bluuebunny/crossref_metadata_2025_split huggingface dataset:
Diagnostic investigation rates and use of prescription and non‐prescription medications amongst dyspeptics: a population‐based study of 2300 Australians
Authors: Westbrook J. I. , Talley N. J. 
Published: December 2004

SummaryBackground : There is limited knowledge of the diagnostic investigation rates and use of prescription and non‐prescription drugs amongst dyspeptics.Aim : To assess the investigation rates and use of prescription and non‐prescription anti‐ulcer medications amongst dyspeptics in the population.Methods : A cross‐sectional survey was performed of 2300 Australians.Results : Of 748 dyspeptics, 422 (56%) had consulted a doctor regarding dyspepsia at some time in their life. Of the consulters, 64% had undergone investigations at some time: 37% an endoscopy, 54% a barium meal and 27% both. A diagnosis of peptic ulcer was reported by 31% of those investigated. The symptom profile of gastroscopy patients differed significantly from that of uninvestigated dyspeptics. Of the consulters, 36% had taken anti‐ulcer prescription drugs in the last 3 months: Histamine‐2 receptor antagonists (73% of prescriptions), proton pump inhibitors (17%), cytoprotectants (5%) and prokinetic drugs (5%). Antacids were taken by 30% of non‐consulting dyspeptics, 44% of consulters not on prescription drugs and 58% of dyspeptics taking prescription drugs. Advancing age, but not gender, was associated with diagnostic investigation and prescription and non‐prescription drug usage.Conclusions : There are high rates of diagnostic investigation amongst dyspeptics who consult doctors. Many individuals with dyspepsia decide to self‐medicate with antacids regardless of consulting or prescriptions, suggesting that current management is suboptimal.
The advent of capsule endoscopy — a not‐so‐futuristic approach to obscure gastrointestinal bleeding
Authors: Lewis B. , Goldfarb N. 
Published: December 2004

SummaryCapsule endoscopy is a new, wireless, endoscopic examination of the small intestine. To date, two small clinical trials have been reported utilizing capsule endoscopy in patients with obscure gastrointestinal bleeding, and have shown its superiority to push enteroscopy in diagnosing the cause of blood loss. No outcome studies have been reported.This paper proposes a change in practice guidelines for obscure bleeding. It is our opinion that, in the future, with the advent of wireless capsule endoscopy, the evaluation of patients with obscure gastrointestinal bleeding will be very different from the practice of medicine today. We believe that capsule endoscopy will become the first‐line method for the evaluation of patients with obscure bleeding, once upper endoscopy and colonoscopy have been shown to be negative.In patients with active bleeding, capsule endoscopy will confirm the small bowel as the site of bleeding, providing a location, or, if the study is negative for the small intestine, may indicate that the bleeding is either colonic or gastric in origin. In a patient with active bleeding within the small intestine, the capsule will guide further evaluation and therapy. A patient with a small bowel tumour detected by capsule endoscopy will proceed directly to laparoscopic surgery. If the site of bleeding is identified in the proximal small bowel and there is no mass, push enteroscopy will be used to re‐identify the site and cauterize it. A distal small bowel site will require surgical intervention, coupled with intra‐operative enteroscopy. Should the patient be too sick to undergo surgery, medical therapy utilizing hormonal agents will be considered. A colonic site will be evaluated by colonoscopy. In patients with a more occult or intermittent type of bleeding and in those whose upper endoscopies and colonoscopies are negative, capsule endoscopy will be used similarly to identify a bleeding lesion and thereby direct subsequent testing or treatment.
Famotidine for infant gastro‐oesophageal reflux: a multi‐centre, randomized, placebo‐controlled, withdrawal trial
Authors: Orenstein S. R. , Shalaby T. M. , Devandry S. N. , Liacouras C. A. , Czinn S. J. , Dice J. E. , Simon T. J. , Ahrens S. P. , Stauffer L. A. 
Published: December 2004

SummaryBackground :  Gastro‐oesophageal reflux afflicts up to 7% of all infants. Histamine‐2 receptor antagonists are the most commonly prescribed medications for this disorder, but few controlled studies support this practice.Aim : To evaluate the safety and efficacy of famotidine for infant gastro‐oesophageal reflux disease.Methods : Thirty‐five infants, 1.3–10.5 months of age, entered an 8‐week, multi‐centre, randomized, placebo‐controlled, two‐phase trial: first 4 weeks, observer‐blind comparison of famotidine 0.5 mg/kg and famotidine 1.0 mg/kg; second 4 weeks, double‐blind withdrawal comparison (safety and efficacy) of each dose with placebo.Results : No serious adverse events were reported. Eleven patients had 16 non‐serious, possibly drug‐related adverse experiences: 6 patients with agitation or irritability (manifested as head‐rubbing in two), 3 patients with somnolence, 2 patients with anorexia, 2 with headache, 1 patient with vomiting, 1 patient with hiccups, and 1 patient with candidiasis. Of the 35 infants, 27 completed Part I. There were significant score improvements for famotidine 0.5 mg/kg in regurgitation frequency (P = 0.04), and for famotidine 1.0 mg/kg in crying time (P = 0.027) and regurgitation frequency (P = 0.004) and volume (P = 0.01). Eight infants completed Part II on double‐blind treatment, which was insufficient for meaningful comparisons.Conclusions : Histamine‐2 receptor antagonists may cause agitation and headache in infants. A possibly efficacious famotidine dose for infants is 0.5 mg/kg (frequency adjusted for age). As 1.0 mg/kg may be more efficacious in some, the dosage may require individualization based on response. Further sizeable placebo‐controlled evaluations of histamine‐2 receptor antagonists in infants with gastro‐oesophageal reflux disease are warranted.
Helicobacter pylori eradication and gastric ulcer healing — comparison of three pantoprazole‐based triple therapies
Authors: Malfertheiner P. , Kirchner T. , Kist M. , Leodolter A. , Peitz U. , Strobel S. , Bohuschke M. , Gatz G. ,   THE BYK ADVANCED GASTRIC ULCER STUDY (BAGUS) GROUP
Published: December 2004

SummaryAim : To study the efficacy of three pantoprazole‐based triple therapy regimens for the eradication of Helicobacter pylori infection and gastric ulcer healing.Methods : In an open, multi‐centre, randomized study, 519 H. pylori‐positive patients with active gastric ulcer were randomized to receive pantoprazole (40 mg) (P) and two of three antibiotics: clarithromycin (500 mg) (C), metronidazole (500 mg) (M) or amoxicillin (1000 mg) (A). Triple therapy (PAC, PCM, PAM) was administered twice daily for 7 days, followed by pantoprazole until the ulcer had healed. Antrum and corpus biopsies were taken to determine the pattern of gastritis, to assess the H. pylori status and to determine the strain susceptibility to antibiotics, and from the ulcer margins and base to exclude malignancy. Scores based on the Sydney system were used to categorize the gastritis phenotypically.Results : The H. pylori eradication rates for the per protocol (intention‐to‐treat) analysis were 89% (67%) for PAC, 83% (68%) for PCM and 76% (60%) for PAM, with a significant difference between PAC and PAM. Healing rates after 4 weeks were 91% for PAM, 90% for PCM and 88% for PAC (per protocol analysis). The eradication rates were lower in patients in whom strains resistant to any antibiotic used in the triple therapies were detected. Successful eradication [odds ratio, 5.2 (3.3; 8.3)] and the ulcer size (< 15 mm) were significant predictors for healing after 4 weeks. The regimens showed a comparable safety profile and compliance.Conclusions : Pantoprazole‐based triple therapies are effective in the eradication of H. pylori infection in gastric ulcer patients, as reported in previous similar sized studies in duodenal ulcer patients. Successful eradication and an ulcer size of < 15 mm are the best predictors of gastric ulcer healing after 4 weeks.
Gastrointestinal transit and release of 5‐aminosalicylic acid from 153Sm‐labelled mesalazine pellets vs. tablets in male healthy volunteers
Authors: Brunner M. , Greinwald R. , Kletter K. , Kvaternik H. , Corrado M. E. , Eichler H. G. , Müller M. 
Published: December 2004

SummaryBackground : Mesalazine (5‐aminosalicylic acid)‐containing formulations, designed to optimize drug delivery to the ileo‐caecal region, represent a cornerstone in the treatment of inflammatory bowel diseases.Aim : To test, by means of pharmaco‐scintigraphy, whether novel mesalazine‐containing pellets release 5‐aminosalicylic acid in the same target region as mesalazine tablets (Salofalk).Methods : Fourteen healthy male volunteers received a single dose of either pellets or tablets containing 500 mg of mesalazine and 2 mg of 152Sm2O3 with a 1‐week washout period. The gastrointestinal transit of 153Sm, incorporated into the formulations, was followed by gamma‐scintigraphy. Mesalazine release was verified by assessing 5‐aminosalicylic acid plasma pharmacokinetics.Results : The formulations reached the ileo‐caecal target region almost at the same time (3.3 ± 1 and 3.8 ± 1 h for pellets and tablets, respectively). Plasma 5‐aminosalicylic acid tmax values were comparable and corresponded to the time during which the formulations were located in the target region. Plasma AUC values were significantly lower for pellets, which might be explained by a more prolonged release of 5‐aminosalicylic acid.Conclusions : Novel mesalazine pellets and Salofalk tablets release active 5‐aminosalicylic acid in the same target region and pass through the gastrointestinal tract under fasting conditions in healthy volunteers in a comparable time. From a comparison of in vitro dissolution and plasma concentration data, a slower and more prolonged release of 5‐aminosalicylic acid from pellets is suggested.
Rabeprazole is superior to omeprazole for the inhibition of peptone meal‐stimulated gastric acid secretion in Helicobacter pylori‐negative subjects
Authors: Ohning G. V. , Walsh J. H. , Pisegna J. R. , Murthy A. , Barth J. , Kovacs T. O. G. 
Published: December 2004

SummaryBackground: Peptone meal‐stimulated gastric acid output is considered to be a reliable means to evaluate drug‐mediated inhibition of stimulated gastric acid output, an important measure of the efficacy of the agents — such as proton pump inhibitors — used to treat acid‐related disorders.Aim: To compare the initial and overall inhibitory effects on peptone meal‐stimulated gastric acid secretion of rabeprazole and omeprazole, 20 mg, in Helicobacter pylori‐negative subjects on the first and eighth days of treatment.Methods: Healthy volunteers (n = 27) were randomized in a single‐centre, double‐blind, double‐dummy, 2 × 2 cross‐over study. Subjects received an oral dose of rabeprazole or omeprazole, 20 mg once daily, for 8 days. After a 2–4‐week washout period, subjects were crossed over to receive the other medication for 8 days. Peptone meal‐stimulated gastric acid secretion was measured at hours 11 and 23 at baseline and on days 1 and 8 of treatment.Results: On days 1 and 8, rabeprazole demonstrated a significantly greater inhibition of peptone meal‐stimulated gastric acid secretion compared with omeprazole at all time points (P < 0.03). Median values of steady‐state inhibition on day 1 were statistically significant at hour 23 (rabeprazole 100% vs. omeprazole 74%, P < 0.02).Conclusions: Rabeprazole, 20 mg, demonstrated superior control of peptone meal‐stimulated gastric acid secretion compared with omeprazole, 20 mg, after the first dose and after the eighth daily dose. Rabeprazole achieved a more rapid onset of acid inhibition and a greater steady‐state reduction in peptone meal‐stimulated gastric acid secretion.
Efficacy of artichoke leaf extract in the treatment of patients with functional dyspepsia: a six‐week placebo‐controlled, double‐blind, multicentre trial
Authors: Holtmann G. , Adam B. , Haag S. , Collet W. , Grünewald E. , Windeck T. 
Published: December 2004

SummaryBackground : This study aimed to assess the efficacy of artichoke leaf extract (ALE) in the treatment of patients with functional dyspepsia (FD).Methods : In a double‐blind, randomized controlled trial (RCT), 247 patients with functional dyspepsia were recruited and treated with either a commercial ALE preparation (2 × 320 mg plant extract t.d.s.) or a placebo. The primary efficacy variable was the sum score of the patient's weekly rating of the overall change in dyspeptic symptoms (four‐point scale). Secondary variables were the scores of each dyspeptic symptom and the quality of life (QOL) as assessed by the Nepean Dyspepsia Index (NDI).Results : Two hundred and forty‐seven patients were enrolled, and data from 244 patients (129 active treatment, 115 placebo) were suitable for inclusion in the statistical analysis (intention‐to‐treat). The overall symptom improvement over the 6 weeks of treatment was significantly greater with ALE than with the placebo (8.3 ± 4.6, vs. 6.7 ± 4.8, P < 0.01). Similarly, patients treated with ALE showed significantly greater improvement in the global quality‐of‐life scores (NDI) compared with the placebo‐treated patients (− 41.1 ± 47.6 vs. − 24.8 ± 35.6, P < 0.01).Conclusion : The ALE preparation tested was significantly better than the placebo in alleviating symptoms and improving the disease‐specific quality of life in patients with functional dyspepsia.
Adherence to proton pump inhibitors or H2‐receptor antagonists during the use of non‐steroidal anti‐inflammatory drugs
Authors: Sturkenboom M. C. J. M. , Burke T. A. , Tangelder M. J. D. , Dieleman J. P. , Walton S. , Goldstein J. L. 
Published: December 2004

SummaryBackground : The efficacy of proton pump inhibitors (PPIs) or histamine‐2 receptor antagonists (H2RAs) prescribed as prophylaxis for NSAID‐related upper gastrointestinal (UGI) toxicity is dependent upon patient adherence.Aim : To describe patient adherence to prophylactically prescribed PPIs and H2RAs in the clinical setting.Methods : We conducted a retrospective observational cohort study using the Integrated Primary Care Information Project database. The study population consisted of incident non‐specific NSAID users prescribed a PPI or H2RA specifically as prophylaxis for NSAID‐related UGI toxicity. Patients were classified as non‐adherent if < 75% of days of NSAID use were covered by one of these agents, and as continuing users after discontinuation of NSAID use if they had a renewed prescription for these agents after their last NSAID prescription.Results : The study cohort comprised 784 patients: 374 with H2RAs, 405 with PPIs, and 5 with both PPI and H2RA. Eighty‐five percent of H2RA users and 7% of PPI users were prescribed these drugs at doses below the minimum recommended/effective dose for NSAID‐associated gastroduodenal ulcer prophylaxis. Thirty‐seven percent of patients were non‐adherent. The lowest rate of non‐adherence was associated with the first NSAID prescription (9%), increasing to 61% for patients with 3 prescriptions. In a cohort of subjects who stopped their NSAID and were followed for up to 2 years (n = 711), there was significant persistent use of acid suppressive agents; 40% of patients had at least one additional prescription for the acid suppressive agent after stopping NSAIDs, and> 30% received enough drug to cover a period longer than 2 months after stopping their NSAID.Conclusions : The pattern of PPI and H2RA prescriptions, when prescribed as prophylactic strategy, does not correspond with the pattern of NSAID use. Physicians should consider the medical impact of non‐adherence with dual therapies and the impact of prolonged use of GPAs on treatment cost.
A pilot study to investigate the use of oxpentifylline (pentoxifylline) and thalidomide in portal hypertension secondary to alcoholic cirrhosis
Authors: Austin A. S. , Mahida Y. R. , Clarke D. , Ryder S. D. , Freeman J. G. 
Published: December 2004

SummaryBackground : Tumour necrosis factor‐α is thought to be important in the pathogenesis of portal hypertension. Oxpentifylline (pentoxifylline) and thalidomide inhibit endotoxin‐induced tumour necrosis factor‐α production in vitro.Aims : To assess the toxicity of oxpentifylline (pentoxifylline) and thalidomide in cirrhosis and their effect on the hepatic venous pressure gradient and tumour necrosis factor‐α production.Methods : In an open‐label pilot study, 20 abstinent patients with stable alcoholic cirrhosis and oesophageal varices were recruited; 12 patients completed haemodynamic measurements before and after treatment with oxpentifylline (pentoxifylline) 1800 mg (n = 6) or thalidomide 200 mg (n = 6) daily for 2 weeks. Tumour necrosis factor‐α production was assessed in ex vivo monocyte cultures stimulated with endotoxin.Results : Thalidomide reduced the hepatic venous pressure gradient from 19.7 mmHg (9.3–23.5 mmHg) to 12.2 mmHg (4.7–19.5 mmHg) (P = 0.03) without reducing the hepatic blood flow or altering systemic haemodynamic parameters. Thalidomide reduced ex vivo tumour necrosis factor‐α production by approximately 50%. Oxpentifylline (pentoxifylline) had no significant effect on any of the parameters measured. Side‐effects led to dose reduction or treatment withdrawal in 40% of patients.Conclusion : Thalidomide, but not oxpentifylline (pentoxifylline), reduces the hepatic venous pressure gradient in stable alcoholic cirrhotics, an effect that may be mediated by the inhibition of tumour necrosis factor‐α production. The role of tumour necrosis factor‐α inhibitory drugs in the therapy of portal hypertension should be investigated in a randomized controlled trial.
Current management of chronic hepatitis B
Authors: Papatheodoridis G. V. , Hadziyannis S. J. 
Published: December 2004

SummaryChronic hepatitis B can be diagnosed in patients with increased aminotransferases, hepatitis B virus viraemia and necroinflammation with fibrosis on liver biopsy. Although, ideally, all patients with chronic hepatitis B should be treated, therapeutic intervention is currently recommended for cases with a relatively satisfactory likelihood of response and/or advanced disease. A realistic therapeutic approach aims to sustain hepatitis B e antigen (HBeAg) loss and hepatitis B e antibody (anti‐HBe) seroconversion in HBeAg‐positive chronic hepatitis B and to sustain biochemical and virological remission in HBeAg‐negative chronic hepatitis B. Currently, three drugs are licensed for chronic hepatitis B: interferon‐alpha, lamivudine and adefovir dipivoxil. In patients with HBeAg‐positive chronic hepatitis B, all of these drugs achieve HBeAg loss (24–33%) and anti‐HBe seroconversion (12–30%) rates significantly superior to those observed in untreated placebo controls. In patients with HBeAg‐negative chronic hepatitis B, the sustained off‐therapy response rate is 20–25% after a ≥ 12‐month course of interferon‐alpha and minimal (< 10%), if any, after a 12‐month course of lamivudine or adefovir. Long‐term lamivudine induces an initial response in 70–90% of patients, but only 30–40% of patients remain in remission after the third year due to progressively increasing viral resistance. Long‐term adefovir achieves a response in approximately 70% of patients at 12 months, which is maintained at 24 months with rare (< 2%) drug resistance. Adefovir is also effective against lamivudine‐resistant strains. Many other anti‐viral agents, immunomodulatory approaches and combination therapies are currently being evaluated in chronic hepatitis B.
Atrophic gastritis as a cause of hyperhomocysteinaemia
Authors: Santarelli L. , Gabrielli M. , Cremonini F. , Santoliquido A. , Candelli M. , Nista E. C. , Pola P. , Gasbarrini G. , Gasbarrini A. 
Published: December 2004

SummaryBackground : Hyperhomocysteinaemia is an independent risk factor for atherosclerosis. It is often related to low levels of vitamin B12 and/or folate, enzymatic co‐factors of methionine metabolism. Atrophic gastritis, often caused by Helicobacter pylori infection, may impair vitamin absorption.Aim : To assess whether the presence of atrophic gastritis is associated with hyperhomocysteinaemia via deficiency of its vitamin co‐factors.Methods : Thirty‐one patients with atrophic gastritis were recruited. The control group consisted of 28 patients with non‐atrophic gastritis, matched with patients for sex, age and body mass index. The presence and degree of gastric atrophy were assessed by histology. H. pylori infection was assessed by histology/serology. Blood samples were collected for the measurement of homocysteine, vitamin B12 and folates.Results : Multiple logistic regression analysis showed that atrophic gastritis (odds ratio, 5.3; 95% confidence interval, 1.23–25.26; χ2 = 5.2; P = 0.01) and low vitamin B12 (odds ratio, 3.7; 95% confidence interval, 1.03–22.08; χ2 = 3.6; P < 0.05) were both predictors of hyperhomocysteinaemia. None of the other variables considered in the analysis, including H. pylori status, showed a significant association with hyperhomocysteinaemia.Conclusions : The present study suggests that atrophic gastritis, rather than H. pylori infection per se, may be a contributing factor to hyperhomocysteinaemia, possibly via vitamin B12 malabsorption.
Lipase inhibition by orlistat: effects on gall‐bladder kinetics and cholecystokinin release in obesity
Authors: Mathus‐Vliegen E. M. H. , Van Ierland‐Van Leeuwen M. L. , Terpstra A. 
Published: December 2004

SummaryBackground : Obese subjects are at risk of developing gallstones as a result of the obese state and during weight reduction.Aim : To study whether orlistat, by lipase inhibition, impairs gall‐bladder emptying, thus further predisposing weight‐losing obese subjects to gallstone formation.Methods : Patients entering a randomized clinical trial of 1 month of diet, followed by treatment with placebo, 3 × 60 mg orlistat or 3 × 120 mg orlistat, underwent gall‐bladder emptying studies measured by ultrasound. Meal‐induced cholecystokinin release and gall‐bladder emptying were investigated at the start, at randomization and after 1 and 12 months.Results : One month of dieting did not change gall‐bladder emptying and cholecystokinin release. After 1 month, placebo treatment resulted in a decreased fasting volume of 11%, compared with increases of 26% and 47% with 60 and 120 mg orlistat, respectively. Gall‐bladder emptying increased by 9% with placebo and decreased by 15% and 53% with 60 and 120 mg orlistat, respectively. Fasting cholecystokinin values and cholecystokinin release decreased significantly in the orlistat group. After 1 year, a persistent but attenuated effect of orlistat on gall‐bladder emptying and cholecystokinin release remained. Three of 40 patients developed gallstones, two on placebo with major weight loss and one on 60 mg orlistat.Conclusions : One month of lipase inhibition by orlistat significantly impaired gall‐bladder motility, which persisted to some extent after 1 year. Obese subjects with diabetes or hyperlipidaemia, who are more at risk of gallstones, should be followed carefully.