bluuebunny/crossref_metadata_2025_split huggingface dataset:
Famotidine (20 mg) b.d. relieves gastrooesophageal reflux symptoms in patients without erosive oesophagitis
Authors: ROBINSON M. , DECKTOR D. L. , STONE R. C. , PEVELERY M. , BARDEN P. , MOYER R. , HOLT S. , ROOT J. , HUFNAGEL K. , HUMPHRIES T. J. , BERLIN R. D. 
Published: July 2010

SUMMARYPrevious clinical trials have evaluated a large number of symptomatic individuals with heartburn. Most studies have documented the need for multiple daily dosing with H2‐antagonists to achieve clinical and statistical efficacy for symptom relief. The purpose of this study was to compare the safety profile and efficacy of famotidine oral dosing regimens, 40 mg nocte and 20 mg b.d. with placebo in the relief of symptoms in patients suffering from frequent heartburn found to have endoscopically normal oesophageal mucosa or mild non‐erosive oesophagitis. Famotidine (20 mg) b.d. reduced and eventually completely relieved gastro‐oesophageal reflux disease symptoms in most patients during the 6‐week trial. Global assessment of improvement at 2 and 6 weeks indicated significantly greater improvement with a b.d. treatment regimen than with either a 40 mg nocte or placebo treatment. No statistically significant differences between famotidine and placebo in the number of patients who experienced clinical adverse experiences were noted and no serious adverse events attributable to famotidine occurred. Based upon these findings, patients with gastro‐oesophageal reflux symptoms experience good relief of their complaints with twice daily famotidine in standard doses.
Role of acid suppressants in patients with Zollinger–Ellison Syndrome
Authors: MATON P. N. 
Published: July 2010

SUMMARYVirtually all symptoms in patients with Zollinger‐Ellison syndrome are due to acid hypersecretion, thus the control of acid secretion is the first and most important step in the management of patients with this syndrome. Antisecretory medication is prescribed as soon as the diagnosis of Zollinger‐Ellison syndrome is made, as patients may bleed or perforate with little warning. Acid output is reduced to < 10 mmol/h to heal mucosal lesions, but in patients with a Billroth I or II gastrectomy and those with severe oesophagitis and stricture formation, acid output is reduced to < 5 or < 1 mmol/h. Acid output and not symptomatic response is a reliable guide of the adequacy of therapy. In sufficient doses, all H2‐receptor antagonists are useful; however, side effects associated with cimetidine therapy limit its use. The ratio of potencies of cimetidine: ranitidine: famotidine is 1:4:32.Ranitidine given as a 50‐mg intravenous bolus, followed by a continuous infusion of 0.5 mg. kg/h, controls acid hypersecretion acutely in patients with Zollinger‐Ellison syndrome. Acid output is checked after 4 h, and the dose increased until acid output is < 10 mmol/h. In 70% of patients with Zollinger‐Ellison syndrome, 1 mg. kg/h reduces acid output to < 10 mmol/h; however, doses up to 4 mg. kg/h have been used. When patients are switched to oral ranitidine, a useful dosage conversion is to administer 1.5 times the total daily intravenous dose in four equal doses every 6 h. Four doses of oral drug are given before the infusion is stopped. Six hours after the first/last oral dose, acid output is checked. In our patients, the mean dose of ranitidine was 2100 mg/day (range, 450–9200 mg/day). No serious toxicity was observed.Omeprazole, which has a long duration of action and is a potent inhibitor of gastric acid secretion, has simplified management. Once‐daily dosing is sufficient in most patients, and a reasonable starting dose is 60 mg daily. The dose may be increased to 120 mg once daily; if this dosage fails to control acid secretion, 60 mg is administered every 12 h. In our studies, the median dose was 90 mg/day (range, 20–120 mg/day). Omeprazole was more effective than H2‐receptor antagonists in providing symptom relief and mucosal healing and did not cause significant toxicity. In particular, no gastric carcinoid tumours developed during four years of use. Omeprazole is, therefore, the treatment of choice for control of acid secretion in patients with Zollinger‐Ellison syndrome.Surgery plays a minor role in the control of acid hypersecretion. Parathyroidectomy in patients with Zollinger‐Ellison syndrome as part of multiple endocrine neoplasia type I, or highly selective vagotomy decrease gastric acid output and lower drug requirements but do not cure the patient. Except when resection of gastrinoma is curative, lifelong medical therapy for control of acid secretion in patients with Zollinger‐Ellison syndrome is required.
Rationale for high‐dose H2‐receptor blockade in the treatment of gastro‐oesophageal reflux disease
Authors: CASTELL D. O. 
Published: July 2010

SUMMARYChronic gastro‐oesophageal reflux disease is a common clinical problem. The underlying pathophysiology is considered to be acid injury to the oesophageal mucosa secondary to reflux of gastric contents across an incompetent lower oesophageal sphincter. Evidence suggests that gastrooesophageal reflux disease is primarily a motility disorder, possibly the combined effect of decreased lower oesophageal sphincter pressure, abnormal oesophageal peristalsis, and, perhaps, delayed gastric emptying. The rationale for the use of acid‐suppressing drugs in chronic gastrooesophageal reflux disease is based on control of the known destructive role of acid and pepsin. Recent evidence indicates, however, that standard doses of H2‐receptor blockers are often inadequate to control gastric acid‐induced injury in many patients with chronic reflux. Long‐term maintenance therapy with standard doses of these drugs has proved unsuccessful in approximately 50% of patients. More recent studies show that greater symptom relief and improved healing can be achieved with the use of larger doses of H2‐receptor antagonists. This has been shown particularly with ranitidine at a dosage of 300 mg four times daily.
The long‐term management of duodenal ulceration using an H2‐antagonist: symptomatic self‐care compared with maintenance treatment
Authors: POUNDER R. E. , FESTEN H. , KORMAN M. 
Published: July 2010

SUMMARYIn a 48‐week study of 319 duodenal ulcer patients, symptomatic self‐care with an histamine H2‐receptor antagonist (flexible self‐chosen dosing with cimetidine 0, 400 or 800 mg/day) was compared with maintenance treatment (cimetidine 400 mg nocte). The rate of withdrawal from the study was similar in both groups. The mean consumption of cimetidine 400 mg tablets was significantly higher in the maintenance group (7.2vs. 5.4 tablets/week; P < 0.0001), but the mean cumulative number of days with ulcer symptoms was higher in the symptomatic self‐care group (47.2vs.29.1 days in 48 weeks). The estimated number of days of work‐loss due to ulcer symptoms was similar in both groups (approximately 4 days in the 48 weeks of observation).It is concluded that symptomatic self‐care using an H2‐antagonist can provide not only an economic but also an effective strategy for the long‐term management of uncomplicated duodenal ulceration.
The effects of lansoprazole, a new H+,K+‐ATPase inhibitor, on gastric pH and serum gastrin
Authors: SANDERS S. W. , TOLMAN K. G. , GRESKI P. A. , JENNINGS D. E. , HOYOS P. A. , PAGE J. G. 
Published: July 2010

SUMMARYThis study examined the effects of dose and time of administration of lansoprazole on gastric pH and serum gastrin in healthy male volunteers. Three groups of six subjects received 10, 20 or 60 mg doses of lansoprazole or placebo. Doses were administered at 22.00 hours daily for 7 days. An additional 18 subjects received once daily 30 mg oral doses of lansoprazole or placebo; these subjects were dosed at either 08.00 hours or 22.00 hours in a randomized, crossover fashion with a 2‐week washout period. Gastric pH was monitored for 24 h following the first and final dose, and 1 week following the completion of dosing.Lansoprazole, at all doses except 20 mg/day, significantly increased the median 24‐hour gastric pH following 7 days of dosing (P < 0.05). In addition, morning dosing in the 30‐mg crossover group led to a higher 24‐h median pH than evening dosing (P= 0.003). There was no difference in night‐time median pH between morning and evening dosing. Morning dosing also led to a significant increase in gastric pH on study Day 1 (P < 0.05). Plasma concentrations of lansoprazole were highly variable between subjects, but there was a significant correlation between AUC and the median 24‐h gastric pH. Plasma concentrations and AUCs were higher on Day 7 than on Day 1 for subjects receiving 10 or 20 mg, but not for those receiving 30 or 60 mg doses. Lansoprazole bioavailability demonstrated a circadian effect manifested by higher plasma concentrations following morning dosing. Serum gastrin concentrations were elevated in all active medication groups.
Short report: twenty‐four‐hour hyperpepsinogenaemia in Helicobacter pylori‐positive subjects is abolished by eradication of the infection
Authors: FRASER A. G. , PREWETT E. J. , POUNDER R. E. , SAMLOFF I. M. 
Published: July 2010

SUMMARYTwenty‐four‐hour plasma pepsinogen I and II concentrations were determined in 8 healthy subjects with antibody to Helicobacter pylori, before and after treatment with tripotassium dicitrato bismuthate, amoxycillin and metronidazole, Therapy was successful in the 5 subjects with active H. pylori infection. In these subjects, median integrated 24‐h plasma pepsinogen I and II concentrations significantly decreased from 2288 and 357 μg.h/L before treatment, respectively, to 1811 and 171 μg.h/L at 4–6 weeks after treatment, and 1643 and 150 μg.h/L at 20–24 weeks. By contrast, in the 3 subjects without evidence of active H. pylori infection, pre‐treatment plasma pepsinogen I and II concentrations were similar to values found in the H. pylori‐infected subjects after successful therapy, and they did not change significantly in response to therapy. H. pylori infection is associated with reversible hyperpepsinogenaemia.
Effecf of treatment with cisapride alone or in combination with domperidone on gastric emptying and gastrointestinal symptoms in dyspeptic patients
Authors: TATSUTA M. , IISHI H. , NAKAIZUMI A. , OKUDA S. 
Published: July 2010

SUMMARYThe effects on gastric emptying and gastrointestinal symptoms of treatment with cisapride alone and in combination with domperidone were investigated in 25 patients with chronic idiopathic dyspepsia. In a double‐blind study, 9 patients were randomly assigned to receive cisapride 2.5 mg three times daily, and 8 patients to receive placebo. After 7 days of treatment, gastric emptying was significantly accelerated and the score of gastrointestinal symptoms was significantly reduced in patients treated with cisapride. Placebo treatment had no significant effect. A randomized, double‐blind crossover study of 8 patients compared the effects of combined treatment with cisapride 2.5 mg plus domperidone 10 mg three times daily for 7 days against the effects of cisapride plus placebo. Administration of cisapride plus domperidone gave significantly higher gastric emptying and lower gastrointestinal symptoms than cisapride plus placebo.
Inhibition of human exocrine pancreatic secretion by the long‐acting somatostatin analogue octreotide (SMS 201‐995)
Authors: KEMMER T. P. , MALFERTHEINER P. , BÜCHLER M. , FRIESS H. , MESCHENMOSER L. , DITSCHUNEIT H. 
Published: July 2010

SUMMARYThe new long‐acting somatostatin analogue octreotide (SMS 201–995) was investigated for its influence on segretatagogue‐stimulated human exocrine pancreatic secretion. Eighteen healthy volunteers participated in the study. During duodenal intubation with a background stimulation of either secretin 1 U.kg/h or secretin 1 U. kg/h + ceruletide, 120 ng.kg/h, octreotide was infused at doses of 5, 20 and 80 μg/h in a placebo‐controlled randomized double‐blind crossover trial. Duodenal juice samples were collected in 10‐min intervals, and amylase, trypsin, chymotrypsin, and bicarbonate were measured in the individual fractions.During secretin stimulation, amylase was inhibited between 41 and 59%, trypsin between 28 and 72%, chymotrypsin between 55 and 70%, and bicarbonate between 0 and 31% with 5, 20 and 80 μg/h octreotide. During secretin and ceruletide stimulation, amylase was significantly inhibited by 84%, 78%, 81%, trypsin by 76%, 55%, 52%, chymotrypsin by 77%, 55%, 60%, and bicarbonate by 25%, 11%, 19% with 5, 20, and 80 μg/h octreotide, respectively (all decreases P < 0.05).The long‐acting somatostatin analogue octreotide was confirmed to be a potent inhibitor of stimulated human exocrine pancreatic secretion. The near maximal inhibitory potency of octreotide was achieved at a dose of only 5 μg/h. This finding may be of value in the planning of therapeutic studies with octreotide.
A comparison of indomethacin with ibuprofen on gastrointestinal mucosal integrity in conventional and germ‐free rats
Authors: MELARANGE R. , MOORE G. , BLOWER P. R. , COATES M. E. , WARD F. W. , RONAASEN V. 
Published: July 2010

SUMMARYThe effects of indomethacin and ibuprofen on gastrointestinal mucosal integrity were studied in conventional and germ‐free rats. Only ibuprofen induced significant gastric erosion formation in both conventional and germ‐free animals, demonstrating that the presence of micro‐organisms is not required in this form of damage. Both indomethacin and ibuprofen caused significant intestinal damage and blood loss in germ‐free animals. However, in the conventional counterparts, damage due to indomethacin was enhanced whereas that induced by ibuprofen was not. The results from the present work would suggest that non‐steroidal anti‐inflammatory drugs such as indomethacin, which are secreted largely in the bile, unlike ibuprofen, may act in concert with bacteria and the constituents of bile to induce, in part, intestinal damage and blood loss.
Influence of the timing of administration of 300 mg ranitidine on 24‐hour gastvic pH in patients with acute duodenal ulcer
Authors: CORTOT A. , GUILLEMOT F. , MOREAU J. , SOULE J. C. , VEYRAC M. , ALBEROLA B. , PAPPO M. 
Published: July 2010

SUMMARYThe 24‐hour intragastric pH of 12 patients with an acute duodenal ulcer was recorded with the aim of comparing the effects of two different times of administration of 300 mg ranitidine: post evening meal, or bedtime. This double‐blind crossover trial involved 3 centres. Twenty‐four‐hour gastric pH was measured under standard conditions (meals, time schedule) at the middle of each 14‐day treatment period. The analysis was performed on the percentage of times spent at pH levels below 1.5, 2, 3 and 4 for different periods and for the total 24 hours. During the whole day and night combined, as well as during the afternoon (12.00 hours‐19.00 hours), there was no difference between the 2 regimens regardless of the pH profile studied. During the morning (07.30 hours‐12.00 hours), the time spent below pH 1.5 and 2 was less when the drug was taken at bedtime (P < 0.05). In contrast, during the whole night (19.00 hours‐07.30 hours) the percentage of time spent below pH 1.5, 2 and 3 was significantly less when the drug was taken at post evening meal (P < 0.05). These results show that in patients with acute duodenal ulcer, 300 mg ranitidine administered at the end of the evening meal provides better control of nocturnal acidity than administration at bedtime and hence is suggested for optimization of therapeutic efficacy.
Short report: cefprozil for the eradication of Helicobacter pylori infection
Authors: MALATY H. , KLEIN P. D. , GRAHAM D. Y. 
Published: July 2010

SUMMARY Helicobacter pylori infection has proven to be extraordinarily difficult to eradicate. Antimicrobial monotherapies have been particularly disappointing, with most eradication rates in the range of 0 to 15%. We evaluated cefprozil (250 mg q.d.s. for 14 days) in 12 H. pylori‐infected subjects. The 13C‐urea breath test was used to evaluate effectiveness of therapy. Eradication was defined as a negative urea breath test 4 to 6 weeks after the end of treatment. Suppression of H. pylori was demonstrated in 4 of 12 (33%) by a negative urea breath test two days after start of treatment. H. pylori infection was not eradicated in any subject (0%). Adverse events were intermittent and mild. Cefprozil does not appear to offer promise as monotherapy for the eradication of H. pylori.
The effect of H2‐blockade on plasma gastrin concentration in patients with an achlorhydric stomach
Authors: FULLARTON G. M. , ARDILL J. E. S. , McCOLL K. E. L. 
Published: July 2010

SUMMARYThe mechanisms of hypergastrinaemia during H2‐receptor antagonist therapy remain unclear. In addition, the effect of food stimulation in conditions of hypergastrinaemia is poorly understood. These effects may be important when considering long‐term therapy with potent acid inhibitory agents. To investigate this we studied the effect of H2‐receptor antagonist therapy on basal and meal‐stimulated plasma gastrin concentrations in 9 patients with pentagastrin fast gastric achlorhydria associated with pernicious anaemia. The subjects received in double‐blind randomized fashion 28‐day courses of 300 mg ranitidine q.d.s. and placebo, with one‐month wash‐out between. The fasting and peptone meal‐stimulated gastrin concentrations were studied on the final day of each course of treatment. The median fasting gastrin concentrations (ng/L) were similar following placebo (1100, range 25–2100), and 300 mg ranitidine q.d.s. (1075, range 15–2600) and both markedly elevated when compared with our laboratory's normal range of 0—100. Despite the elevated basal levels the pernicious anaemia patients still showed a further increase in response to the peptone meal. Their median peak percentage rise over basal in response to the meal was similar following placebo (96%, range 0–375) and 300 mg ranitidine q.d.s. (100%, range 25–425) (both P < 0.02 c.f. basal).This study shows that: (a) in hypergastrinaemia in pernicious anaemia subjects, meal stimulation leads to a marked and prolonged increase in plasma gastrin concentrations; (b) H2‐receptor antagonists have no effect on plasma gastrin in the neutral stomach and this is consistent with their gastrin effect being entirely secondary to acid inhibition.
Nine years of maintenance treatment with ranitidine for patients with duodenal ulcer disease
Authors: PENSTON J. G. , WORMSLEY K. G. 
Published: July 2010

SUMMARYFour hundred and sixty‐four patients with duodenal ulcer disease received continuous maintenance treatment with ranitidine for up to 9 years. Treatment failure was defined as either the first symptomatic recurrence of ulcer or the first ulcer recurrence accompanied by haemorrhage. Life tables were constructed using the Kaplan‐Meier product‐limit method; comparisons of survival curves were performed using the log‐rank test; and multivariate analysis was carried out using the Cox proportional hazards model.Results. The proportion of patients remaining free from symptomatic recurrence of ulcer during maintenance treatment with either 150 mg/day or 300 mg/day ranitidine was: 95% at 1 year; 88% at 3 years; 86% at 5 years; and 81% at 7 and 9 years (95% C.I. 76–86%). Young age and the absence of exposure to non‐steroidal anti‐inflammatory drugs (NSAIDs) at the time of diagnosis of ulcer were shown to increase the likelihood of developing ulcer recurrence. The rate of ulcer recurrence after 9 years of maintenance treatment (17%) was significantly less than that after 5 years without active anti‐ulcer therapy (80%),P= 0.0001.The proportion of patients who remained free from ulcer haemorrhage during maintenance treatment was: 99.1% at 1 year and 98.1 % at 5 and 9 years (95 % C.I. 96.7–99.6%). The risk of haemorrhage was significantly greater in patients who were not receiving active treatment (12.4% at 5 years) than in patients receiving maintenance treatment (< 2% at 9 years),P= 0.0001 (log‐rank test). Patients who had originally presented with haemorrhage had an increased risk of further ulcer bleeding compared with patients who presented with pain (P= 0.0013). A significantly greater proportion of patients with NSAID‐associated duodenal ulcers remained free from ulcer recurrence during maintenance treatment compared with patients suffering from‘idiopathic’ ulcers (P= 0.0238), although there was no difference between the two groups in respect of haemorrhage during maintenance treatment.Concltisions(a) Continuous maintenance treatment with ranitidine for up to nine years successfully prevents ulcer recurrence in more than 80% of patients with duodenal ulcer disease.(b) Young age increases the risk of ulcer recurrence during maintenance treatment with ranitidine. Ulcers associated with NSAID‐intake at the time of diagnosis have a lesser risk of recurrence during maintenance treatment.(c) The risk of haemorrhage in patients with ulcer disease receiving maintenance treatment with ranitidine for nine years was < 2% compared with > 12% in untreated patients observed for 5 years.(d) Patients whose ulcer disease presents with haemorrhage have a greater risk of further bleeding than patients who present with pain.
Review article: promotility drugs in the treatment of gastro‐oesophageal reflux disease
Authors: RAMIREZ B. , RICHTER J. E. 
Published: July 2010

SUMMARYProkinetic agents are drugs that increase contractile force and accelerate intraluminal transit. They are often used in treating disorders of gastrointestinal motility including gastro‐oesophageal reflux disease (GERD). The most widely studied agents include bethanechol, metoclopramide, domperidone and cisapride. These drugs act either by enhancing the effect of acetylcholine or by blocking the effect of an inhibitory neurotransmitter such as dopamine. With the exception of cisapride, the clinical efficacy of the various prokinetic agents in treating GERD has not been confirmed consistently. These agents have variable effects on oesophageal and gastric motor function and are fraught with side‐effects. They are effective in relieving mild reflux symptoms but do not predictably heal oesophagitis. On the other hand, cisapride is thus far the most effective prokinetic agent studied for the treatment of GERD. It relieves reflux symptoms and promotes healing of grade I–II oesophagitis, with few side‐effects or tachyphylaxis. Its most important role may be in the maintenance treatment of GERD either as a single agent or in combination therapy with an H2‐antagonist after oesophagitis healing.
Ileo‐caecal ulceration associated with the use of diclofenac slow release
Authors: HUDSON N. , WILKINSON M.J. , SWANNELL A. J. , STEELE R. J. , HAWKEY C. J. 
Published: July 2010

SUMMARYA 38‐year‐old man with seropositive arthropathy on long‐standing treatment with diclofenac slow release presented with abdominal pain, diarrhoea and anaemia. Upper gastrointestinal endoscopy and barium series were unremarkable. Five months later he presented with a right iliac fossa mass. Investigations revealed discrete ulceration in the terminal ileum and caecum confirmed at laparotomy. Other possible causes of intestinal ulceration were excluded suggesting a diagnosis of non‐steroidal anti‐inflammatory drug associated intestinal ulceration.