bluuebunny/crossref_metadata_2025_split huggingface dataset:
Is there any acid peptic disease that is refractory to proton pump inhibitors ?
Authors: BARDHAN K. D. 
Published: July 2010

SUMMARYNon‐healing and delayed healing during acid inhibition treatment depend on the extent to which acid and‘non‐acid’factors are causative in the particular acid peptic disease, and on the effectiveness and duration of acid suppression. Refractoriness (defined arbitrarily) occurs less often with proton pump inhibitors than with H2‐receptor antagonists as the former decrease acid more effectively; H2‐receptor antagonist‐refractory disease usually responds to treatment with proton pump inhibitors. In Rotherham, 5–10% of duodenal ulcer and gastric ulcer patients are refractory (not healed after 3 months of standard‐dose H2‐receptor antagonist). In patients with oesophagitis 15% are refractory to high‐dose H2‐receptor antagonist (for example, 3.2 g cimetidine daily) and 5% to standard‐dose proton pump inhibitors (for example, 20 mg omeprazole daily). In controlled clinical trials of patients with refractory duodenal ulcer, healing at 8 weeks with 40 mg omeprazole o.m. vs. continued standard‐dose H2‐receptor antagonist was 98%vs. 60%; and with 40 mg omeprazole vs. continued high‐dose H2‐receptor antagonist (2 g + 3 g cimetidine, that is, ultra‐refractory disease) was 92%vs. 67%. After healing, in open studies, relapse with maintenance 400‐800 mg cimetidine nocte was 45‐69% at one year, but 0% with 40 mg omeprazole administered for up to 6.5 years. For 53 patients with refractory gastric ulcer, in an open study, healing with omeprazole 40 mg o.m. occurred in 94% at 8 weeks, and none relapsed on long‐term maintenance treatment at this dose. In controlled trials of patients with refractory oesophagitis, healing at 12 weeks with 40 mg omeprazole o.m. vs. high‐dose ranitidine (300 mg b.d.) was 90%vs. 47%, and with maintenance 20 mg omeprazole o.m. vs. 150 mg ranitidine b.d., relapse at 1 year was 32%vs. 88%. In conclusion, acid peptic disease refractory to H2‐receptor antagonists is uncommon and treatment with proton pump inhibitors is effective. Refractoriness to proton pump inhibitors is rare.
Lack of evidence of neurotoxicity following 8 weeks of treatment with tripotassium dicitrato bismuthate
Authors: NWOKOLO C. U. , FITZPATRICK J. D. , PAUL R. , AL R. DY , SMITS B. J. , LOFT D. E. 
Published: July 2010

SUMMARY Objective: To search for evidence of subclinical neurotoxicity in patients treated with tripotassium dicitrato bismuthate. Design: Prospective, controlled, triplicate study using urinary bismuth concentration, magnetic resonance imaging (MRI), nerve conduction studies, visual evoked response and a battery of 10 neuropsychological screening tests. Setting: Out‐patient clinics, Walsgrave Hospital, Coventry, UK. Subjects: Fourteen dyspeptic patients; 8 (treatment group) treated with tripotassium dicitrato bismuthate one tablet q.d.s and 6 (control group) treated with ranitidine 150 mg b.d. for 8 weeks. Main outcome measures: Changes in urinary bismuth, MRI, nerve conduction studies, visual evoked response, and neuropsychological tests performed before, immediately after and 8 weeks after the cessation of treatment. Results: In the treatment group the median (range) urinary bismuth concentration was 1 (1–12) ng/ml before treatment, increased to 560 (140–1300) immediately after treatment (P < 0.01, Wilcoxon Rank Sum test) and was still significantly elevated (23 (7–53) ng/ml) 8 weeks after the cessation of treatment. In the patient who recorded the highest urinary bismuth, a high intensity signal appeared in the globus pallidus immediately after treatment and was still present (though diminished in intensity) 8 weeks after the cessation of treatment. This isolated MRI finding was not associated with evidence of subclinical neurotoxicity. No changes in the MRI, nerve conduction studies, visual evoked response and neuropsychological tests were observed among the other patients studied. Conclusions: Bismuth accumulation occurs in patients receiving a conventional course of treatment with tripotassium dicitrato bismuthate but this is not associated with significant changes in the nervous system.
Comparison of pantoprazole and ranitidine in the treatment of acute duodenal ulcer
Authors: JUDMAIER G. , KOELZ H. R. ,   PANTOPRAZOLE‐DUODENAL ULCER‐STUDY GROUP
Published: July 2010

SUMMARYBackground:Pantoprazole is a new substituted benzimidazole that blocks the H+/K+‐ATPase in the gastric mucosa and thus inhibits acid secretion.Methods: Efficacy and tolerability of pantoprazole (40 mg at breakfast) and ranitidine (300 mg at bedtime) in the treatment of uncomplicated acute duodenal ulcer were compared in a double‐blind, randomized multicentre trial.Results:Of 202 outpatients who entered the study, 185 terminated the treatment without violation of the protocol. After 2 weeks of treatment, healing rates (protocol correct) with pantoprazole and ranitidine were 81 and 53%, respectively (P> 0.001), the corresponding results after 4 weeks were 97 and 83% (P> 0.01). Pantoprazole was more effective with respect to symptom relief. Both treatments were well tolerated.Conclusion:Pantoprazole 40 mg at breakfast is superior to ranitidine 300 mg at bedtime in the short‐term treatment of acute, uncomplicated duodenal ulcer.
Short report: a comparative study of the interaction between antacid and H2‐receptor antagonists
Authors: SULLIVAN T. J. , REESE J. H. , JAUREGUI L. , MILLER K. , LEVINE L. , BACHMANN K. A. 
Published: July 2010

SUMMARYThe influence of concomitant antacid administration on the relative bioavailability of the H2‐receptor antagonists cimetidine, famotidine, nizatidine and ranitidine, was investigated in a panel of 21 healthy, adult male volunteers in an eight‐way crossover trial. Administration with antacid reduced the bioavailability of all agents tested. The reduction in area under the serum concentration‐time curve (AUC) was greatest for cimetidine (23%) and ranitidine (26%) and least for nizatidine (12%) and famotidine (19%). Reductions in peak serum concentration (Cmax) followed a similar pattern. The times of peak serum concentrations were not affected by antacid. Comparison of the relative bioavailability among all drugs tested showed no statistically significant differences in the effect of antacid administration on these agents. However, a high degree of intersubject variability was observed.
Short report: zinc sulphate supplementation corrects abnormal erythrocyte membrane long‐chain fatty acid composition in patients with Crohn's disease
Authors: BELLUZZI A. , BRIGNOLA C. , CAMPIERI M. , GIONCHETTI P. , RIZZELLO F. , BOSCHI S. , CUNANNE S. , & M. MIGLIOLI , BARBARA L. 
Published: July 2010

SUMMARYPatients with Crohn's disease may become zinc‐deficient and, in such patients, an altered metabolism of radiolabelled long‐chain fatty acids has been reported. We have investigated the possible reversal by zinc supplementation of altered long‐chain fatty acid profiles of red cells in Crohn's disease. Twenty patients with long‐standing Crohn's disease in clinical remission received 200 mg of zinc sulphate daily for 6 weeks. Phospholipid fatty acid profiles of washed red cells were analysed before and after zinc treatment and compared to those of 20 unsupplemented healthy controls.Plasma zinc levels in Crohn's were 72 ± 8 μg/dL before zinc treatment and increased to 114 ± 10 μg/dl after the therapy. Prior to zinc supplementation, the percentage of palmitic, stearic and oleic acids was significantly higher in Crohn's disease, while linoleic, arachidonic and n‐3 fatty acids were reduced in Crohn's disease compared to healthy controls. Zinc supplementation abolished these pre‐treatment differences in red‐cell long‐chain fatty acid profiles but did not affect plasma fatty acid values. Further studies are needed to clarify whether these fatty acid changes can be related to the clinical course of the disease.
Review article: aspirin and gastrointestinal bleeding
Authors: HAWKEY C.J. 
Published: July 2010

SUMMARYMany animal and human studies have shown aspirin to cause gastric mucosal erosions and enhanced spontaneous microbleeding. Chronic use is associated with uncomplicated gastric ulcer (but not clearly with uncomplicated duodenal ulcer) and with presentation with haematemesis and melaena. Sub‐group analysis suggests that the risks of bleeding duodenal ulcer as well as bleeding gastric ulcer (and possibly non‐ulcer bleeding) are increased. These data imply that an anti‐haemostatic as well as an ulcerogenic effect contributes to such presentation and acute data support this proposition. A broken mucosa and inhibition of thromboxane synthesis both appear to be necessary for bleeding to occur. Aspirin enhances the bleeding associated with mucosal biopsy analogous to its prolongation of the skin bleeding time. Anti‐haemostatic properties could account for the apparent increase in presentation with haematemesis and melaena in patients taking low doses of aspirin for cardiovascular prophylaxis. However, acute studies also show aspirin 300 mg to cause a level of mucosal injury which is substantial, though significantly less than with aspirin 600 mg q.d.s. The risk attached to aspirin consumption needs to be kept in perspective. It can be calculated that aspirin use is associated with approximately 700 bleeds per annum in the UK. The relative risk for upper gastrointestinal bleeding is roughly similar to that for non‐aspirin non‐steroidal anti‐inflammatory drugs but those affected are generally younger, in an age group where death from upper gastrointestinal bleeding is very uncommon. In keeping with this and in contrast to non‐aspirin nonsteroidal anti‐inflammatory drugs, no study has shown increased mortality from aspirin‐related upper gastrointestinal complications.
Comparison of acid inhibition by either oral high‐dose ranitidine or omeprazole
Authors: HURLIMANN S. , ABBÜHL B. , INAUEN W. , HALTER F. 
Published: July 2010

SUMMARYBackground:High‐dose once daily oral omeprazole dosing can inhibit acid secretion almost completely but several days elapse before maximum efficacy is established. The acid inhibitory effect obtained with high doses of a histamine H2‐receptor antagonist is built up rapidly but has the tendency to fade‐the term tolerance’has been applied to characterize this phenomenon.Methods: To obtain more information on the dynamics of acid inhibition during prolonged dosing, we compared the acid suppressory effects of oral high‐dose omeprazole with high‐dose ranitidine. Twenty‐eight healthy volunteers were randomly assigned to a 2‐week dosing with omeprazole or ranitidine in a double‐blind, double‐dummy, parallel‐group study design. Omeprazole was given as 1 capsule of 40 mg mane and ranitidine as 2 tabs of 150 mg q.d.s. The median 24‐h pH, daytime pH and night‐time pH were measured by ambulatory continuous 24‐h pH metry on days ‐8, ‐6, 1. 2, 7 and 14.Results: High reproducibility was observed for the two baseline acidity measurements. Ranitidine exerted its peak acid suppressant effect on day 1 of dosing; the degree of acid inhibition faded from day 2 to 7, with no significant change thereafter. The decline in antisecretory activity was more pronounced during the day than the night. In contrast, acid inhibition by omeprazole increased throughout the first week, and antisecretory activity was stable thereafter. Despite the considerable differences in median intragastric pH values at the end of the 14‐day study, plasma gastrin levels were elevated to a similar degree with both medications.Conclusions: This study confirms the ‘tolerance’phenomenon previously observed with high‐dose histamine H2‐receptor antagonist dosing. The dynamics with which it occurs exclude a typical exaggerated first‐dose response. Prolonged high‐dose histamine H2‐receptor dosing compromises the feedback mechanism regulating gastrin release, whilst this is maintained during dosing with omeprazole.
Rapid healing of gastric ulcers with lansoprazole
Authors: BARDHAN K. D. , AHLBERG J. , HISLOP W. S. , LINDHOLMER C. , LONG R. G. , MORGAN A. G. , SJOSTEDT S. , SMITH P. M. , STIG R. , WORMSLEY K. G. , LANGWORTHY H H. , MOULES I. K. 
Published: July 2010

SUMMARY Background: Lansoprazole is a new proton pump inhibitor which powerfully decreases acid secretion. Methods: We compared the efficacy and short‐term safety of lansoprazole against ranitidine in the healing of gastric ulcer. This was a parallel group, comparative multicentre, prospectively randomized, double‐blind study which included 250 patients with gastric ulcer, 219 of whom had follow‐up endoscopic data. Results: Both lansoprazole 30 mg and 60 mg daily produced significantly more rapid healing of gastric ulcer than ranitidine 300 mg nightly with healing rates after 4 weeks of 78% (P < 0.05), 84% (P < 0.01) and 61%, respectively. After 8 weeks, the corresponding healing rates were 99%, 97% and 91% (P = 0.08). Symptom relief was similar for all treatment groups, but fewer antacids were used by patients receiving lansoprazole. Sixty‐nine patients experienced 91 adverse events; the incidence, pattern and severity was similar across all three treatment groups. Conclusions: Lansoprazole 30 mg and 60 mg once daily had similar efficacy. Both were superior to ranitidine 300 mg nocte in healing gastric ulcer. The short‐term safety profile of lansoprazole was similar to ranitidine. These data indicate that lansoprazole should be used at a dose of 30 mg once daily for the treatment of gastric ulcers.
Rolling review–the pathogenesis, diagnosis and management of viral hepatitis
Authors: DUSHEIKO G. M. 
Published: July 2010

SUMMARYFive major hepatotrophic viruses have been identified. The pathogenesis, diagnosis and treatment of chronic viral hepatitis continues to be intensely researched. Experimental evidence suggests that HLA restricted virus‐specific T cells play a role in hepatocellular injury in type A hepatitis. The absence of chronic infection indicates the effectiveness of the host immune response to hepatitis A virus (HAV). It is postulated that HAV may rarely trigger an autoimmune chronic hepatitis. Active prophylaxis of hepatitis A is possible.The elimination of hepatitis B is dependent on the recognition of viral determinants in association with HLA proteins on infected hepatocytes by cytotoxic T cells. The specific epitopes recognized by B and T cells are being mapped. Polymerase chain reaction (PCR) amplification and sequencing of genomic DNA in patients with chronic hepatitis B has indicated that nucleotide substitutions in the genome are not uncommon. Their pathogenicity is being explored. Antiviral therapy for hepatitis B remains difficult. Interferon is effective in a proportion of patients. Thymosin may prove to be more effective immunomodulatory therapy. New nucleoside analogues suppress HBV replication, but the safety of these drugs has been questioned after the appearance of severe liver toxicity with fialuridine.The data that hepatitis D virus is pathogenic has recently been challenged with the observation that HDV re‐occurs in transplanted liver after engrafting, but without signs of HBV recurrence or evidence of liver damage. Treatment of hepatitis D virus remains difficult.Several isolates of hepatitis C virus have been cloned, and the sequence divergence of these isolates indicates that there are several major genotypes and component subtypes of this polymorphic virus. Hypervariability of regions of the HCV envelope proteins may be important in persistence of HCV infection and immunopathogenesis. Type C hepatitis has a complex natural history, and several systemic manifestations as well as autoimmune disease have been linked to hepatitis C infection. Alpha interferon is beneficial in 25–30% of patients; certain genotypes may be more sensitive to interferon therapy.The hepatitis E virus causes acute, and in susceptible populations, fulminant hepatitis. The diagnosis can now be made with tests for anti‐HEV and Polymerase chain reaction.Other forms of viral hepatitis, particularly those associated with fulminant hepatitis, severe sporadic hepatitis and autoimmune disease are being sought.
Review article: the transjugular intrahepatic portosystemic shunt (TIPS) in the treatment of portal hypertension
Authors: McCORMICK P. A. , DICK R. , BURROUGHS A. K. 
Published: July 2010

SUMMARYThe transjugular intrahepatic portosystemic shunt (TIPS) is a non‐surgical intrahepatic shunt connecting the hepatic and portal veins. The shunt can be inserted successfully in more than 90% of patients and it effectively decompresses the portal venous circulation. Serious complications, such as intraperitoneal bleeding, occur but they are uncommon. The role of TIPS in the treatment of portal hypertension is currently being evaluated. There are few controlled data available to compare TIPS with established treatments such as drugs, injection sclerotherapy, endoscopic banding or shunt surgery. TIPS has also been used to treat ascites, the Buddxhiari syndrome and cirrhotic hydrothorax. Concerns over the long‐term patency and the true incidence of encephalopathy following TIPS raise doubts about its long‐term efficacy. Controlled trials are required to demonstrate the cost‐effectiveness of TIPS for individual indications before it is widely adopted. TIPS may find its most immediate application in the emergency treatment of active variceal haemorrhage refractory to standard medical and endoscopic therapy, as there is no satisfactory treatment currently available for this high‐risk group. TIPS may also have a role in patients awaiting liver transplantation who bleed from varices. Long‐term patency should not be an issue in this patient group and portal decompression may reduce blood transfusion requirements during transplant surgery.
Effect of decaffeination of coffee or tea on gastro‐oesophageal reflux
Authors: WENDL B. , PFEIFFER A. , PEHL C. , SCHMIDT T. , KAESS H. 
Published: July 2010

SUMMARY Background: Coffee and tea are believed to cause gastrooesophageal reflux : however, the effects of these beverages and of their major component, caffeine, have not been quantified. The aim of this study was to evaluate gastro‐oesophageal reflux induced by coffee and tea before and after a decaffeination process, and to compare it with water and water‐containing caffeine. Methods: Three‐hour ambulatory pH‐metry was performed on 16 healthy volunteers, who received 300 ml of (i) regular coffee, decaffeinated coffee or tap water (n = 16), (ii) normal tea, decaffeinated tea, tap water, or coffee adapted to normal tea in caffeine concentration (n= 6), and (iii) caffeine‐free and caffeine‐containing water (n= 8) together with a standardized breakfast. Results: Regular coffee induced a significant (P < 0.05) gastro‐oesophageal reflux compared with tap water and normal tea, which were not different from each other. Decaffeination of coffee significantly (P < 0.05) diminished gastro‐oesophageal reflux, whereas decaffeination of tea or addition of caffeine to water had no effect. Coffee adapted to normal tea in caffeine concentration significantly (P < 0.05) increased gastro‐oesophageal reflux. Conclusions: Coffee, in contrast to tea, increases gastrooesophageal reflux, an effect that is less pronounced after decaffeination. Caffeine does not seem to be responsible for gastro‐oesophageal reflux which must be attributed to other components of coffee.
A dose‐response study of orally administered torsemide in patients with ascites due to cirrhosis
Authors: APPLEFELD J. J. , KASMER R. J. , HAK L. J. , DUKES G. E. , WERMELING D. P. , McCLAIN C. J. 
Published: July 2010

SUMMARYBackground: This study evaluated the dose‐response relationship of torsemide, the first pyridine‐sulphonylurea loop diuretic, in patients with ascites due to cirrhosis.Methods: During a 13‐day hospitalization period, 17 patients received single, oral doses of 5 mg, 10 mg, or 20 mg of torsemide or placebo in a randomized, double‐blind, crossover fashion. All the patients received a constant dose of spironolactone concomitantly beginning at least 7 days before the study. Electrolyte excretion and urine volume were measured for 24 h after each dose. Body weight was measured before, and 24 h after each dose.Results: Torsemide was effective in producing statistically significant, dose‐related increases in urinary sodium and chloride excretion, with little effect on potassium or magnesium excretion. Urine volume increased and body weight decreased in a dose‐related manner.Conclusion: Torsemide increased sodium excretion substantially in patients with cirrhosis and ascites who were receiving spironolactone.
Alosetron does not affect the visceral perception of gastric distension in healthy subjects
Authors: ZERBIB F. , VARANNES S. BRULEY des , ORIOLA R. C. , McDONALD J. , ISAL J. P. , GALMICHE J. P. 
Published: July 2010

SUMMARYBackground: The effect of alosetron, a new specific 5‐HT3, receptor antagonist, on the visceral perception in response to gastric distension was assessed in 12 healthy male subjects in a randomized, double‐blind, placebo controlled crossover trialMethods: Each subject was given orally either alosetron 1 mg b.d. or placebo b.d. for 6 days (wash‐out period 7–28 days). At the end of each dosing period, both isobarometric and isovolumetric gastric distensions were performed using an electronic barostat.Results: Alosetron did not modify the gastric wall compliance (pressure‐volume relationship). Alosetron had an effect similar to placebo on the visceral perception scores in both isobarometric and isovolumetric distensions. The mean (± SEM) thresholds for abdominal discomfort were, respectively, 16.8 ±0.7 mmHg and 825 ± 61 mL with alosetron, 16.7±0.6 mmHg and 883±45 mL with Placebo (P = NS).Conclusions: 5‐HT3 receptors do not appear to be involved in the visceral perception of gastric distension in healthy subjects.
Ulceration, fibrosis and diaphragm‐like lesions in the caecum of rats treated with indomethacin
Authors: ANTHONY A. , DHILLON A. P. , SIM R. , NYGARD G. , POUNDER R. E. , WAKEFIELD A. J. 
Published: July 2010

SUMMARYBackground: Patients on nonsteroidal antiinflammatory drugs can develop curious intestinal fibrotic diaphragms.Methods: Groups of rats received indomethacin mixed into a powdered diet at 3 mg.kg/day for 6 and 12 weeks and 6 mg. kg/day for up to 6 weeks. In an attempt to reproduce a human dosing regimen, another group of rats, for a total of 30 weeks, received consecutive periods of indomethacin at 3 mg. kg/day for 12 weeks, 4.5 mg.kg/day for 1 week, 6 mg.kg/day for 1 week, control diet for 6 weeks, 4.5 mg.kg/day for 2 weeks and finally, a control diet for a healing period of 8 weeks. Control rats received powdered diet alone. At termination, the small and large intestines were examined macroscopically and histologically.Results: Indomethacin caused microcytic anaemia, hypoalbuminaemia, small intestinal ulceration, caecal ulceration and inconspicuous raised mucosal lesions in the caecum that histologically showed submucosal fibrosis with disruption and thickening of the apical muscularis mucosae. No control rats showed any abnormality.Conclusion: These fibrotic lesions of the rat caecum resemble human diaphragms and may arise from healed caecal ulcers.