bluuebunny/crossref_metadata_2025_split huggingface dataset:
Short report: sedation for upper gastrointestinal endoscopy—diazepam versus midazolam
Authors: GILVARRY J. M. , CRAIG M. , FIELDING J. F. 
Published: July 2010

SUMMARYIntravenously injected midazolam was associated with a greater degree of sedation, as assessed by 24‐h retrograde amnesia, than the longer acting benzodiazepine, diazepam. No differences in the frequency of pain on injection or the occurrence of venous sequelae were noted between the two preparations.
Prolonged inhibition of acid secretion causes hypergastrinaemia without altering pH inhibition of gastrin release in humans
Authors: KARNES W. E. , BERLIN R. G. , MAXWELL V. , SYTNIK BOYZENA , ROOT JANET K. , WALSH J. H. 
Published: July 2010

SUMMARYHypergastrinaemia induced by potent inhibitors of acid secretion is thought to occur as a result of the elimination of the inhibitory effects of intragastric acid on gastrin release. The present study was designed to determine if the mechanisms responsible for feedback inhibition of gastrin release and acid secretion by intragastric acid are preserved during four weeks of varying degrees of drug‐induced acid inhibition. Forty‐eight healthy male volunteers were randomly assigned to one of four treatments for four weeks: 10 mg omeprazole o.m., 20 mg omeprazole o.m., 40 mg omeprazole o.m. or 150 mg ranitidine b.d. Gastrin release and acid secretion in response to peptone meals maintained at pH 2.5 and pH 5.5 by intragastric titration, and 24‐hour gastrin profiles in response to standard meals were determined before treatment, at the fourth week of treatment and two weeks after discontinuing treatment. As expected, omeprazole produced dose‐related effects on acid secretion and gastrin concentrations that were largely reversed after treatment was discontinued. Gastrin release in response to pH 5.5 peptone meals remained significantly greater than gastrin release in response to pH 2.5 meals during treatment with all doses of omeprazole. The ratio of pH 5.5/pH 2.5 peptone meal‐stimulated gastrin release was approximately 1.5, and remained constant for all treatment groups throughout the study period. These data indicate that four weeks of drug induced hypochlorhydria causes an apparent increase in overall G‐cell function, but it does not interfere with normal feedback inhibition of gastrin release and acid secretion mediated by intragas tric acidity.
Comparison of three regimens in the management of acute gastroenteritis in infants
Authors: McCLEAN P. , LYNCH A. B. , DODGE J. A. 
Published: July 2010

SUMMARYSixty infants were randomly assigned to one of three groups on admission to hospital with a diagnosis of gastroenteritis. After rehydration, Group A received a low‐lactose, low‐fat feed (HN25) in full strength; Group B were regraded on to a conventional formula (SMA); Group C received a hydrolysed soya and collagen feed (Prejomin) in full strength. All feeds were continued for 5 days. The median duration of loose stools from starting the feed was 24 hours in Group A, compared to 119 hours and 95 hours in Groups B and C, respectively. Group A showed a mean percentage increase in weight of 2.34%, Group B showed a mean loss of 1.45%, and Group C a mean increase of 0.15%. These differences were statistically significant. Recovery from gastroenteritis is hastened by the use of a low‐lactose, low‐fat feed in the initial post‐rehydration phase of the disease.
Pharmacological profile of duodenal alkaline secretion
Authors: GARNER A. , HEYLINGS J. R. , HAMPSON S. E. , STANIER A. M. 
Published: July 2010

SUMMARYStimulation of mucosal alkaline secretion represents an opportunity for discovering novel drugs of potential benefit in maintenance therapy of duodenal ulcer disease. We screened over 200 agents representing the full spectrum of pharmacological categories in order to characterize stimulatory pathways and identify mechanistic leads. A variety of eicosanoids, phospho‐diesterase inhibitors and adrenoreceptor agonists together with forskolin, 6–hydroxy‐dopamine, 2–chloroadenosine, diazepam, testosterone, dipyridamole and dihydropyridazinone caused a reproducible increase in the metabolism‐dependent component of alkaline secretion in bullfrog proximal duodenum. PGE2(ED500.02 μg/ml) was the most potent agent in vitro and was also the most effective stimulant of duodenal alkalinization in vivo in an anaesthetized cat preparation. Agents without effect on spontaneous alkaline secretion by amphibian duodenum included agonists and antagonists of histamine, 5–hydroxy‐tryptamine, γ‐aminobutyric acid, dopamine, muscarinic and nicotinic receptors, inhibitors of amine uptake, monoamine oxidase and cholinesterase, plus various corticoids, diuretics, oestrogens, chemotherapeutic (anticancer) and antimicrobial agents. The major mechanism of stimulating alkaline secretion in the isolated duodenum is by increasing intracellular cyclic AMP levels. This may occur by either inhibiting metabolism of the nucleotide or by stimulating its formation.
Effects of low‐dose cimetidine on nocturnal acid secretion in healthy subjects
Authors: ACTON G. , BROOM C. , WAREHAM K. , LAROCHE J. , BURNHAM D. , FRIEDMAN C. 
Published: July 2010

SUMMARYThe effects of 100 mg and 200 mg bedtime doses of cimetidine on nocturnal gastric acid secretion were examined in nine healthy subjects in a double blind, placebo controlled, randomised three way crossover study. Treatment was given at 23.00 hours and the gastric contents continually aspirated from midnight until 07.00 hours the following morning. Hourly aliquots were analysed for pH and acid output. Relative to placebo the 100 mg and 200 mg doses of cimetidine respectively increased mean pH by 2.22 and 2.63 units/h (P < 0.001) with mean acid output decreasing by 0.95 and 0.98 mmol/h (P < 0.001). Whilst mean pH was higher and mean acid output was lower for 200 mg cimetidine compared to 100 mg cimetidine the difference was not statistically significant. Mean hourly pH was consistently above pH 3 for 100% of the time for both doses of cimetidine whereas mean pH failed to reach this value at anytime on placebo.Low doses of cimetidine taken at bedtime effectively reduced nocturnal gastric acid secretion in healthy individuals.
Long‐term effects of elemental and exclusion diets for Crohn's disease
Authors: GIAFFER M. H. , CANN P. , HOLDSWORTH C D. 
Published: July 2010

SUMMARYPrevious studies have confirmed the therapeutic value 61 elemental diets in promoting remission in active Crohn's disease, but their long‐term benefit has not been established. Twenty‐seven patients with established Crohn's disease who attained clinical remission after four weeks of enteral feeding were followed prospectively for up to 36 months. Twenty of these were willing to be tested for specific food intolerance using a predefined dietary elimination protocol; the others continued on a normal unrestricted diet. Eighteen patients (67%) have since relapsed; 89% of the relapses occurred within the first 6 months. Of the 15 patients with colonic involvement, 12 (80%) relapsed by 6 months. In contrast only 3 of 11 with isolated small bowel disease experienced early relapse. Of the 14 patients who completed the process of dietary testing, 5 could not identify any trigger foods; the remaining 9 were maintained on exclusion diets, 3 of whom relapsed early. Of the 11 taking a normal diet, 9 relapsed. Disease duration, previous intestinal resection or prior steroid therapy did not affect the relapse rate. Eight patients (31 %) obtained a long‐term remission, mean 23 months (range 12–36 months), without any medication. Long‐lasting remissions can be obtained in about one‐third of patients with Crohn's disease following treatment with a defined formula diet. Colonic involvement is associated with a high early relapse rate.
The effects of renzapride, a novel prokinetic agent, in diabetic gastroparesis
Authors: MACKIE A. D. R. , FERRINGTON C , COWAN S. , PALMER K. R. 
Published: July 2010

SUMMARYGastric emptying was measured in 9 diabetic patients with autonomic neuropathy (Group 1) and 8 normal controls (Group 2) on 4 occasions after swallowing placebo, 0.5, 1.0 or 2.0 mg of the newly developed prokinetic drug renzapride given double‐blind and in random order. The liquid component of the test meal was labelled with In113mand the solid with Tc99m. Liquid emptying was uni‐exponential. Solid emptying comprised an initial lag phase, followed by a linear component. Following placebo, the mean lag phase of solid emptying was 40 ± 7 (S.E.M.) min in Group 1 and 16 ± 2 min in Group 2 (P< 0.01). In Group 1 subjects renzapride reduced the mean lag phase by 20–26 min at all doses (P< 0.01). No effect was seen in Group 2. The linear rate of solid emptying was similar in both groups (0.9 ± 0.1 and 1.0 ± 0.2%/min) and was not altered by renzapride. Mean liquidt1/2was similar in Groups 1 and 2 after placebo (30 ± 6 and 29 ± 4 min, respectively) and was decreased with increasing doses of renzapride in both groups. No adverse effects were encountered in any subjects. Renzapride may be useful in the treatment of diabetic gastroparesis.
Morphometric studies in duodenal biopsies from patients with coeliac disease: the effect of the steroid fluticasone propionate
Authors: ZAITOUN A. , RECORD C. O. 
Published: July 2010

SUMMARYMorphometric measurements have been performed on small intestinal biopsy specimens from patients with untreated coeliac disease before and after six weeks oral treatment with a steroid of low systemic bioavailability (fluticasone propionate). Measurements were obtained by point counting and also by a computer‐aided measuring system with reference to a constant area of the muscularis mucosa.Fluticasone propionate led to a parallel reduction in the intra‐epithelial lymphocyte count within the surface (P < 0.001) and crypt epithelium (P < 0.01). The intra‐epithelial lymphocyte count assessed by reference to constant areas of the muscularis mucosa and surface epithelium were decreased two‐fold (P < 0.01) and seven‐fold (P < 0.001) respectively. Fluticasone propionate treatment also led to significant increases in the absorptive surface epithelium as shown by an increase in the villus: crypt ratio (P < 0.01), the epithelial cell height (P < 0.01) and two‐ to three‐fold increases in the area and length of the surface epithelium (P < 0.001).Short‐term fluticasone propionate treatment appears to exert a powerful beneficial effect upon duodenal morphology in patients with coeliac disease. Whether the alterations seen are comparable to a similar period of gluten withdrawal is not yet known.
A controlled study of 20 mg famotidine nocte vs. 150 mg ranitidine nocte for the prevention of duodenal ulcer relapse
Authors: PORRO G. BIANCHI , LAZZARONI M. , BARBARA L. , CORINALDESI R. , BLASI A. , MANGIAMELI A. , CAPURSO L. , KOCH M. , CHELI R. , BOVERO E. , FRANCHIS R. DE , GUSLANDI M. , FRANCAVILLA A. , INGROSSO M. , GASBARRINI G. , ZOLI G. , MAZZACCA G. , SABBATINI F. , NACCARATO R. , MARIO F. DI , PAOLUZI P. , AGNELLO M. , SCURO L. A. , CAVALLINI G. , SURRENTI C. , CALACRO A. 
Published: July 2010

SUMMARYA 24‐week, double‐blind, randomized study at 13 centres compared the efficacy and safety of 20 mg famotidine nocte and 150 mg ranitidine h.s. for the prevention of duodenal ulcer recurrence. All participants had been successfully treated for an acute duodenal ulcer with 40 mg famotidine nocte. Patients were endoscoped at baseline and at 24 weeks, unless symptoms warranted earlier examination: of the 208 patients enrolled, 86 who received famotidine and 84 who received ranitidine met all protocol criteria and were considered evaluable.Intention to treat and per protocol analyses showed non‐significant trends in favour of famotidine (P= 0.44 and 0.16, respectively). During the 24‐week observation period, 16.3% of the famotidine group and 25% of the ranitidine group had an ulcer recurrence (95% CI of percentage difference –0.22 + 0.04). At 24 weeks, relief of day and night pain was reported by 81.2% and 91.8% of the famotidine‐treated patients, respectively. The corresponding figures in the ranitidine group were 73.5% and 85.5%.No laboratory abnormalities related to the study‐drugs were noted and only two drug related (possibly or probably) adverse experiences were reported, both in the famotidine group. The data from this study therefore, supports the conclusion that the efficacy of 20 mg famotidine nocte is comparable to that of ranitidine in preventing duodenal ulcer recurrence, with comparable tolerability for long‐term therapy.
Review article: dietary and nutritional management of Crohn's disease
Authors: RUSSELL R. I. 
Published: July 2010

SUMMARYThe value of dietary alteration and the nutritional management of Crohn's disease is assessed in this review.Lactose restriction, low‐fat diets and low‐residue diets may be of value in specifically indicated clinical situations. A fibre‐rich, unrefined carbohydrate diet has not been shown to alter the course of the disease, and the value of ‘exclusion diets’remains to be confirmed in controlled, prospective studies.Nutritional insufficiency of varying degrees is common in Crohn's disease and can be corrected by the efficient use of enteral diets (usually with polymeric preparations) or intravenous nutritional support. Growth retardation in adolescents with Crohn's disease can usually be improved by enteral nutrition.Nutritional support of various kinds may be of value in the management of local complications of Crohn's disease; sub‐acute obstruction, anal, perianal and rectal lesions, fistulas and ileostomy complications, and the management of bile acid‐induced diarrhoea.The use of nutrition as ‘primary therapy; in Crohn's disease is considered. Theoretical reasons why nutritional support and bowel rest may possibly induce remission of the disease are discussed. The evidence to date suggests that intravenous nutrition and bowel rest may not be effective in inducing a primary remission of the disease, and the possible value of elemental diets and polymeric diets in this respect are assessed. Further prospective controlled studies of elemental diets as primary therapy in Crohn's disease are required.
Suppression of castor oil‐induced diarrhoea by α2‐adrenoceptor agonists
Authors: THOLLANDER M. , HELLSTRÖM P. M. , SVENSSON T. H. 
Published: July 2010

SUMMARYThe effects of systemic administration of α2‐adrenoceptor agonists on migrating myoelectric complexes and castor oil‐induced diarrhoea of the small intestine were studied in conscious rats. Castor oil (1 mg/kg, intraduodenally) disrupted the migrating myoelectric complexes and induced irregular spiking activity with sporadic bursts of myoelectric activity. This change of motility pattern was present concomitant with diarrhoea 1–2 h after instillation of castor oil and during the whole period of diarrhoea. Pre‐treatment with clonidine (5–10 μg/kg i.v.) or oxymetazoline (5.6–11.2 μg/kg i.v.), a peripherally active α2‐agonist, inhibited the irregular spiking induced by castor oil and no diarrhoea occurred during the experimental period of 6 h. Thus, the antidiarrhoeal action of peripherally acting α2‐adrenoceptor agonists such as oxymetazoline, may be of clinical value in the treatment of diarrhoea.
A comparison of roxatidine and ranitidine for the acute treatment of duodenal ulcer
Authors: WALT R. P. , LOGAN R. F. A. , HAWKEY C. J. , DANESHMEND T. K. , LONG R. G. , COOPER B. T. , LANGMAN M. J. S. , COLLINS M. , STREET R. 
Published: July 2010

SUMMARYRoxatidine acetate is a new histamine H2‐antagonist of about twice the potency of ranitidine on a weight‐for‐weight basis. Two hundred and thirty‐two patients participated in a double‐blind randomized trial of duodenal ulcer healing comparing 300 mg ranitidine nocte with 150 mg roxatidine nocte. Endoscopy was repeated fortnightly to 4 weeks in each of four participating centres. Usual exclusion criteria applied but NSAID users were allowed. There were no important demographic differences between treatment recipients. Three analyses were used: protocol (dropouts and violators not included), intention‐to‐treat I (dropouts considered failures), and intention‐to‐treat II (dropouts considered failures, but violators outcome included). Healing rates differed markedly (but not significantly) with each analysis. After 2 weeks of treatment ulcers had healed in 51% versus 45% using the intention to treat I analysis with roxatidine and ranitidine, respectively; by the protocol analysis the healing proportions were 60% and 55%. These differences between treatments were not significant. After 4 weeks of treatment healing rates ranged from 71% to 83% on roxatidine and between 69% and 84% on ranitidine depending on the analysis. Differential healing proportions of smokers and non‐smokers were nonsignificant (83% vs. 79%). Both drugs were well tolerated and adverse events were similar with each agent. Roxatidine should prove as effective as ranitidine for acute duodenal ulcer treatment.
Effects of ranitidine on maternal gastric juice and neonates when administered prior to caesarean section
Authors: IKENOUE T. , IITO J. , MATSUDA Y. , HOKANISHI H. 
Published: July 2010

SUMMARYRanitidine hydrochloride, a histamine H2‐receptor antagonist, was intravenously administered to 61 pregnant women at a dose of 50 mg as premedication for caesarean section; its effects on gastric secretion were studied in the mother and the newborn.The volume of the maternal gastric juice collected immediately after the induction of anaesthesia averaged 14.0 ± 10.0 ml with pH 3.48 ± 1.70, and at the time of extubation, 3.6 ± 2.8 ml with pH 4.19 ± 1.79, respectively.Forty‐four full‐term neonates whose mothers had received ranitidine were selected to investigate the effects of ranitidine. Another 45 full‐term normal newborns delivered vaginally, and 14 by caesarean section, served as controls.No effects of ranitidine infusion in the mothers were detected in the newborn children. The gastric pH of the newborn at birth and 24 hours after birth, gastrointestinal symptoms and the general growth checked at the regular one‐month work‐up after birth did not differ in test and control groups.
Omeprazole
Authors: LANGMAN M. J. S. 
Published: July 2010

SUMMARYOmeprazole is a potent and effective antisecretory drug. Benefits in gastric and duodenal ulceration nevertheless seem marginal because standard treatments are very effective. More obvious advantages are discernible in oesophageal reflux disease where more profound acid inhibition may be needed to obtain symptom relief. Fears of important adverse effects either through inducing ECL cell hyperplasia or outright carcinogenesis, do not seem firmly founded, nor is there convincing evidence of significant interactions with other xenobiotics. Nevertheless, continued caution seems justified.
Rebound hypersecretion after H2‐antagonist withdrawal—a comparative study with nizatidine, ranitidine and famotidine
Authors: FULLARTON G. M. , MACDONALD A. M. I. , McCOLL K. E. L. 
Published: July 2010

SUMMARYOur previous study demonstrated rebound nocturnal acid hypersecretion after a 4‐week course of nizatidine. Nocturnal acid output was increased by 77% two days after discontinuing treatment compared with pretreatment values. To confirm this effect with other H2‐blockers we assessed daytime intragastric pH, fasting and meal‐stimulated plasma gastrin and nocturnal acid output in 9 duodenal ulcer patients in remission before, during and two days after treatment with three different drugs. Each patient received 4‐week courses of 300 mg ranitidine, 40 mg famotidine or 300 mg nizatidine, taken at 20.00 hours in randomized order with a ‘washout’period of 4 weeks between each course of drug. Median nocturnal acid output (mmol/10 h) decreased during treatment with ranitidine to 3 (range 0–17), famotidine to 4 (1–12) and nizatidine 6 (0–40) compared with the respective pre‐treatment values, 49 (20–126;P< 0.01), 52 (22–105;P< 0.01) and 32 (23–114;P< 0.01). Two days after discontinuing treatment nocturnal acid output was increased after ranitidine at 77 (28–237;P< 0.04) and after nizatidine at 64 (17–130;P< 0.05) compared with pre‐treatment values.There was no significant change in nocturnal acid output after famotidine at 57 (27–107) compared with the pre‐treatment value. There was no change in daytime intragastric pH with any drug during or after treatment compared with the pre‐treatment values. Fasting and meal‐stimulated plasma gastrin concentrations were increased on the final treatment day with ranitidine and famotidine but had returned to pretreatment levels two days after treatment. The rebound acid hypersecretion may contribute to the high ulcer relapse rate after discontinuation of H2‐receptor antagonists.
Effect of anti‐obesity drugs promoting energy expenditure, yohimbine and ephedrine, on gastric emptying in obese patients
Authors: JONDERKO K. , KUCIO C. 
Published: July 2010

SUMMARYThe effect of ephedrine, a non‐selective adrenoreceptor agonist, and yohimbine, a selective alpha2‐adrenolytic drug, on gastric emptying of a radiolabelled solid meal was examined in groups of 8 (all women) and 15 (4 men and 11 women) obese patients, respectively. Patients were given orally, double‐blind in random order, placebo or 50 mg ephedrine in the first group, and placebo or 15 mg yohimbine in the second group, 1.5 h prior to the gastric emptying measurement performed with the use of a gamma camera. Yohimbine did not significantly affect gastric emptying—the fraction of the meal retained within the stomach at the end of the examination (that is after 90 min), F90, amounted to 71.0 ± 3.8% (placebo) and 66.8 ± 4.1% (yohimbine); the gastric emptying index, Ix, was 0.737 ± 0.106 min−1× 10−2 (placebo) and 0.885 ± 0.128 min−1× 10−2 (yohimbine). A significant delay in gastric emptying was observed after administration of ephedrine: F90 increased from 70.3 ± 5.1% after placebo to 80.9 ± 3.0% after ephedrine, P < 0.02, and Ix decreased from 0.747 ± 0.142 min−1× 10−2 to 0.461 ± 0.080 min−1× 10−2 after ephedrine, P < 0.02. We conclude that the inhibitory influence of ephedrine on gastric emptying, and thus possibly on satiety, makes it a candidate for trial as pharmacological support of a low‐energy diet treatment of obesity.
Protection from gastrointestinal side‐effects by azapropazone by its incorporation into a glucose—sodium acid citrate formulation
Authors: RAINSFORD K. D. , DIEPPE P. A. , PRITCHARD M. H. , RHODES J. , LEACH H. , RUSSELL R. I. , WALKER F. S. , UPADHYAY R. , HORT J. F. 
Published: July 2010

SUMMARYAddition of glucose and sodium citrate to azapropazone, in proportions of 1:1:1 by weight reduced gastric mucosal damage in rats and there was a trend towards reduction in radiolabelled faecal red cell loss in human volunteers compared with that with azapropazone alone. The glucose and citrate did not affect the pharmacokinetics of azapropazone, or its therapeutic efficacy. While no difference was observed in endoscopic injury and in symptomatic gastrointestinal complaints in a multicentre comparison in rheumatic patients, a striking reduction in symptoms was observed in those patients with a history of severe gastrointestinal intolerance to non‐steroidal anti‐inflammatory drugs.