bluuebunny/crossref_metadata_2025_split huggingface dataset:
Double‐blind, randomized trial of roxatidine 150 mg in the early evening versus bedtime administration in the short‐term treatment of duodenal ulcer
Authors: LAZZARONI M. , CANALI A. , PORRO G. BIANCHI 
Published: July 2010

SUMMARY Aim: To compare the efficacy and tolerability of early evening (19.00–21.00 hours) vs. bedtime (22.00–00.00 hours) oral administration of roxatidine 150 mg in the short‐term treatment of active duodenal ulcer. Methods: The trial was randomized, double‐blind and double‐dummy, with parallel groups. A total of 276 patients were recruited and randomly assigned either to roxatidine in the early evening (n= 139) or roxatidine at bedtime (n= 137). Results: After 4 weeks, 78% of patients receiving roxatidine in the early evening and 74% of those treated at bedtime had achieved complete healing, as determined by per‐protocol analysis. With intention‐to‐treat analysis the healing rates were 70.5% and 70.8%, respectively. After 8 weeks the healing rates in the early evening and bedtime treatment groups were 92% and 95% (per‐protocol analysis) and 78% and 84% (intention‐to‐treat analysis). Both treatments proved effective in reducing the frequency and severity of daytime and nocturnal epigastric pain, as well as other ulcer‐related symptoms. Conclusions: This study confirmed the healing and analgesic properties of roxatidine in duodenal ulcer disease. Early evening or bedtime dosing with roxatidine 150 mg resulted in similar 4‐ to 8‐week rates of duodenal ulcer healing.
Effect of omeprazole and feeding on plasma gastrin in patients with achlorhydria
Authors: BANERJEE S. , ARDILL J. E. S. , BEATTIE A. D. , McCOLL K. E. L. 
Published: July 2010

SUMMARY Background: The mechanism of hypergastrinaemia during omeprazole therapy is unclear, but is generally assumed to be entirely a consequence of acid suppression. However, direct stimulation of G cells by omeprazole could also be a factor. In order to further investigate the mechanism of omeprazole‐induced hypergastrinaemia, we have studied the effects of the drug on plasma gastrin in patients with achlorhydria, in whom altered acid secretion cannot play a role. Methods: We estimated fasting and peptone meal stimulated plasma gastrin in nine patients (seven female) with pernicious anaemia and achlorhydria, before and on the final day of 4 weeks’dosing with omeprazole 40 mg daily. Results: Despite the high fasting gastrin concentrations, the peptone meal produced a further elevation in plasma gastrin concentrations, median gastrin concentrations rising from 1500 ng/L (range 225–10875 ng/L) to 3750 ng/L (range 585–15600 ng/L) post‐prandially (P = 0.004). The median post‐prandial rise in plasma gastrin at this initial visit was 44% (3–260%), and the median time interval until plasma gastrin concentrations returned to fasting levels was 120 min (range 10‐ > 150 min). There was a significant negative correlation between fasting plasma gastrin concentrations and the percentage increase in plasma gastrin levels in response to meal stimulation (Spearman correlation coefficient ‐0.79, P= 0.01). Fasting plasma gastrin concentrations were similar pre‐omeprazole (median 1950 ng/L, range 240–16500 ng/L) and postomeprazole (median 1500 ng/L, range 315–7650 ng/L). Likewise, peak plasma gastrin concentrations were also similar pre‐omeprazole (median 2700 ng/L, range 585–16500 ng/L) and post omeprazole (median 3420 ng/L, range 720–11250 ng/L). Conclusions: (i) The hyperplastic G cell mass in patients with pernicious anaemia can be further stimulated by a peptone meal, which causes a prolonged rise in plasma gastrin concentrations. (ii) There is a negative correlation between fasting plasma gastrin concentrations and the percentage increase in plasma gastrin levels in response to meal stimulation. (iii) Omeprazole has no effect on plasma gastrin in achlorhydric patients, which is consistent with its hypergastrinaemic effect being entirely secondary to acid inhibition.
A comparison of three doses of lansoprazole (15, 30 and 60 mg) and placebo in the treatment of duodenal ulcer
Authors: AVNER D. L. , DORSCH E. R. , JENNINGS D. E. , GRESKI‐ROSE P. A. 
Published: July 2010

SUMMARYBackground: Lansoprazole is a new proton pump inhibitor for the treatment of peptic ulcer disease. Methods: A double‐blind, multicentre study was undertaken in 2 9 6 patients with endoscopically proven duodenal ulcer to compare the efficacy and safety of lansoprazole 15, 30 or 60 mg with placebo. Ulcer healing was documented by endoscopy at 2 and 4 weeks; patients whose ulcers healed after 4 weeks were followed for up to 6 months post‐treatment. Results: Four‐week healing rates of 89.4% 91.7% and 89.9% were obtained with lansoprazole 15, 30 and 60 mg, respectively, compared with 46.1 % on placebo (P < 0.001). All three doses of lansoprazole produced rapid symptom relief, although patients taking 60 mg lansoprazole required fewer antacids than did those taking 15 mg. At 6 months, the percentages of patients healed were 45.3%, 40.0% and 38.4% in the lansoprazole 15, 30 and 60 mg dosage groups, respectively, and 2 5.3 % for the placebo group. No significant adverse events were documented during the period of this trial. Conclusion: Lansoprazole is an effective and safe treatment for duodenal ulcer and the 15 mg dose is as effective as 30 or 60 mg.
Erythromycin shortens orocaecal transit time in diabetic male subjects : a double‐blind placebo‐controlled study
Authors: MINOCHA A. , KATRAGADDA R. , RAHAL P. S. , RIES† A. 
Published: July 2010

SUMMARYBackground: The effects of erythromycin on small bows motility are controversial. Orocaecal transit time (OCTT) is considered to be a valid measure of small bowel motility.Methods: We studied the effect of erythromycin on OCTT in diabetic male subjects in a double‐blind placebo‐controlled crossover fashion. After an overnight fast, subjects received erythromycin 500 mf 250 mg or placebo, on 3 different days. A standard solid meal containing 20 g lactulose was administered 30 min after the erythromycin ingestion. Exhaled breath was collected and hydrogen concentration was assessed over 5 h. Breath hydrogen concentrations for each session were analysed over time by a generalized logistic function generating a sigmoidal curve. Front transit time was recorded as the time point when a sustained rise in breath hydrogen concentration of at least 5 p.p.m. was first observed.Results: The mean ± S.E.M. time taken for the front of the meal to reach the caecum was 92.5 ± 9.5, 86.1±16.5 and 62.3 ± 12.1 min for placebo, erythromycin 250 mg and erythromycin 500 mg, respectively. The OCTT was significantly decreased with erythromycin 500 mg compard to placebo (P< 0.05).Conclusion: Oral administration of 500 mg erythromycin has prokinetic effect on orocaecal transit in male patients with diabetes mellitus.
Comparison of budesonide and 5‐aminosalicylic acid enemas in active distal ulcerative colitis
Authors: LÉMANN M. , GALIAN A. , RUTGEERTS P. , HEUVERZWIJN R. VAN , CORTOT A. , VITEAU J. M. , ELEWAUT A. , BELAICHE J. , FROGUEL E. , MODIGLIANI R. 
Published: July 2010

SUMMARY Background: Budesonide is a new corticosteroid with high topical anti‐inflammatory activity but little systemic effect. The aim of the present study was to compare the efficacy and safety of budesonide enema (2 mg/100 mL) and 5‐ASA enema (mesalazine 1 g/ 100 mL) given for 4 weeks in the treatment of active distal ulcerative colitis and proctitis. Methods: Ninety‐seven patients were studied in a multicentre single‐blind randomized group‐comparative trial. The primary efficacy variables were endoscopy and histopathology scores obtained at 0, 2 and 4 weeks. Clinical symptoms were the secondary efficacy variables. Haematology, chemistry and adverse events were the safety variables. Results: Budesonide and 5‐ASA enemas both resulted in a significant improvement in endoscopy and histopathology scores but no difference could be demonstrated between the two treatment groups. There was also a significant improvement of symptoms (number of bowel movements per day, quality of stools, presence of blood and mucus, and state of well‐being) within both groups but no difference between the two treatment groups. The clinical remission rate at 4 weeks was, however, 38% for patients treated with budesonide enema but 60% for those treated with 5‐ASA enema (P= 0.03). No adverse events attributed to the study drugs were recorded in either of the groups. Conclusions: Budesonide enema 2 mg/100 mL appears to be as efficient and well‐tolerated as 5‐ASA enema in the treatment of active distal ulcerative colitis and proctitis.
A comparative study of cisapride and ranitidine at controlling oesophageal acid exposure in erosive oesophagitis
Authors: POUDEROUX P. , KAHRILAS P. J. 
Published: July 2010

SUMMARY Background: The severity of gastro‐oesophageal reflux disease is generally considered to be related to the extent of oesophageal acid exposure. Current therapies include antisecretory and prokinetic agents. We compared two of these, ranitidine and cisapride, in their ability to lower oesophageal acid exposure in patients with erosive oesophagitis. Methods: Seven patients with Savary–Miller's grade II–IV oesophagitis and with oesophageal contact time ± 8% were studied. Mean lower oesophageal sphincter pressure was 4.6 mmHg. Oesophageal acid contact time was 25.6 ± 5.6%. Each patient received ranitidine 150 mg b.d., ranitidine 150 mg q.d.s., or cisapride 10 mg q.d.s. in a randomized 3‐way cross‐over design. Intra‐oesophageal pH was monitored during 24 h for each of these treatments in a controlled hospital environment, while consuming a high fat, high calorie diet. Results: Cisapride and ranitidine at both doses decreased the acid contact time and the number of reflux episodes. However, a minority of patients treated with ranitidine, and none with cisapride, diminished their oesophageal acid contact time to a normal value of < 5%. No treatment significantly decreased nocturnal acid exposure. Conclusion: In patients with severe gastro‐oesophageal reflux disease both cisapride and ranitidine demonstrably lower oesophageal acid exposure, but neither therapy predictably normalizes it.
Intravenous administration of lansoprazole: a preliminary study of dose ranging and eflcacy in upper gastrointestinal bleeding
Authors: AOKI T. 
Published: July 2010

SUMMARYUsing 24‐h pH monitoring, we studied the optimal dose and mode of administration of lansoprazole (LAN) injection in healthy adult male volunteers in three tests of antisecretory effect. We followed this with a dosefinding study, using the drug's suppressive effect on increased gastric acid secretion due to surgical stress as the indicator. Finally, we conducted a pilot study to determine the optimal mode of administration and efficacy of the drug in patients with haemorrhage from the upper gastrointestinal tract.Twenty‐four‐hour intragastric pH monitoring established the order of potency of the different regimens: LAN 30 mg b.d. > LAN 15 mg bed.: and LAN 30 mg b.d., intravenous drip infusion = LAN 30 mg b.d., bolus injection.Lansoprazole 30 mg b.d. appeared to be slightly more effective than LAN 15 mg b.d. in suppressing increased gastric acid secretion due to post‐operative stress and in haemostasis in patients with upper gastrointestinal bleeding. No severe adverse effects were observed in either study.
Review article: The medical management of Crohn's disease
Authors: ELTON E. , HANAUER S. B. 
Published: July 2010

SUMMARYThe choice of medical therapies for Crohn's disease continues to grow. Although our understanding of the mechanisms of the disease is incomplete, increasing knowledge of the pathogenesis of inflammation in general and Crohn's disease in particular allows targeting of therapies at various points in the immunoinflammatory cascade. In addition, the division of Crohn's disease into subtypes by location, aggressiveness, and the presence or absence of perianal and fistulizing disease allows the tailoring of medical therapy to the individual patient. For those patients with moderate to severe symptoms or frequent flares of disease activity, and those who have required surgical resection, maintenance therapy can substantially reduce the rate of recurrence. Despite these advances, available medical therapies for Crohn's disease remain imperfect, as evidenced by their sometimes substantial toxicities and the continued frequent need for surgery.
Clinical Economics Review: gastroenterology
Authors: BODGER K. , DALY M. J. , HEATLEY R. V. , WILLIAMS D. R. R. 
Published: July 2010

SUMMARYIn the prevailing climate of cost containment, doctors are increasingly expected to consider the economic consequences of treatment choices. Clinical (or medical) economics attempts to apply economic principles to the description and analysis of the costs of medical interventions, so as to identify how best to spend scarce health care resources. Such economic evaluations may assess the overall financial burden of a disease to society as a whole (macro‐economics), or attempt to compare alternative treatment strategies for a specific clinical situation (micro‐economics). In addition to expenditure on drugs and investigations (direct medical costs), economic studies may consider a variety of other costs. These include direct costs borne by patients (e.g. prescription charges, travel, food), indirect costs to society owing to lost productivity (resulting from morbidity or premature mortality) and even intangible costs which assign a monetary value to outcomes of disease such as pain, distress and anxiety.Four main types of economic analysis are in current use.Cost minimization analysisattempts to identify the least expensive option in situations where there are a range of equally effective treatments for a given clinical condition, whereascost‐effectiveness analysisallows management strategies differing both in cost and efficacy to be compared. The cost‐effectiveness of health care programmes targeting different disease states may also be compared usingcost‐utility analysis, in which health benefits are translated into a common utility‐based unit of outcome, such as the Quality Adjusted Life Year (QALY).Cost‐benefit analysisattempts to quantify health outcomes in monetary terms, so that the net result provides an assessment of value‐for‐money of health interventions.Gastrointestinal disorders are amongst the commonest of complaints, and considerable health care resources are consumed in treatment. Issues of cost‐effectiveness are likely to assume increasing importance in gastroenterologybecause of the everexpanding range of drug choice, the increasing number of high costtreatments and the development of new therapeuticinterventions.
Significance of activated mast cells in submucosa and muscularis propria of patients with Crohn's disease detected by a novel antimast cell surface molecule antibody
Authors: OSHITANI N. , KAMATA N. , INAGAWA M. , YAMAGAMI H. , WATANABE K. , FUJIWARA Y. , HIGUCHI K. , ARAKAWA T. , OKADA T. 
Published: July 2010

SummaryBackgroundDegranulated mast cells may be missed by histochemical and immunohistological techniques, making the histological assessment of activated mast cells difficult.AimTo use a novel mast cell surface antigen 1 (MASA‐1) to detect activated mast cells.MethodsSurgical samples of human intestine were obtained from 15 patients with ulcerative colitis (UC), 14 patients with Crohn's disease (CD) and 11 controls. Frozen sections were cut and MASA‐1 was detected and quantified by enzyme immunohistology. Immunohistological double staining with anti‐MASA‐1 and either anti‐CD68 or anti‐c‐Kit antibody was also performed.ResultsThe number of MASA‐1‐positive cells was significantly higher in the submucosal layer and muscularis propria in patients with CD than in patients with UC or controls. The number of MASA‐1‐positive cells was significantly higher in the muscularis propria in patients with UC in highly inflamed colon compared with controls and less inflamed colon. Human intestinal MASA‐1‐positive cells are not from the macrophage lineage and showed heterogeneous expression of c‐Kit.ConclusionThe increased number of mast cells in the submucosa and muscularis propria in patients with CD suggests that the involvement of activated mast cells in transmural inflammatory responses possibly including tissue remodelling.
Comparison of efficacies of dual therapy and triple therapy using rabeprazole in second‐line eradication ofHelicobacter pyloriin Japan
Authors: KAWAI T. , KAWAKAMI K. , KATAOKA M. , TAIRA S. , ITOI T. , MORIYASU F. , TAKAGI Y. , AOKI T. , RIMBARA E. , NOGUCHI N. , SASATSU M. 
Published: July 2010

SummaryBackgroundThe only authorized second‐lineHelicobacter pyloriregimen in Japan is proton pump inhibitor + amoxycillin + clarithromycin. However, it has been reported that this second‐line regimen is not effective. In this study, we evaluated the efficacy of dual and triple eradication therapies using rabeprazole as second‐lineH. pylorieradication regimens.AimTo evaluate the efficacy of dual and triple eradication therapies using rabeprazole as second‐lineH. pylorieradication therapy.MethodsSixty‐twoH. pylori‐positive patients with first‐line eradication failure were randomly assigned to two groups. The RAM group was administered rabeprazole 20 mg + amoxycillin 1500 mg + metronidazole 500 mg daily for 1 week. The RA group was administered rabeprazole 40 mg + amoxycillin 2000 mg daily for 2 weeks. Eradication ofH. pyloriinfection was determined by13C‐urea breath testing at 8 weeks after completion of treatment. Prior to treatment, amoxycillin, clarithromycin and metronidazole susceptibility, and CYP2C19 phenotype status were determined.ResultsEradication rates for the RAM and RA groups were 97% and 74%, respectively. Eradication rates were not influenced by CYP2C19 phenotype in either group. Eradication rates for clarithromycin‐resistant patients were 100% in the RAM group and 77% in the RA group.ConclusionsOne week with RAM therapy and 2 weeks with RA therapy were effective as second‐line eradication therapy forH. pyloriinfection; moreover, RAM was more effective than RA therapy.
Efficacy of proton pump inhibitors for cellular proliferation and apoptosis in Barrett's oesophagus with different mucin phenotypes
Authors: AMANO Y. , CHINUKI D. , YUKI T. , TAKAHASHI Y. , ISHIMURA N. , KAZUMORI H. , KUSHIYAMA Y. , KARIM RUMI M. A. , ISHIHARA S. , KINOSHITA Y. 
Published: July 2010

SummaryBackgroundControversy exists concerning the efficacy of acid suppressants in the regression of Barrett's oesophagus.AimTo evaluate the effect of proton pump inhibitors on cyclooxygenase‐2 expression, cellular proliferation and apoptosis in Barrett's oesophagus with different mucin phenotypes.MethodsFour hundred and sixty‐six biopsy samples of Barrett's oesophagus from 358 non‐treatment patients and 81 from 61 chronic proton pump inhibitor users were immunohistochemically examined using anti‐cyclooxygenase‐2 protein, anti‐proliferating cell nuclear antigen and anti‐single stranded DNA antigens in both mucin phenotypes of Barrett's oesophagus.ResultsPrevalence of the cyclooxygenase‐2 expression pattern did not significantly differ between the non‐treatment and proton pump inhibitor users. In those using proton pump inhibitors, significant suppression of the proliferating cell nuclear antigen index was found in Barrett's oesophagus with the gastric‐predominant mucin phenotype, but not with the intestinal‐predominant mucin phenotype. Apoptosis indices in chronic proton pump inhibitor users did not significantly differ between the two mucin phenotypes.ConclusionsProton pump inhibitors suppress cellular proliferation in Barrett's oesophagus with the gastric‐predominant mucin phenotype but not in that with the intestinal‐predominant mucin phenotype. This finding may at least partly explain the ongoing controversy surrounding the notion that all cases of Barrett's oesophagus respond to acid‐suppressive therapy.
Intravenous ghrelin administration enhances gastric acid secretion – evaluation using wireless pH capsule
Authors: MORI M. , SUZUKI H. , MASAOKA T. , IMAEDA H. , NOMOTO Y. , HOSODA H. , NISHIZAWA T. , KANGAWA K. , HIBI T. 
Published: July 2010

SummaryBackgroundGhrelin, a recently discovered peptide hormone, has been shown to be produced mainly by the A‐like cells of the gastric mucosa. Ghrelin not only stimulates growth hormone (GH) release but also promotes gastric motility. While the effect of ghrelin on the gastric acid secretion in rats has been reported, no such reports appeared to date from studies in humans.AimTo investigate the effect of ghrelin administration on the gastric pH in humans, using a novel wireless pH capsule (Bravo, Medtronic, Shoreview, MN, USA).MethodsFour healthy volunteers (male; average age, 35.0 years; Helicobacter pylori‐negative) were enrolled. The pH capsule was attached endoscopically to the gastric mucosa and the data were transmitted to a portable receiver. Thirty minutes after a stabilization period, synthetic ghrelin (5 μg/kg body weight) was injected intravenously into the subjects and the data were monitored for more than 120 min while the subjects lay supine.ResultsThe average minimum gastric pH in four cases (1.2 ± 0.10) was significantly decreased after injection of ghrelin, as compared with the basal pH value (1.8 ± 0.06). The serum gastrin level, however, showed no change after the ghrelin injection.ConclusionThese results suggest that exogenous ghrelin could enhance gastric acid secretion in humans.
Increased levels of plasma ghrelin in peptic ulcer disease
Authors: SUZUKI H. , MASAOKA T. , NOMOTO Y. , HOSODA H. , MORI M. , NISHIZAWA T. , MINEGISHI Y. , KANGAWA K. , HIBI T. 
Published: July 2010

SummaryBackgroundGhrelin is a novel appetite‐promoting peptide secreted primarily from the A‐like cells in the gastric fundic mucosa. As gastric inflammation caused by Helicobacter pylori infection extends, the number of ghrelin‐producing A‐like cells is diminished and gastric ghrelin content decreases significantly. We previously reported that plasma levels of ghrelin, which correlated well with the serum levels of pepsinogen (PG) I and PG I/II ratio, decreased as gastric mucosal atrophy increased in non‐ulcerogenic conditions and that plasma ghrelin level increased in rats with cysteamine‐induced duodenal ulcer.AimTo investigate the plasma levels of ghrelin in patients with peptic ulcer disease.Patients and MethodsTwo hundred and eighty‐six patients with epigastric symptoms, who underwent upper gastrointestinal endoscopy, were enrolled. Blood samples were collected after a 12‐h fast before endoscopy. Patients were divided into four groups, namely chronic gastritis with high PG (n = 197), chronic gastritis with low PG (n = 58), duodenal ulcer (n = 14) and gastric ulcer (n = 17) and plasma concentrations of total and active ghrelin as well as serum concentrations of PG I and PG II were measured by radioimmunoassay. Six patients with duodenal ulcer and seven with gastric ulcer were also examined after ulcer healing.ResultsPlasma ghrelin levels were significantly higher in patients with duodenal ulcer or gastric ulcer than in those without ulcers. Elevated plasma total ghrelin levels did not significantly change after the healing of ulcers.ConclusionsPlasma ghrelin levels were significantly higher in patients with peptic ulcer than in those with gastritis without ulcer. This finding suggests a possible relationship between mucosal injury susceptibility and elevated fasting plasma ghrelin.