bluuebunny/crossref_metadata_2025_split huggingface dataset:
The eflects of 300 mg ranitidine at night, twice daily and four times daily on intragastric acidity in normal subjects
Authors: PRIMROSE J. N. , ROGERS M. J. , HOLMFIELD J. H. M. 
Published: July 2010

SUMMARYThe aim of this study was to compare to placebo the effects of 300 mg ranitidine nocte, b.d. and q.d. on intragastric acidity. The study was performed on healthy male subjects and intragastric acidity measured by radiotelemetry. All active treatments significantly decreased 24‐hr acidity, with a median suppression of 61.0% with 300 mg ranitidine nocte, 77.7% with 300 mg b.d. and 78.0% with 300 mg q.d.s. There was no significant difference between the effects of two higher dose regimens: although the 300 mg q.d.s. suppressed daytime acidity more than 300 mg b.d. (88.9%vs. 77.8%), it suppressed nocturnal acidity less effectively (65.5%) than either 300 mg nocte (92.9%) or 300 mg b.d. (90.0%). These data suggest that only modest additional therapeutic acid inhibition can be achieved by increasing the dose of ranitidine above 600 mg daily.
Thrornboxanes in inflammatory bowel disease—pathogenic and therapeutic implications
Authors: RAMPTON D. S. , COLLINS C. E. 
Published: July 2010

SUMMARYRecent work suggests that thromboxanes may play a major pathogenic role in inflammatory bowel disease. Thromboxanes are produced in excess not only in inflamed mucosa but also in Crohn's disease, by uninflamed bowel and by isolated intestinal and peripheral blood mononuclear cells. Their cellular source is likely to include platelets, neutrophils, endothelial and epithelial cells as well as mononuclear cells, possible stimuli to their overproduction being chemotactic peptides, lipopolysaccharide, leucotrienes, platelet activating factor, interleukin‐1, bradykinin and angiotensinII. The pro‐inflammatory effects of thromboxanes are both direct (diapedesis and activation of neutrophils, mucosal ulceration, reduction of suppressor T‐cell activity) and indirect (vasoconstriction, platelet activation). Although corticosteroids and aminosalicylates inhibit thromboxane synthesis, this action does not necessarily explain their therapeutic effect in inflammatory bowel disease. Selective thromboxane synthesis inhibitors and receptor antagonists, however, ameliorate experimental colitis in animals. Picotamide and ridogrel are dual thromboxane pathway blockers already used in man. Drugs of this type could prove useful not only for the prevention of systemic thrombo‐embolism but also for suppressing intestinal mucosal inflammation in patients with inflammatory bowel disease.
Pharmacokinetics of budesonide enema in patients with distal ulcerative colitis or proctitis
Authors: DANIELSSON Å. , EDSBÄCKER S. , LÖFBERG R. , NILSSON Å. , NYMAN‐PANTELIDIS M. , OLSSON O. , SUHR O. , WILLÉN R. 
Published: July 2010

SUMMARYPharmacokinetic data obtained after one dose of a 2‐mg budesonide enema were compared with data obtained after the last dose of four weeks of daily treatment in 24 patients with active distal ulcerative colitis or proctitis. This open multicentre study involved 28 eligible patients. Sigmoidoscopy and biopsy scores improved significantly (P < 0.002) during the four‐week treatment period. Maximal plasma concentration (Cmax) of budesonide was 2.1 nmol/L 1.3 h after the first dose and 2.5 nmol/L 1.2 h after the last dose; the difference was not significant. The area under the curve (AUC) of plasma concentration vs. time was after the first dose 9.7 nmol h/L and after the last dose 11.6 nmol h/L (P < 0.03). The small increase in AUC may be attributed to improved absorption. During the last dose interval, minimal plasma concentration was below the limit of quantitation in most subjects. The Cmax and AUC of budesonide increased slightly after four weeks of treatment, but budesonide did not accumulate. Mean morning plasma cortisol values did not change significantly during treatment (P= 0.083), although a small change in cortisol levels between the first visit (pre‐treatment) and last visit was positively correlated to the C. of budesonide measured at the last visit (P= 0.012).
Omeprazole versus famotidine in the healing and relapse of duodenal ulcer
Authors: MISRA S. C. , DASARATHY S. , SHARMA M. P. 
Published: July 2010

SUMMARYSixty patients with symptomatic duodenal ulcer were randomized to receive either omeprazole (20 mg each morning) or famotidine (40 mg at night time) for 2–4 weeks in a double‐blind parallel group clinical trial. Healing rates were higher with omeprazole in comparison with famotidine after 2 weeks (77%vs. 40%, P < 0.001) and 4 weeks (93%vs. 80%, P= 0.2) of treatment. Assessment of daily diary cards completed by all patients revealed that omeprazole rapidly relieved ulcer‐related day pain and nocturnal pain in comparison to famotidine. Treatment with omeprazole for 2 weeks was also associated with lower cumulative antacid intake (P < 0.05) and reduced absenteeism from work. Helicobacter pylori infection was present in all patients and remained unaffected by treatment with either of the drugs. None of the drugs produced any significant adverse effects. During 6 months follow‐up of all the patients after ulcer healing (without maintenance therapy), ulcer relapse was seen in 40% of omeprazole‐ and 37% of famotidine‐treated patients (P > 0.1). The duration of ulcer‐free period following initial healing of ulcer was also similar in both the groups (median time: 22 weeks for omeprazole, 21 weeks for famotidine). We conclude that omeprazole is superior to famotidine in rapidly healing duodenal ulcers and achieving more rapid pain relief, but does not influence subsequent ulcer relapse.
The management of Zollinger—Ellison syndrome
Authors: MATON P. N. 
Published: July 2010

SUMMARYAwareness of the sometimes subtle features of Zollinger–Ellison syndrome is important in order not to miss the diagnosis. Immediately after initial diagnostic tests, the patient should be given antisecretory medication, while tests for the type of Zollinger–Ellison syndrome and tumour extent can be delayed. Acid output should be decreased to < 10 mmol/h to control symptoms and prevent complications. Histamine H2‐ antagonists remain the best available intravenous therapy but omeprazole is the most effective long‐term oral therapy and has proved to be safe in nearly 10 years of continuous use. The management of the gastrinoma has changed in recent years since the discovery that the majority of gastrinomas arise outside the pancreas. Exploratory surgery with tumour resection is the treatment of choice in sporadic Zolliiger‐Ellison syndrome but there are few indications for surgery in patients with Zollinger–Ellison syndrome and multiple endocrine neoplasia type‐1. None of the available therapies for metastatic gastrinoma is very effective.
Review article: the use of gastric acid‐inhibitory drugs—physiological and pathophysiological considerations
Authors: WALDUM H. L. , BRENNA E. , KLEVELAND P. M. , SANDVIK A. K. , SYVERSEN U. 
Published: July 2010

SUMMARYAll vertebrates secrete gastric acid. Acid denatures the proteins in the food and thus makes them more accessible to proteolytic enzymes, and it kills swallowed micro‐organisms. Gastric acid plays an important pathogenetic role in peptic ulcer disease and reflux oesophagitis. In these diseases, drugs that inhibit secretion of gastric acid will heal the lesions and suppress the symptoms. However, both reflux oesophagitis and peptic ulcer tend to recur when the acid‐inhibitory treatment is stopped. Therefore, these patients often require long‐term treatment with acid‐inhibitors. In this overview the potential risks of long‐term profound inhibition of acid secretion, raising the pH above 4 for a considerable time, resulting in reduced killing of micro‐organisms and secondary hypergastrinaemia, are discussed. Gastrin regulates both the function (production and release of histamine) and growth of the enterochromaffin‐like (ECL) cell. Hitherto, the role that this cell plays in gastric carcinogenesis appears to have been underestimated.
Lansoprazole in the treatment of reflux oesophagitis: a survey of clinical studies
Authors: BERSTAD A. , HATLEBAKK J. G. 
Published: July 2010

SUMMARYThe newly developed proton pump inhibitor lansoprazole has been compared to placebo, ranitidine and with omeprazole in a number of clinical studies in patients with reflux oesophagitis. In three comparative studies against ranitidine, lansoprazole was found to be superior in terms of healing rates and symptom relief. In two studies against omeprazole, no significant difference was found in healing rates, while a Scandinavian study demonstrated more prompt relief from heartburn. Further studies are presently being conducted to evaluate the potential of lansoprazole in long‐term treatment of reflux oesophagitis. It is concluded that lansoprazole is a safe, effective therapy for reflux oesophagitis, superior to ranitidine and comparable with omeprazole.
Acute treatment of duodenal ulcer: experience with lansoprazole
Authors: MIGNON M. , VALLOT T. 
Published: July 2010

SUMMARYClinical experience with lansoprazole in the acute treatment of duodenal ulcer patients has been compared with treatment using placebo, H2‐antagonists or omeprazole. Among the various lansoprazole dosage regimens that have been tested, 30 mg daily for 4 weeks appears to be the optimal regimen to relieve pain rapidly and to heal ulceration in up to 90–95% of patients. Lansoprazole tolerability in the short term appears excellent, most adverse effects are trivial and not dose related. Duodenal ulcer relapse after ulcer healing with lansoprazole appears to occur at a rate similar to that observed after treatment with omeprazole or histamine H2‐antagonists.
A decade of experience with long‐term continuous treatment of peptic ulcers with H2‐receptor antagonists
Authors: PENSTON J. G. 
Published: July 2010

SUMMARYPatients with peptic ulcer disease are troubled by recurrent episodes of ulcer pain, and remain at risk of developing the serious and occasionally lethal complications of haemorrhage and perforation. As the disease is chronic and persists over many years, a long‐term strategy for the management of patients with peptic ulcer is required. Continuous, long‐term treatment with H2‐receptor antagonists successfully achieves the dual objectives of preventing painful ulcer recurrence and reducing the risk of complications. During nine years of continuous therapy with ranitidine, more than 80% of patients with duodenal ulcers remain free from symptomatic ulcer recurrence, less than 2% suffer from ulcer haemorrhage, and the risk of perforation is 0%. Similar beneficial effects of long‐term treatment have been observed in patients with gastric ulcer. Long‐term continuous treatment with H2‐receptor antagonists may not alter the natural history of ulcer disease. Even after seven years of continuous therapy with ranitidine, ulcers recur in 50% of patients within six months of stopping treatment. Hence, long‐term therapy with H2‐receptor antagonists may need to be continued beyond 10 years. Patients with peptic ulcer who are elderly, those taking NSAIDs, aspirin or anti‐coagulants, those with a previous history of an ulcer complication and those with serious co‐existent disease are at increased risk from haemorrhage and perforation. These patients should receive long‐term prophylactic therapy with an H2‐receptor antagonist.
Oral mesalazine (5‐aminosalicylic acid; Asacol) for the prevention of post‐operative recurrence of Crohn's disease
Authors: CAPRILLI R. , ANDREOLI A. , CAPURSO L. , CORRAO G. , ALBASIO G. D. , GIOIENI A. , ASSUERO LANFRANCHI G. , PALADINI I. , PALLONE F. , PONTI V. , RIGO G. P. , ROSSINI F. P. , STURNIOLO G. C. , TONELLI F. , VALPIANI D. ,   THE GRUPPO ITALIANO PER LO STUDIO DEL COLON E DEL RETTO (GISC)
Published: July 2010

SUMMARYMethods:A multicentre randomized controlled trial was conducted to evaluate the efficacy of oral mesalazine (5‐aminosalicylic acid) for the prevention of post‐operative recurrence in 110 patients operated on for Crohn's disease by first intestinal resection. Patients were randomly allocated to receive 2.4 g/day of mesalazine, or no treatment at all. The protocol included colonoscopy with ileoscopy at 6 months and yearly thereafter. Recurrence was denned on the basis of endoscopic criteria and classified as mild or severe.Results: The demographic and pre‐trial characteristics were very similar in the two groups of patients. The cumulative proportion of recurrence at 6, 12 and 24 months was significantly lower in the mesalazine group than in untreated group (P= 0.002). At 24 months the cumulative proportions of endoscopic recurrence were 0.52 + 0.12 (± S.E.M.) and 0.85 (±0.07), respectively. At the same time the cumulative proportions of symptomatic recurrence were 0.18 + 0.09 and 0.41 + 0.09 (P= 0.006). The cumulative proportions of the severe recurrence was also significantly lower in the mesalazine group (0.17±0.09vs.0.38±0.09;P= 0.021).Conclusions: The preliminary results of this study show that administration of oral mesalazine soon after surgery is effective in preventing post‐operative endoscopic recurrence in Crohn's disease over a 2‐year period. It is estimated that this treatment prevents 39% of all recurrences and 55% of the severe recurrences.
Randomized, placebo‐controlled comparison of famotidine 20 mg b.d. or 40 mg b.d. in patients with erosive oesophagitis
Authors: SIMON T. J. , BERENSON M. M. , BERLIN R. G. , SNAPINN S. , CAGLIOLA A. 
Published: July 2010

SUMMARY Methods: this US multicentre, randomized, double‐blind, placebo‐controlled, parallel group study determined the effects of two twice daily oral famotidine regimens on symptom relief and healing of erosive oesophagitis in patients with gastro‐oesophageal reflux disease. Three hundred and eighteen patients were enrolled: 66 received placebo, 125 received famotidine 20 mg b.d., and 127 received famotidine 40 mg b.d. Patients maintained diaries of their symptoms. Endoscopy was performed at weeks 0 and 6, and again at week 12 if healing had not occurred. Results: healing at 6 and 12 weeks was (respectively) 48% (P < 0.01 vs. placebo) and 69% (P≫ 0.01 vs.placebo) for famotidine 40 mg b.d.; 32% and 54% (P≫ 0.01 vs. placebo) for famotidine 20 mg b.d., and 18% and 29% for placebo. At both 6 and 12 weeks the healing rates of famotidine 40 mg b.d. were significantly greater than placebo and famotidine 20 mg b.d. Compared to placebo, famotidine produced more frequent global symptom improvement and more rapid heartburn relief. There were no significant differences among treatment groups in the incidence of clinical or laboratory adverse events. Conclusions: famotidine 40 mg b.d. was a better regimen than famotidine 20 mg b.d. or placebo. The clinical efficacy paralleled the previously documented effect of the famotidine regimens on decrease of oesophageal acid exposure.
Addition of cisapride shortens colonoscopy preparation with lavage in elderly patients
Authors: UEDA S. , HSHI H. , TATSUTA M. , ODA K. , OSAKA S. 
Published: July 2010

SUMMARY Methods: The effect of pre‐treatment with cisapride on colonoscopy preparation with lavage solution was compared in 120 out‐patients less than 60 years and 73 out‐patients 60 years or older, who were scheduled for total colonoscopy. By random allocation, patients were assigned to receive cisapride 10 mg or placebo 30 minutes before ingesting the magnesium citrate lavage solution. Results: The cleansing results and patients’acceptance did not differ significantly in the two treatment groups in either age group. The time from the start of ingesting magnesium citrate until the rectal effluent became clear was significantly shorter in cisapride‐treated patients of 60 years or more. Moreover, the residual fluid volume removed by suction during colonoscopy was significantly less in the patients above aged 60 years who received cisapride. Conclusion: These findings indicate that the combination of cisapride and magnesium citrate is more effective than magnesium citrate alone in cleansing the colon for colonoscopy in elderly patients.
Efsect ofursodeoxycholic acid on in vivo and in vitro toxic liver injury in rats
Authors: SIMKO V. , MICHAEL S. 
Published: July 2010

SUMMARY Background: Benefits of ursodeoxycholic acid (UDCA) cholestatic disorders have been well documented. However, the therapeutic potential of UDCA in parenchymal liver disease is unclear. Methods: We tested UDCA in rat models of hepatotoxicity: (a) in subacute liver injury induced by repetitive CCl4 and dietary ethyl alcohol (ETH) over seven weeks while receiving oral UDCA; and, (b) in liver slides incubated with CCI4, ETH or p‐acetaminophen (APAP) when UDCA was added to the incubating solution. Results: Experiment 1: CCI4 combined with ETH reduced the body weights and resulted in 43% mortality. There was a significant rise in serum ALT, alkaline phosphatase, lipoperoxides (LPO) and in hepatic weight, triglycerides, LPO and histological scores of liver injury. Experiment 2: When liver slides were incubated with hepatotoxins there was an increased transfer of AST and LPO from the tissue into the incubate and a reduction in the valine and thymidine incorporation into the liver proteins or DNA. In none of these situations, whether the liver damage was severe or mild, in vivo or in vitro, UDCA did abolish these hepatotoxic effects. Conclusion: In contrast to clinical cholestatic disorders where the reported benefits of UDCA depend on replacement of the accumulated hydrophobic bile acids, these bile acids have a less prominent role in toxic liver injury and UDCA is ineffective.
Comparative effects of intraduodenal psyllium and senna on canine small bowel motility
Authors: ASHRAF W. , LOF J. , JIN G. , QUIGLEY E. M. M. 
Published: July 2010

SUMMARYBackground/aim: To define the possible contribution of altered small intestinal motor activity to side‐effects of bulking fibres, we sought to compare the relative effects of intraduodenal and intracolonic administration of the bulking fibre psyllium and the anthraquinone laxative senna on canine small intestinal motor activity.Methods: Motor activity was recorded by serosal strain gauges implanted along the small intestine in 6 dogs. In random order, the motor responses to the instillation of psyllium (in doses of 5 or 10 g), senna (10 mg/kg) or appropriate vehicle (200 ml water infusion or saline 5 ml bolus) into either the proximal duodenum or proximal colon were assessed.Results: The intra‐duodenal administration of psyllium in either dose consistently induced a prolonged burst of‘clustered’contractions; in contrast, clusters were infrequent and of short duration following instillation of either vehicle or senna (P< 0.05). Intraduodenal instillation of psyllium inhibited migrating motor complex (MMC) migration and consistently delayed the onset of the next MMC cycle; a similar inhibition occurred with vehicle, however. Neither senna nor its vehicle inhibited MMC migration. None of these agents had any effect on small intestinal motor activity when instilled directly into the colon.Conclusions: Psyllium administered directly into the duodenum inhibits MMC activity and consistently induces‘clustered’contractions. Whilst the MMC‐inhibitory effect appears to be a non‐specific volumerelated phenomenon, the induction of clusters is independent of volume or laxation. These motor effects of psyllium may contribute to the gastrointestinal symptomatology related to such agents and could be avoided by the preferential release of psyllium in the colon.
Review article: gastroduodenal bicarbonate secretion
Authors: HOGAN D. L. , AINSWORTH M. A. , ISENBERG J. I. 
Published: July 2010

SUMMARYThe gastroduodenal epithelium is covered by an adherent mucus layer into which bicarbonate is secreted by surface epithelial cells. This mucus‐bicarbonate barrier is an important first line of defence against damage by gastric acid and pepsin, and has been demonstrated in all species including human. Similar to gastric acid secretion, regulation of gastric and duodenal bicarbonate secretion can be divided into three phases: cephalic, gastric and duodenal. In humans, sham‐feeding increases bicarbonate secretion in both the stomach and duodenum which is mediated by cholinergic vagal fibres in the stomach, but seems to be noncholinergic in the duodenum. Gastric distention and luminal acidification increases gastric bicarbonate production. Whereas there are no data relating to the gastric phase of human duodenal bicarbonate secretion, in animals, food and acid in the stomach independently stimulate duodenal bicarbonate output. To date, the duodenal phase of human gastric bicarbonate secretion has not been studied, but data from animals reveal that duodenal acidification augments bicarbonate secretion in the stomach. In all species tested, direct acidification of the duodenum is a potent stimulant of local bicarbonate production. In humans, the pH threshold for bicarbonate secretion is pH 3.0. Mediation of gastroduodenal bicarbonate secretion is provided by a variety of agonists and antagonists, tested mainly in animals, but some have been evaluated in humans. Prostaglandins of the E class and VIP are major factors that control bicarbonate secretion. Bicarbonate secretion, and the mucus‐bicarbonate layer in general, is adversely effected by ulcerogenic factors such as aspirin, NSAIDs, bile salts, and cigarette smoking. Furthermore, duodenal ulcer patients have an impairment in bicarbonate production within the duodenal bulb, at rest and in response to stimulation. These findings indicate that the mucus‐bicarbonate barrier is an important first line of defence in the pathogenesis of peptic ulcer disease.
Oral budesonide for treatment of autoimmune chronic active hepatitis
Authors: DANIELSSON Å. , PRYTZ H. 
Published: July 2010

SUMMARY Objectives: To see if budesonide, a second generation glucocorticosteroid with a high topical effect and a high first‐pass metabolism of 90% in the healthy liver, can induce biochemical remission in autoimmune chronic active hepatitis before being metabolized, and further to study the effect on endogenous plasma cortisol levels and corticosteroid‐related side effects. Patients and design: Thirteen patients with autoimmune chronic active hepatitis (11 females) were treated openly for up to 9 months by oral budesonide capsules. The initial dose was 6–8 mg (mean 6.3 mg) daily for 6–10 weeks, and then the dose was individualized. Results: The pre‐treatment values of alanine aminotransferase and immunoglobulin (IgG) were 7.1 ± 1.2,μkat/L (mean ± S.E.M.) and 26.4 ± 3.9 g/L, respectively. After 6 weeks of treatment, significant decreases in alanine aminotransferase (to 2.1 ± 0.9 μkat/L) and immunoglobulin (to 18.4 ± 2.4 g/L) were recorded. After 9 months the corresponding values (n= 9) were 1.2 ± 0.9 μkat/L and 15.9 ± 1.3 g/L, respectively. The mean value of plasma cortisol remained within normal ranges or was only slightly subnormal for the whole group (364 ± 44 nmol/L at start, 165 ± 46 after 6 weeks and 138 ± 44 after 9 months). However, significantly reduced plasma cortisol levels were found in patients with biopsy‐proven liver cirrhosis. Conclusion: Oral budesonide appears to decrease liver inflammation in autoimmune chronic active hepatitis while causing a low frequency of systemic side effects and a marginal reduction in plasma cortisol in non‐cirrhotic patients over a study period of 9 months.