bluuebunny/crossref_metadata_2025_split huggingface dataset:
Treatment of steatorrhoea in cystic fibrosis: a comparison of enteric‐coated microspheres of pancreatin versus non‐enteric‐coated pancreatin and adjuvant cimetidine
Authors: STEAD R. J. , SKYPALA I. , HUDSON M. E. 
Published: July 2010

SUMMARYEnteric‐coated microspheres of pancreatin were compared with non‐enteric‐coated pancreatin combined with cimetidine taken 40 min before meals in the treatment of patients with cystic fibrosis. Fourteen adults with steatorrhoea due to cystic fibrosis were investigated in an open, randomized crossover study, over two consecutive 28‐day treatment periods. Lipase intake was adjusted to each patient's previous requirements and was the same during both months; they were instructed to continue with their normal diet. Patients collected faeces for 72 h at the end of each month and completed diary cards daily throughout. Bowel actions were less frequent on enteric‐coated microspheres of pancreatin than on non‐enteric‐coated pancreatin/cimetidine (1.7 vs. 2.4/day; P < 0.001) and stool character was improved (P < 0.001). Mean daily faecal weight was similar on enteric‐coated microspheres of pancreatin to that on the combination (254 g vs. 291 g; N.S.), whereas daily faecal fat excretion tended to be less on enteric‐coated microspheres of pancreatin (21 g vs. 27 g; N.S.), and percentage fat absorption tended to be greater (81%vs. 73%; N.S.). Mean body weight increased by 0.3 kg on enteric‐coated microspheres of pancreatin and fell by 0.1 kg on the combination (N.S.). These data indicate that enteric‐coated microspheres of pancreatin are at least as effective as non‐enteric‐coated pancreatin with cimetidine in the treatment of steatorrhoea in cystic fibrosis.
Loss of predictive value of gastric ulcer symptoms in a randomized treatment trial
Authors: FEURLE G. E. , BRÖKER H.‐J. , BLUM A. L. 
Published: July 2010

SUMMARYAnalysis of clinical data obtained in a double‐blind randomized study, which compared liquid antacid (neutralizing capacity 120 mmol per day) with 1 g cimetidine in the treatment of 125 patients with gastric ulcer, revealed that, before starting treatment 71 % of the patients complained of epigastric pain, approximately 50% of bloating, and approximately 30 % of nausea, heartburn, constipation or vomiting.Epigastric pain before treatment was significantly more frequent in patients with large ulcers (P < 0.05) and in patients with ulcers unhealed after 4 weeks of therapy (P < 0.05). This finding was the result of a highly significant correlation between diurnal epigastric pain and ulcer size and delayed healing (P < 0.005). Nocturnal pain did not correlate with prognosis.In contrast to this correlation between pain before therapy and healing, the disappearance of epigastric pain with therapy did not signify ulcer healing. Only 14 (38%) of the 37 patients with healed ulcer were free from pain after the 4 weeks of therapy, whereas 25 (49%) of the 52 patients with persistent ulcers had no pain at this time. Placebo pain tablets relieved ulcer pain effectively in more than 85% of the patients, irrespective of whether the ulcer was healing or not. The other symptoms (bloating, nausea, heartburn, constipation or vomiting) were also alleviated by 4 weeks of therapy but no correlation was found with ulcer size or prognosis.The loss of the prognostic significance of ulcer pain is probably due to a complex interaction of the trial schedule on the patient's level of consciousness. The highly effective placebo pain tablets and improvement of symptoms, which are unlikely to be due to gastric ulcer symptoms that are also unlikely to be affected by a decrease in gastric acidity such as bloating and constipation), suggest that ulcer treatment in a controlled trial changes pain perception. We conclude that treatment trials have effects that go beyond the rates of healing.
Meta‐analysis of randomized controlled trials as a method of estimating rare complications of non‐steroidal anti‐inflammatory drug therapy
Authors: CHALMERS T.C. , BERRIER J. , HEWITT P. , BERLIN J. , REITMAN D. , NAGALINGAM R. , SACKS H. 
Published: July 2010

SUMMARYThe design of randomized controlled trials to assess the efficacy of pharmacological measures for the prevention of the gastrointestinal side‐effects of anti‐inflammatory drugs requires an accurate estimate of excess risk under controlled conditions. Photocopies of 952 randomized controlled trial publications were obtained after scanning titles and abstracts of a MEDLINE computer search, 427 were excluded for obvious reasons, and 525 were again photocopied after obliterating source and results. Selection criteria were: the presence of a non‐anti‐inflammatory drug control group; at least 4 days of therapy; at least 3 days without anti‐inflammatory drugs before randomization; no complicating background drugs; mention of side‐effects; and a clear differentiation of gastrointestinal complications. Observer error, with two independent readings, for inclusion suitability in the study was 19% for Methods and 9% for Results. For the 44 aspirin trials, the mean therapy duration was 357 days; the unweighted rate difference between therapy and control groups (± 1 S.E.M.) for ulcer was 0.006 ± 0.003, for gross haemorrhage 0.006 ± 0.002 and for unspecified gastric symptoms 0.03 ± 0.01. In 123 non‐aspirin non‐steroidal anti‐inflammatory drug (NA—NSAID) trials, the mean duration was 67 days; the unweighted rate difference for ulcer was 0.0005 ± 0.0003, for gross haemorrhage 0.007 ± 0.004 and for unspecified gastric symptoms 0.02 ± 0.005. Risk differences were also pooled using the DerSimonian and Laird method, which weights studies inversely according to variance. Using this method, only the unspecified gastric symptoms for non‐aspirin non‐steroidal anti‐inflammatory drugs (NA—NSAIDs) and the haemorrhage for aspirin were found to be statistically significant. Longer studies have higher risk differences. Randomized control trials to determine prophylactic efficacy against haemorrhage (that is, to demonstrate a reduction of ulcer rate in the therapy group to the rate of controls) would require 190 patients in each group for NA—NSAIDs in studies of 2–6 months; 950 subjects would be needed to detect a 50% reduction. Randomized control trials to determine a reduction in ulcer rate to that of controls in patients on aspirin for more than 6 months would require 700 subjects in each group; 3346 subjects would be needed to detect a 50% reduction. Such studies are feasible.
Ulcer and ulcer complications from non‐steroidal anti‐inflammatory drugs: what is the risk?
Authors: LANGMAN M. J. S. 
Published: July 2010

SUMMARYGastroenterologists believe that non‐steroidal anti‐inflammatory drugs (NSAIDs) cause dyspepsia, may cause ulcers to developde novoand cause ulcer bleeding and perforation. Regulatory authorities are aware that NSAID‐associated adverse events are reported more often than for any other drug class, and that gastrointestinal events are most common and often serious. A case‐control study in the UK indicates that those who use NSAIDs may be between two and four times as liable to gastrointestinal bleeding and probably perforation as non‐users, particularly if elderly. It has further been suggested that the chances of dying of ulcer complications are very high in NSAID users. By contrast, studies in the USA conducted prospectively and post‐marketing surveillance in the UK have appeared to show little risk. Differences may be partially, if not completely, explained by the variable methodologies employed. Dispute also exists about the rank order and significance of toxic effects among the various agents.
Treatment of endoscopy‐negative NSAID‐induced upper gastrointestinal symptoms with cimetidine: an international multicentre collaborative study
Authors: BIJLSMA J.W.J. 
Published: July 2010

SUMMARYIn this double‐blind multicentre trial, 127 patients on non‐steroidal anti‐inflammatory drugs (NSAIDs) who experienced gastrointestinal symptoms significant enough to warrant endoscopic evaluation, but without endoscopic evidence of mucosal damage, were randomized to receive cimetidine 400 mg b.d. or placebo for 4 weeks. Non‐steroidal anti‐inflammatory drug therapy was maintained at pre‐trial doses for the duration of the study. After 4 weeks, 72 % of cimetidine‐treated patients experienced complete symptom resolution, as defined by a global symptom score of zero, compared with 49% on placebo. Complete disappearance of upper abdominal pain was achieved in 72 % of the cimetidine‐treated patients as opposed to 47% on placebo. Relief of heartburn was experienced by 87 % of patients on cimetidine compared with 60 % on placebo. Throughout treatment, the proportion of cimetidine‐treated patients with nausea was consistently lower than in patients on placebo, while the two groups were similar with respect to disappearance of vomiting. At the completion of acute treatment, 27% of placebo‐treated patients but only 12% of those on cimetidine were ineligible to continue maintenance due to persisting gastrointestinal symptoms. Patients who were symptom‐free and required continuation of NSAID therapy were followed for 6 months during which they were re‐randomized to receive cimetidine 400 mg nocte or placebo. Of the 105 patients included in this maintenance treatment phase of the study, 11% of the cimetidine‐treated patients and 10% of those on placebo experienced relapse of symptoms. However, the mean time to relapse was 120 days with cimetidine compared with 35 days with placebo. The results of this study indicate that cimetidine is effective in the treatment of endoscopy‐negative NSAID‐induced GI symptoms, specifically pain and heartburn, in patients continuing NSAID therapy.
Surgery in the management of the gastric side‐effects of NSAIDs
Authors: VENABLES C. W. 
Published: July 2010

SUMMARYIt is now accepted that the administration of non‐steroidal anti‐inflammatory drugs (NSAIDs) can result in peptic ulceration. Not infrequently, the first presentation of the ulcer is as a life‐threatening complication such as a perforation or gastrointestinal bleed. Surgeons often become involved in management when one of these complications occurs. This paper discusses the ways in which NSAID‐induced peptic ulceration may present to the surgeon and the special features that distinguish patients with NSAID‐induced ulcers from the remainder of patients with peptic ulcer disease. It is pointed out how little has been written on the surgical management of this group of patients. The importance of the overall assessment of these patients, with the correction of nutritional deficiencies and the use of appropriate prophylactic therapeutic measures in their surgical management, is stressed. The criteria for determining what surgical procedure is used and results are described.
Cost of treating arthritis and NSAID‐related gastrointestinal side‐effects
Authors: BLOOM B. S. 
Published: July 2010

SUMMARYNon‐steroidal anti‐inflammatory drugs (NSAIDs) are efficacious in the treatment of arthritis. However, side‐effects particularly gastrointestinal toxicity, have been well documented with their use. Thus, in assessing total direct medical costs in the treatment of arthritis, the expenses involved in treating these side‐effects must be taken into account. A retrospective analysis was undertaken of all direct medical costs related to care of a group of Medicaid recipients treated for arthritis during a 2‐year period. Data were obtained from the Medicaid Management Information System of Washington, D.C., USA. The actual expenditure of treating arthritis as well as the medical costs of associated NSAID‐induced gastrointestinal side‐effects were determined. Arthritis treatment costs per quarter were found to be $145 per patient. Approximately 25 % of the population experienced NSAID‐related gastrointestinal side‐effects requiring further medical care. Treatment of these adverse effects cost an additional $66 per quarter per patient, thus adding 45.5% to the cost of arthritis treatment. Pharmaceutical claims comprised 42.4% of total adverse drug reaction treatment costs, while the few hospital claims accounted for 37.9% and physician charges 19.7%. It has been estimated that in 1983 direct medical costs of arthritis treatment in the USA was $8.6 billion. By extrapolating the costs in this study, it can be estimated that a further $3.9 billion was spent on treating gastrointestinal side‐effects of NSAIDs, making a total of $12.5 billion.
Effect of the bile‐acid sequestrant colestipol on postprandial serum bile‐acid concentration: evaluation by bioluminescent enzymic analysis
Authors: ROSSI S. S. , WAYNE M. L. , SMITH R. B. , WRIGHT C. E. , ANDREADIS N. A. , HOFMANN A. F. 
Published: July 2010

SUMMARYChronic ingestion of bile‐acid sequestrants has been shown to decrease the serum cholesterol concentration and coronary events in hypercholesterolaemic patients. To develop improved sequestrants, a rapid, convenient method for testing the bile‐acid binding efficacy of sequestrants is needed. Serum bile‐acid concentrations could be used to detect bile‐acid binding by an administered sequestrant, since the serum bile‐acid concentration is determined largely by the rate of intestinal absorption in healthy individuals. To test this, serum bile‐acid concentrations were measured at frequent intervals over 24 h in five otherwise healthy hypercholesterolaemic subjects during the ingestion of three standard meals, with or without the addition of 5 g colestipol granules administered 30 min before each meal.Total serum bile‐acid concentration was measured with a previously reported bioluminescent enzymic assay, that uses a 3α‐hydroxysteroid dehydrogenase, an oxido‐reductase, and a bacterial luciferase co‐immobilized on to Sepharose beads. Bile acids in 1 ml of serum were isolated by solid‐phase extraction chromatography with reversed‐phase C18 cartridges.
Symptom relief and duodenal ulcer healing with omeprazole or cimetidine
Authors: CROWE J. P. , WILKINSON S. P. , BATE C. M. , WILLOUGHBY C. P. , PEERS E. M. , RICHARDSON P. D. I. ,   OPUS (OMEPRAZOLE PEPTIC ULCER STUDY) RESEARCI GROUP
Published: July 2010

SUMMARYIn a double‐blind parallel‐group study, 98 patients with symptomatic duodenal ulcer received omeprazole 20 mg o.m. and 91 cimetidine 800 mg nocte for 2 or, if then not healed, 4 weeks. After 2 weeks the healing rates on an intention‐to‐treat basis were: for omeprazole 62% and for cimetidine 33% (P < 0.001), and at 4 weeks 85% and 61%, respectively (P < 0.001). The proportions symptom‐free at 2 weeks were 83% of the omeprazole and 63% of the cimetidine‐group (P < 0.01) and at 4 weeks 84% and 72% (P= 0.01). Patients receiving omeprazole took fewer antacid tablets than those receiving cimetidine. Patient tolerance of both drugs was similar and good. In the treatment of duodenal ulcer, omeprazole 20 mg o.m. gives faster symptom relief than cimetidine 800 mg nocte, as well as healing a greater proportion of ulcers within 2 and 4 weeks.
A multicentre, randomized, double‐blind study comparing nocte famotidine or ranitidine for the treatment of active duodenal ulceration
Authors: SANTAELLA R. ALCALÁ , GUARDIA J. , PAJARES J. , PIQUÉ J. , PITA L. , ALVÁREZ E. , CASTELLANOS P. , GUARNER L. , ORTIZ J. , PESQUERA R. , VARGAS V. , RUIZ‐CAPELLÁN R. 
Published: July 2010

SUMMARYThe efficacy and safety of famotidine and ranitidine in the treatment of active duodenal ulcer were compared in a multicentre, randomized, double‐blind study. The study was carried out in five centres which included a total of 143 patients with endoscopically documented active duodenal ulcer. The patients received either famotidine (one tablet of 40 mg at night) or ranitidine (two tablets of 150 mg at night). Endoscopic examinations were performed at 4 and 6 weeks of active treatment. Daytime and nocturnal pain were also monitored, and the laboratory and clinical profiles evaluated. One hundred and thirty‐three patients fulfilled the evaluation criteria (66 patients in the famotidine group and 67 in the ranitidine group). Healing rates at 4 or 6 weeks of treatment showed no significant differences between the famotidine and ranitidine groups. The healing rates were 80% at week 4 and 97% at week 6 in the famotidine group, and 77% at week 4 and 96% at week 6 in the ranitidine group. Similar results were observed in both treatment groups with regard to pain resolution, decrease in antacid intake and safety profile.
Acute treatment of reflux oesophagitis: a multicentre study to compare 150 mg ranitidine twice daily with 300 mg ranitidine at bedtime
Authors: HALVORSEN L. , LEE F. I. , WESDORP I. C. E. , JOHNSON N. J. , MILLS J. G. , WOOD J. R. 
Published: July 2010

SUMMARYA randomized, double‐blind, clinical trial was undertaken to compare 150 mg ranitidine b.d. with 300 mg ranitidine nocte in the treatment of reflux oesophagitis. Endoscopy data were evaluable for 336 patients after 8 weeks of treatment. At this time 75% of patients who received 150 mg ranitidine b.d., and 73% of those who received 300 mg nocte, had healed or showed endoscopic improvement to grade I oesophagitis. At 12 weeks these rates had increased to 89 and 88%, respectively. Oesophageal biopsies from 258 patients at 8 weeks showed histological improvement in 44 and 47% of those treated with 150 mg ranitidine b.d. and 300 mg ranitidine nocte, respectively. After 12 weeks histological improvement was apparent in 57 and 54% of biopsies from each group, respectively. Symptom severity and frequency was reduced to a similar extent by both treatments. Adverse events were reported by 15 patients. A 300–mg bedtime dose of ranitidine was found to be a well‐tolerated, effective alternative to twice daily treatment in reflux oesophagitis.
Human gastric acid secretion following repeated doses of AG‐1749
Authors: MÜLLER P. , DAMMANN H. G. , LEUCHT U. , SIMON B. 
Published: July 2010

SUMMARYThe effect of increasing doses (15 mg, 30 mg and 60 mg) of the substituted benzimidazole, AG‐1749, on gastric acid secretion and fasting serum gastrin concentration has been studied after repeated administration to healthy volunteers.AG‐1749 produced a dose‐dependent and profound decrease in basal and stimulated gastric acid secretion in all volunteers, with almost total suppression at the highest dose. The extent of inhibition increased between Day 2 and Day 8 with the 15 and 30 mg doses of AG‐1749. The inhibitory effect of AG‐1749 appears to be fully reversible as control levels of acid output were reached 7 days after drug withdrawal.Seven days’dosing with 60 mg AG‐1749 induced a more than threefold increment of fasting serum gastrin concentration, but this increase was still within the normal range. Seven days after cessation of dosing, fasting serum gastrin concentration returned to a pre‐dose level.
A single night‐time dose of famotidine is equivalent to ranitidine in decreasing 24‐hour gastric acidity in asymptomatic duodenal ulcer subjects
Authors: THOMSON A. B. R. , PINCHBECK B. R. , KIRDEIKIS J. , ZUK L. , MARRIAGE B. , PRAT A. 
Published: July 2010

SUMMARYSix asymptomatic, non‐smoking men with endoscopically proven duodenal ulcer disease received single nocturnal doses of placebo, 40 mg famotidine and 300 mg ranitidine each for 1 week prior to serial measurement of pH, peptic activity and serum gastrin concentrations over 24 h and of acid output. The intragastric pH fluctuated between 1.53 and 5.07 when subjects were given placebo but within 2 h of taking famotidine or ranitidine it rose to 5.57 or higher; the effect lasted for 12 h from midnight. Peptic activity fell during famotidine and ranitidine treatment and the decline was somewhat greater 8–15 h after using famotidine. Serum gastrin levels did not change materially with any treatment. The study shows the equivalent effect of standard bed‐time doses of famotidine and ranitidine on intragastric pH, acid output and serum gastrin concentrations in asymptomatic men with duodenal ulcer disease.
Evaluation of three oral rehydration solutions designed for use in developed communities
Authors: ELLIOTT E. J. , FERREIRA R. M. DA CUNHA , CAMERON D. , FARTHING M. J. G. , WALKER‐SMITH J. A. 
Published: July 2010

SUMMARYOne hundred and sixteen children (less than 2 years old) admitted to a London hospital with acute gastroenteritis were randomized to receive either an oral rehydration solution (ORS) with low sodium and high glucose concentration (Na+ 35, glucose 200 mmol/L), an ORS with a high sodium but low glucose concentration (Na+ 60, glucose 111 mmol/L), or an ORS containing glycine and a glucose polymer (Na+ 50, glucose 50, glycine 50 mmol/L). Clinical, biochemical and haematological features of the three groups were similar on admission. Rotavirus was common (31%); the majority of children had minimal dehydration or acid–base disturbance.The clinical outcome, including ORS intake, prevention of dehydration, rehydration, and duration of hospital stay was similar in the three treatment groups. All initial electrolyte abnormalities were corrected; no child developed hypernatraemia or hyponatraemia. At 24 h, the mean serum urea was higher in those who received the ORS containing glycine than in other groups, and it had not fallen significantly since admission. Eighteen per cent of children had carbohydrate intolerance : four children with ≥2% reducing substances in their stool had all received ORS with a high glucose content and had numerous watery green stools containing rotavirus.All ORS solutions were safe and effective for rehydration and correction of biochemical abnormalities, however carbohydrate intolerance was more prevalent in children who received the ORS with a high glucose content.
Comparison between single morning and bedtime doses of 40 mg famotidine for the treatment of duodenal ulcer
Authors: DE PRETIS G. , DOBRILLA G. , FERRARI A. , FONTANA G. , MAIOLO P. , MARENCO G. , MENARDO G. , PALLINI P. , ROSSINI F. P. , SAGGIORO A. 
Published: July 2010

SUMMARYThe aim of this study was to compare the duodenal ulcer healing effects of morning (08.00 hours) vs. single bedtime (22.00 hours) doses of 40 mg famotidine, bearing in mind that the known efficacy of bedtime doses of H2–antagonists is regarded as evidence of the predominance of nocturnal gastric acidity in the pathogenesis of duodenal ulcer.This randomized double‐blind multicentre trial was conducted in a total of 127 patients with endoscopically proven active duodenal ulcer. Nine patients dropped out and thus 118 were included in the final analysis. The duration of treatment was 4 weeks, and this was extended to 8 weeks in patients whose ulcers failed to heal by week 4. The patients in the two treatment groups were well matched for age and sex.The therapeutic efficacy parameters were endoscopic healing of the ulcer lesion and disappearance of pain. Results were compared using the χ‐square method.The 4–and 8–week (cumulative) ulcer healing rates in the patients treated with the morning dose of famotidine were 77.2% and 86%, respectively, compared with 78.6% and 91.8% in those who received the bedtime dose. The differences failed to prove statistically significant either at week 4 (P= 0.85) or at week 8 (P= 0.31). The percentages of patients with ulcer pain, evaluated weekly, were similar in the two treatment groups.The equivalent efficacy of the morning and bedtime famotidine regimens raises doubts concerning the predominance of nocturnal gastric acidity in the pathogenesis of duodenal ulcer.