscle in vitro
Authors: FEELEY T. M. , CLANACHAN A. S. , SCOTT G. W. 
Published: July 2010

SUMMARYThis study examined the effects of transmural nerve stimulation, acetylcholine, adrenoceptor agonists and several peptides on the contractility of strips of human gallbladder in vitro. Acetylcholine caused concentration‐related contractions of the tissues and the sensitivity to acetylcholine was similar in gallbladders with mild and severe chronic cholecystitis. Noradrenaline and adrenaline relaxed gallbladder strips, probably via β2‐adrenoceptor stimulation. Transmural nerve stimulation always caused contractions, but in the presence of atropine inhibitory responses were demonstrable and these were antagonized by propranolol. There was no evidence of non‐adrenergic inhibitory neural responses. Of the peptides tested, only cholecystokinin octapeptide (CCK‐OP), gastrin, pentagastrin, substance P and caerulein caused contractions. Responses to CCK‐OP, gastrin and pentagastrin were antagonized by dibutyryl cyclic GMP. Hormones which had no effect upon human gallbladder strips included motilin, secretin, bombesin, neurotensin, glucagon, vasopressin, VIP and somatostatin. Considerable differences therefore exist between human tissues and those from experimental animals with respect to the direct actions of neural and hormonal stimuli on gallbladder contractility.
The effect of two α2‐adrenoreceptor agonists and an antagonist on gastric emptying and mouth to caecum transit time in humans
Authors: BAXTER A. J. , EDWARDS C. A. , HOLDEN S. , CUNNINGHAM K. M. , WELCH I. McL. , READ N. W. 
Published: July 2010

SUMMARYExperiments were performed to investigate the effect of two α2‐adrenoreceptor agonists, clonidine and lidamidine, and a specific α2‐adrenoreceptor antagonist, idazoxan, on gastric emptying and mouth to caecum transit time (MCTT) of a radiolabelled meal in 27 healthy male subjects. Lidamidine (20 mg p.o.) and clonidine (0.3 mg p.o.), given alone had no significant effect on gastric emptying or MCTT suggesting that the anti‐diarrhoeal action of clonidine and lidamidine are unlikely to be explained by a slowing of small intestinal transit. Idazoxan (20 mg p.o.) reversed the effect of clonidine in 10 subjects, who showed a delay in MCTT after taking clonidine, but did not alter MCTT under basal conditions. These results suggest that although the sympathetic nervous system can influence upper gastrointestinal motility by an action on α2‐adrenoreceptors, this action does not exert a tonic influence on upper gastrointestinal motility under basal conditions.
Is it really more difficult to treat prepyloric ulcers?
Authors: HALTER F. , EIGENMANN F. 
Published: July 2010

SUMMARYPrepyloric and duodenal ulcers have some common characteristics: gastric acid secretion is increased and there is an association with blood group O. Many, therefore, have considered prepyloric ulcers to be a variety of duodenal ulcer disease. From an anatomical point of view, however, prepyloric ulcers are clearly gastric ulcers. After proximal selective vagotomy, the recurrence rate is very high, amounting to more than 30% in 5 years; this is significantly higher than the rate for duodenal ulcers. Better results are obtained in prepyloric ulcers, if vagotomy is combined with a drainage procedure. In recent years, some evidence, primarily from Scandinavia, has accumulated indicating that prepyloric ulcers are more resistant to treatment with histamine H2‐receptor antagonists than duodenal ulcers or ulcers located in other parts of the stomach. In addition, the recurrence rate is particularly high in prepyloric ulcers. One must, however, consider that not only have all of these studies included relatively small numbers of patients, but also the prepyloric ulcer healing rates in other studies were similar to those observed for both duodenal ulcers and ulcers located elsewhere in the stomach. Prospective studies with large numbers of patients are, therefore, necessary before a clear‐cut conclusion can be reached.There are several reasons why prepyloric ulcers could be more resistant to treatment. Impaired gastric emptying, duodeno‐gastric reflex or choric gastritis, especially in conjunction with Campylobacter pylori infection, must be considered. At present one can only speculate on the validity of any of these hypotheses.
When and why do ulcers bleed and what can be done about it?
Authors: SWAIN C P. 
Published: July 2010

SUMMARYThis article reviews the pathophysiology and management of bleeding peptic ulcer. Ulcers bleed when and because they erode into a blood vessel, and bleed massively when they erode into a medium‐ or large‐sized artery. Focal pathology at the bleeding point (such as arteritis, aneurysmal dilatation or recanalized thrombus) contributes to the timing and clinical pattern of ulcer bleeding. Big bleeds are probably associated with erosion into big arteries. The identification of a visible vessel in the floor of an ulcer that has recently bled is predictive of further bleeding, while the absence of a visible vessel or stigmata of recent haemorrhage is strongly predictive that further bleeding will not occur. Unfortunately, no conventional method of managing gastrointestinal bleeding from ulcers has been convincingly shown to be better than placebo in controlled clinical trials. The value of transfusion and surgery has never been tested in controlled trials, while many small studies of drug therapy, especially of H2‐receptor blocking agents, and a few small studies of early surgery afford generally negative or equivocal results. There is some evidence that new physical methods such as lasers or bipolar probes applied at endoscopy are superior to placebo though negative trials have also been reported. Studies randomizing larger numbers of patients with bleeding ulcers are required if therapeutic benefit of any aspect of management is to be demonstrated or refuted.
The place of famotidine in anti‐ulcer therapy
Authors: MANN S. G. 
Published: July 2010

SUMMARYFamotidine now presents physicians in the USA and many European countries with a third option when considering H2‐antagonist therapy. A dose of 40 mg in the evening decreases nocturnal gastric acidity for 10–12 hours, leaving daytime‐stimulated acidity virtually unaffected. This single evening dosage regimen produces effective healing of gastric and duodenal ulceration; maintenance of healing can then be achieved satisfactorily with 20 mg in the evening. In extensive clinical studies, the adverse effect profile of famotidine is similar to placebo. Famotidine has no known drug interactions and there are no identified mechanisms by which it might be expected to produce them. Circulating plasma hormone concentrations in man are not affected by famotidine and no antiandrogenic properties have been observed in animal studies. Future potential uses of famotidine may include the treatment of haemorrhage from peptic ulcers and the healing of oesophageal ulceration.
Omeprazole in the treatment of Zollinger—Ellison syndrome: a 4‐year international study
Authors: LLOYD‐DAVIES K. A. , RUTGERSSON K. , SÖLVELL L. 
Published: July 2010

SUMMARYThe H+, K+‐ATPase inhibitor omeprazole has been made available on a compassionate basis for patients with Zollinger—Ellison syndrome considered resistant to, or with side‐effects on, histamine Hz ‐receptor antagonists. By December 1985, the first 80 patients, from 46 centres in 11 countries, had been treated for periods of 2 days to 4 years. Basal acid output was decreased to the desired level of less than 10 mmol · hour1, and symptoms were rapidly relieved. Acid secretion and laboratory variables were checked regularly and endoscopic examinations made at intervals. Dosage was adjusted primarily on the basis of basal acid output, but also if symptoms recurred. The starting dose was generally 60 mg daily and the median dose ranged between 60 and 70 mg daily over the study period. There was no evidence of tachyphylaxis. More than 90 % of the patients were successfully controlled on total daily doses of 120 mg or less; one‐third of patients required divided doses. Tolerance was good: there were no obvious drug‐related effects on laboratory variables, including fasting serum gastrin, and there were very few adverse events. Thirteen patients died (11 of the primary disease and two of other causes), four underwent successful tumour resection, six underwent total gastrectomy (though acid secretion was controlled in five), four patients’ treatment was changed to other medical therapy, and one was lost to follow‐up. Omeprazole thus appears to be both safe and very effective in controlling acid hypersecretion in this group of patients, and to provide a suitable alternative to total gastrectomy.
Effect of a slow‐release formula of trimoprostil on intragastric acidity in healthy volunteers
Authors: EMDE C. , CILLUFFO T. , BAUERFEIND P. , FIMMEL C. J. , BLUM A. L. 
Published: July 2010

SUMMARYWe investigated the effect of a slow‐release formula of trimoprostil, a prostaglandin E2 analogue, at a dose of 3 mg b.d. on circadian intragastric acidity in nine healthy volunteers using ambulatory pH‐metry in a placebo‐controlled study. The effect of trimoprostil was long lasting (8 hours during the night). However, it lowered gastric pH on average only by 0.4 pH units. In four of the six women severe side‐effects occurred in the form of abdominal cramping, metrorrhagia, and/or diarrhoea. These disadvantages may limit the clinical use of this drug.
Somatostatin compared with cimetidine in the treatment of bleeding peptic ulcer without visible vessel
Authors: SAPERAS E. , PIQUÉ J. M. , PÉREZ‐AYUSO R. , FUSTER F. , TERÉS J. , BORDAS J. M. , RODÉS J. 
Published: July 2010

SUMMARYIn a randomized double‐blind trial 100 patients with severe bleeding peptic ulcers were treated with an intravenous (i.v.) infusion of cimetidine or somatostatin. Only those patients in whom endoscopy performed within 6 h of admission showed non‐arterial bleeding or signs of recent haemorrhage without a visible vessel entered the trial. The two treatment groups were well matched for age, sex, presence of underlying disease, prior ingestion of ulcerogenic drugs, tobacco habits, type of bleeding, haematocrit at admission, presence of hypovolaemic shock, source of bleeding and endoscopic findings. Four patients in each group were excluded after randomization. Further haemorrhage occurred in eight (17.3%) patients in the somatostatin group and in 10 (21.7%) in the cimetidine group, but the difference was not statistically significant. The number of surgical procedures, blood transfusion requirement, duration of hospitalization and mortality rates were similar in the two treatment groups. These results suggest that somatostatin does not improve the results obtained with cimetidine in patients with bleeding peptic ulcer, in whom the endoscopy discloses non‐arterial bleeding or signs of recent haemorrhage without a visible vessel.
The effects of the 5‐hydroxytryptamine (5HT3) receptor antagonist ICS 205‐930 in the carcinoid syndrome
Authors: COUPE M. O. , ANDERSON J. V. , MORRIS J. A. , ALSTEAD E. M. , BLOOM S. R. , HODGSON H. J. F. 
Published: July 2010

SUMMARYTherapy for diarrhoea associated with the carcinoid syndrome is often unsatisfactory. In an open study ICS 205‐930 (Sandoz Limited), a novel 5HT3‐antagonist, controlled diarrhoea in five of six patients studied. This drug may be a useful advance in the symptomatic treatment of the carcinoid syndrome.
Balsalazide in the maintenance treatment of patients with ulcerative colitis, a double‐blind comparison with sulphasalazine
Authors: McINTYRE P. B. , RODRIGUES C. A. , LENNARD‐JONES J. E. , BARRISON I. G. , WALKER J. G. , BARON J. H. , THORNTON P. C. 
Published: July 2010

SUMMARYBalsalazide (BSZ) is a pro‐drug which releases 5‐aminosalicylic acid (5ASA) and 4‐aminobenzoyl‐β‐alanine (an inert carrier) in the colon of various species including man. BSZ was compared with sulphasalazine (SASP) (both 1 g b.d. orally) in the maintenance of remission in patients with ulcerative colitis (UC). Seventy‐nine patients (5.3 male, 26 female), mean age 49 years (range 19–79 years), with UC were randomly allocated to either treatment (41 BSZ, 38 SASP) for 6 months. The groups were similar in respect of age, sex, duration and extent of disease. Seven patients defaulted (3 BSZ, 4 SASP) leaving 38 on BSZ and 34 on SASP. Two male patients, both receiving SASP, were withdrawn because of severe side‐effects. One of these patients, with an exfoliative rash, was maintained satisfactorily on open BSZ. Remission rates at 6 months (51% BSZ, 63% SASP) were not significantly different (life‐table analysis P < 0.1). Twelve patients (15%) reported troublesome side‐effects (2 BSZ 5%, 10 SASP 26%, P= 0.017 Fisher Exact Test). Mean haemoglobin concentrations, similar on entry, increased after 6 months with BSZ (0.2 g/dl) but decreased with SASP (0.5 g/dl) (P < 0.0002). BSZ was not significantly different from SASP in maintaining remission in patients with UC but had fewer side‐effects.
Effect of low‐dose omeprazole on gastric acid secretion in duodenal ulcer patients
Authors: McLAUCHLAN G. , CREAN G. P. , McCOLL K. E. L. 
Published: July 2010

SUMMARYThe effect of 7 days of oral dosing with 5 mg day−1 and 20 mg day−1 omeprazole on basal and pentagastrin‐stimulated gastric acid output was studied in nine duodenal ulcer patients. Basal acid output measured 5–6 h post‐dosing was decreased by a mean of 75% on 5 mg omeprazole and by 90% on 20 mg omeprazole (P < 0.05 and P < 0.01, respectively). Peak acid output measured 6–7 h post‐dosing was decreased by a mean of 75% on 5 mg omeprazole and 90% on 20 mg omeprazole (P < 0.01 for each). There was a wide interindividual variation in response to the 5 mg dose, with five of the nine patients having more than 90% inhibition of peak acid output, but two patients having less than 40% inhibition. This unpredictable response to daily low‐dose omeprazole therapy makes it unsuitable for maintenance treatment.
Review: the enterochromaffin‐like cell, intragastric acidity and the trophic effect of plasma gastrin
Authors: POLAK J. M. , BLOOM S. R. 
Published: July 2010

SUMMARYAlthough enterochromaffin‐like (ECL) cells form the major endocrine cell population of the non‐antral stomach, they have been largely overlooked in the study of gastric disease. In the human, their product and functions are unknown, but they are associated with histamine secretion in rodents. The cells are controlled by neural and hormonal factors, the most significant of the latter being gastrin. Interest in ECL cells has been stimulated by the observation that hyperplasia of these cells, sometimes leading to formation of gastric carcinoid tumours, occurs in conditions of persistent hypergastrinaemia — for example, in response to the achlorhydria of individuals with pernicious anaemia. The advent of new highly potent inhibitors of gastric acid secretion is allowing more information to be obtained on the physiology and functions of the ECL cell. However, there is clearly a great deal more to be discovered about this enigmatic endocrine cell type.
Gastro‐oesophageal reflux associated with nifedipine
Authors: JENKINSON L. R. , NORRIS T. L. , WATSON A. 
Published: July 2010

SUMMARYA 57‐year‐old woman presented with a 3‐week history of dysphagia for solids, 6 months after starting treatment with nifedipine. Endoscopy demonstrated oesophagitis and a benign oesophageal stricture. Twenty‐four‐hour ambulatory pH monitoring demonstrated decreased acid reflux 8 weeks after withdrawal of nifedipine, with coincidental symptomatic and endoscopic improvement. Nifedipine may induce, or aggravate, pre‐existing, gastro‐oesophageal reflux.