bluuebunny/crossref_metadata_2025_split huggingface dataset:
A randomized trial of polyurethane and silicone percutaneous endoscopic gastrostomy catheters
Authors: Van Den Hazel S. J. , Mulder C. J. J. , Den Hartog G. , Thies J. E. , Westhof W. 
Published: March 2003

Background:No data are available on differences in complication rate and long‐term functioning between polyurethane and silicone percutaneous endoscopic gastrostomy (PEG) catheters.Methods:We randomized patients who qualified for PEG placement to receive either a polyurethane or silicone PEG catheter. Patients were prospectively monitored for 28 days after placement for the occurrence of complications. Data on long‐term PEG survival were obtained retrospectively from the Hospital and general practitioner’s medical records.Results:One hundred and six patients were randomized (polyurethane 50, silicone 56). During the first four weeks of follow‐up, major complications occurred twice with both polyurethane and silicone PEGs (relative risk 1.1, 95% confidence interval: 0.11–11). Overall complications occurred four times with polyurethane and 17 times with silicone PEGs (relative risk 3.8, 95% confidence interval: 1.37–10.5). Long‐term follow‐up was available in 96 patients. Seven polyurethane PEGs and 10 silicone PEGs were removed because of PEG malfunctioning, the remainder functioned well until death or the reinstitution of oral feeding. The median complication‐free survival was 916 days for the polyurethane PEG and 354 days for the silicone PEG (Log rank test: P=0.24).Conclusion:Polyurethane PEG catheters were associated with less short‐term complications than silicone catheters, but major complications and long‐term function were comparable.
Serum transforming growth factor‐β1 levels increase in response to successful anti‐inflammatory therapy in ulcerative colitis
Authors: Sambuelli A. , Diez R. A. , Sugai E. , Boerr L. , Negreira S. , Gil A. , Camartino G. , Huernos S. , Doldán I. , Felstiner D. , Bai J. C. 
Published: March 2003

Objective:To investigate serum levels of transforming growth factor‐β1 and interferon‐γ in active ulcerative colitis and to assess changes during treatment.Methods:We prospectively evaluated serum from 25 patients with untreated active ulcerative colitis and 19 healthy controls. Disease activity score (DAI), serum transforming growth factor‐β1 and interferon‐γ levels were measured at baseline and after 7 days of conventional treatment. Disease activity score and transforming growth factor‐β1 were also assessed at 42 days.Results:Baseline transforming growth factor‐β1 levels were significantly higher in patients than in controls (P < 0.02). On the 7th day, transforming growth factor‐β1 levels increased only in patients who responded (P < 0.01); variations in transforming growth factor‐β1 levels and disease activity score were inversely correlated (r=– 0.72, P < 0.001). At day 42, serum transforming growth factor‐β1 decreased significantly compared with the 7th day (P < 0.05). While in controls, interferon‐γ was undetectable; untreated patients had higher, widely variable, levels. At day 7, responders had higher interferon‐γ values than unresponsive cases. Variations in interferon‐γ correlated moderately with changes in transforming growth factor‐β1 (r=0.53, P < 0.05). Cytokine response did not depend upon the type of treatment.Conclusions:Both transforming growth factor‐β1 and interferon‐γ may play a role in the injury–repair process in active ulcerative colitis. Variations in circulating transforming growth factor‐β1 levels in the first week of treatment seem to be related to the therapeutic response.
A lyophilized and inactivated culture of Lactobacillus acidophilus increases Helicobacter pylori eradication rates
Authors: Canducci F. , Armuzzi A. , Cremonini F. , Cammarota G. , Bartolozzi F. , Pola P. , Gasbarrini G. , Gasbarrini A. 
Published: March 2003

Background:Acid suppression plus two antibiotics is considered the reference anti‐Helicobacter pylori treatment. Reported eradication rates are around 65–80%. Human Lactobacillus acidophilus shows an in vitro inhibitory effect on the attachment of H. pylori to gastric epithelial cell lines. Culture supernatant of this bacillus seems to decrease the in vitro viability of H. pylori.Aim:To evaluate whether the supplementation with an inactivated preparation of L. acidophilus could improve the efficacy of a standard anti‐H. pylori therapy.Methods:One‐hundred and twenty H. pylori‐positive patients were randomly assigned to a 7‐day triple therapy based on rabeprazole (20 mg b.d.), clarithromycin (250 mg t.d.s.) and amoxicillin (500 mg t.d.s.) (RCA group: 60 subjects), or to the same regimen supplemented with a lyophilized and inactivated culture of Lactobacillus acidophilus (t.d.s.) (RCAL group: 60 subjects).Results:In the RCA group, eradication was successful in 72% (42 out of 58 patients) from a per protocol (PP) analysis, or 70% (42 out of 60 patients) using an intention‐to treat (ITT) analysis. In the RCAL group a significant increase in the eradication rate was observed: 88% (52 out of 59 patients) from PP analysis (P=0.03), 87% (52 out of 60 patients) from ITT analysis (P=0.02).Conclusions:These results seem to confirm the in vitro anti‐H. pylori effect of L. acidophilus, suggesting that the inactivated L. acidophilus could be effective in increasing eradication rates of a standard anti‐H. pylori therapy.
One‐week triple therapy with esomeprazole provides effective eradication of Helicobacter pylori in duodenal ulcer disease
Authors: Veldhuyzen Van Zanten S. , Lauritsen K. , Delchier J.‐C. , Labenz J. , De Argila C. M. , Lind T. , Treichel H.‐C. , Stubberöd A. , Cockeram A. , Hasselgren G. , Göthe L. , Wrangstadh M. , Sinclair P. 
Published: March 2003

Background:Esomeprazole is the first proton pump inhibitor to be developed as an optical isomer for the treatment of acid‐related diseases.Methods:Four hundred and forty eight duodenal ulcer patients with Helicobacter pylori infection, confirmed by 13C‐urea breath test (UBT), and no current ulcer, were randomised to double‐blind treatment with esomeprazole 20 mg twice daily (b.d.) (n=224) or omeprazole 20 mg b.d. (n=224), in combination with amoxicillin 1 g b.d. and clarithromycin 500 mg b.d. for 1 week (EAC and OAC, respectively). A negative UBT at both 4 and 8 weeks after completing therapy indicated successful H. pylori eradication.Results:Intention‐to‐treat (ITT) analysis comprised 400 patients (EAC, n=204; OAC, n=196) and per protocol (PP) analysis 377 patients (EAC, n=192; OAC, n=185). Eradication rates (95% confidence intervals) for ITT and PP populations were: EAC, 90% (85–94%) and 91% (86–94%); OAC, 88% (82–92%) and 91% (86–95%). Between‐group differences in eradication rates were not statistically significant. Both regimens were well tolerated, with an adverse event profile and frequency typical of proton pump inhibitor plus antibiotic combination therapy.Conclusions:Esomeprazole‐based triple therapy for 1 week is highly effective in eradicating H. pylori infection in duodenal ulcer disease, offers comparable efficacy to omeprazole‐based therapy, and is well tolerated.
Effect of activin on cell growth in primary cultures of guinea pig gastric epithelial cells
Authors: Ogihara S. , Kudo T. , Yamada M. , Seki T. , Kawaguchi M. , Saito T. 
Published: March 2003

Summary Background: The effect of activin on differentiated cells is known to be different from that on undifferentiated cells. Cultured gastric epithelial cells in complete serum‐free conditions grew into matured mucous cells after treatment with epidermal growth factor (EGF). Aim: To elucidate the effect of activin on the growth of differentiated and undifferentiated gastric mucosal cells. Methods: Cultured guinea pig gastric epithelial cells were prepared using the method of Ogihara et al.
1Synthesis of activin was analysed by Western blot using monoclonal anti‐activin A antibody. Cell proliferation was assessed by counting the number of cells. Mucin production was assessed by histochemical study using periodic acid‐Schiff (PAS) reaction. Results: Western blot analysis indicated that activin was synthesized in cultured guinea pig gastric mucosal cells. One hundred nanomolar EGF induced a 3‐fold increase in cell count and the appearance of PAS‐positive granules. Five nanograms activin per millilitre without EGF stimulated proliferation of the cells that showed almost negative PAS staining. When activin was added after treatment with 100 n
m EGF for 24 h, cell proliferation induced by EGF was inhibited by activin at concentrations higher than 5 ng/mL. Conclusion: These results suggest that activin stimulates proliferation of undifferentiated cells and inhibits growth of differentiated cells.
Helicobacter pylori and NSAID gastropathy
Authors: Lazzaroni M. , Bianchi porro G. 
Published: March 2003

Non‐steroidal anti‐inflammatory drugs (NSAIDs) and Helicobacter pylori are known to share a number of pathogenic mechanisms, but there is no evidence to show a significant synergic action between the two risk factors. Studies assessing this subject have differed in almost every aspect of their methodology, including the definition of a NSAID user as well as the types, doses, duration and their indications for NSAID use. They also differed in their end‐points, the definition of dyspepsia and the regimes used for eradication of H. pylori. However, some conclusions may be drawn from the results of clinical trials.In H. pylori‐positive patients without mucosal lesions, NSAIDs may aggravate dyspeptic symptoms but, with the exception of elderly patients, they do not present a definite major risk of gastric and duodenal lesions and, above all, of ulcer‐correlated complications.So what recommendations can be made with regard to H. pylori eradication in patients requiring treatment with NSAIDs? The microorganism and the anti‐inflammatory drugs are undoubtely independent causes of gastric and duodenal damage. Patients taking NSAIDs who are found to have gastric or duodenal ulcers should therefore be tested for the bacterium and specifically treated, since H. pylori and NSAID‐induced ulcers may be macroscopically indistinguishable.Whether asymptomatic patients taking NSAIDs should be tested and treated for H. pylori infection is still a matter of debate.
Review article: should we kill or should we save Helicobacter pylori?
Authors: Hunt R.H. , Sumanac K. , Huang J.‐Q. 
Published: March 2003

Results from epidemiological studies and therapeutic clinical trials have shown that Helicobacter pylori infection causes acute and chronic active gastritis and is the initiating factor for the majority of peptic ulcer disease. Eradication of the infection with antibiotics resolves gastritis and restores normal gastric physiology, accelerates healing of peptic ulcer disease, and virtually eliminates recurrence of duodenal ulcer disease.The infection also plays an important role in the initiation and/or progression of gastric atrophy and intestinal metaplasia, which may eventually lead to the development of distal gastric cancer. Furthermore, almost all patients with gastric MALT lymphoma are infected with H. pylori and cure of the infection leads to histological regression of the tumor and maintains the regression in over 80% of patients during long‐term follow‐up.Preliminary uncontrolled data from Japan show that eradication of the infection significantly reduced metachronous intestinal‐type gastric cancer following initial endoscopic resection of early gastric cancer and might also prevent the progression of gastric adenoma to gastric dysplasia or gastric cancer.Although this overwhelming evidence has demonstrated that H. pylori infection is bad for humans, some have questioned the wisdom of eradicating the infection in all those infected. Their arguments are largely based on hypothesis and circumstantial evidence: 1) Less than 20% of all H. pylori infected persons will develop significant clinical consequences in their lifetime. 2) H. pylori strains are highly diverse at a genetic level and are of different virulence. 3) The antiquity of H. pylori infection in humans and their co‐evolution suggests that H. pylori may be a commensal to humans. Eradication of H. pylori may remove some beneficial bacterial strains and may provoke esophageal disease or gastric cancer at the cardia.However, careful review of the literature confirms that H. pylori infection is a serious pathogen albeit in a minority of those infected. It remains for carefully designed prospective studies, rather than hypothesis to make changes in the current consensus position.
Post‐treatment diagnostic accuracy of a new enzyme immunoassay to detect Helicobacter pylori in stools
Authors: Costa F. , Mumolo M. G. , Bellini M. , Romano M. R. , Manghetti M. , Paci A. , Maltinti G. , Marchi S. 
Published: March 2003

Background: Helicobacter pylori has attracted increasing attention among gastroenterologists because of its pathogenic potential, stimulating the search for non‐invasive diagnostic tests.Aims:In this study the efficacy of a new enzyme immunoassay designed to detect H. pylori antigens in stools (HpSA) was evaluated before and after eradication therapy.Methods:HpSA was performed on stool samples collected from 268 patients whose H. pylori status was defined on the basis of concordant results for the 13C‐urea breath test, rapid urease test and histology. The H. pylori‐positive patients were treated with a 1‐week triple therapy to eradicate the infection. One (T30) and 3 months (T90) after the end of therapy, 13C‐urea breath test and HpSA were repeated in the treated patients.Results:The overall diagnostic accuracy of HpSA at T30 (83%, 95% confidence interval (CI) 77–89%) was significantly lower in comparison to the values obtained at baseline (94%, 95% CI: 91–97%) and at T90 (97%, 95% CI: 94–99%). No significant difference was found between the diagnostic accuracy of HpSA at baseline and at T90 (P=0.253).Conclusions:The present data suggest that HpSA provides a low diagnostic accuracy when used shortly after treatment. It needs a longer period of follow‐up (8–12 weeks) to reach a reliability comparable to the 13C‐urea breath test.
The prevention of colorectal cancer
Authors: Dove‐Edwin I. , Thomas H. J. W. 
Published: March 2003

Colorectal cancer is a leading cause of cancer mortality in the industrialized world. Survival remains poor because most cases are diagnosed at an advanced stage. It is a preventable disease as colorectal cancers usually develop slowly from an identifiable precursor lesion, the adenoma.The existing strategies for colorectal cancer prevention include dietary prevention, chemoprevention and endoscopic intervention. The exact relationship between diet, particularly fibre, and colorectal cancer remains unclear, with the most recent studies suggesting that dietary fibre may not decrease colorectal cancer risk as previously thought.Non‐steroidal anti‐inflammatory drugs have been shown to have a protective effect against colorectal cancer, but the adverse effect profile of the non COX‐2 selective drugs, particularly the risk of gastrointestinal haemorrhage, precludes their widespread use.There is increasing evidence that colorectal cancer incidence and mortality can be decreased from endoscopic polypectomy and early detection of cancer. Faecal occult blood testing in the general population (‘average‐risk’) has been shown in randomized trials to decrease mortality from colorectal cancer by 15–33%. Long‐term results of randomized trials of the effectiveness of flexible sigmoidoscopy and colonoscopy screening in the general population are awaited.Targeting high risk individuals may also be an effective and efficient way to decrease the colorectal cancer burden. As many as 15–30% of colorectal cases may be due to hereditary factors. Individuals with one or two direct relatives affected are at moderate risk for colorectal cancer (empirical lifetime mortality from colorectal cancer approximately 10%) and approximately 2–3% of cases arise in individuals harbouring highly penetrant autosomal dominant mutations, which puts them at high‐risk for colorectal cancer. Surveillance colonoscopy is offered to individuals at moderate and high risk for colorectal cancer.
Effect of an enteric‐release formulation of naloxone on intestinal transit in volunteers taking codeine
Authors: Hawkes N. D. , Richardson C. , Evans B. K. , Rhodes J. , Lewis S. J. , Thomas G. A. O. 
Published: March 2003

Introduction:Constipation is a common side‐effect of opioid therapy; in addition to their analgesic effect, opioids reduce intestinal secretion and motility with an increase in whole‐gut transit time. Naloxone, a specific opioid antagonist, reverses these effects but may also cause symptoms of opioid withdrawal in patients on long‐term therapy.Aim:To use an enteric‐release formulation, designed to produce a topical effect in the gut, with minimum systemic effects.Methods:Naloxone 10 mg b.d. and codeine 30 mg b.d. were used with identical placebo capsules in four sets of studies; 12 male volunteers were given the drugs alone and in combination, with a control study involving double placebo, during each of four study periods. Whole‐gut transit time was calculated and compared for each treatment period.Results:Naloxone, both alone and with codeine, significantly shortened the mean whole‐gut transit time compared with the control period, respectively, from 53.1 to 42.1 h (P=0.005) and to 40.7 h (P=0.024). Urgency to defecate was reported by two volunteers on naloxone alone and by three on combination therapy.Conclusions:The results show that the naloxone formulation counteracts the effect of codeine on intestinal transit, suggesting that it may have useful clinical applications.
Fish oil (Eicosapen) is less effective than metronidazole, in combination with pantoprazole and clarithromycin, for Helicobacter pylori eradication
Authors: Meier R. , Wettstein A. , Drewe J. , Geiser H. R. ,   THE SWISS HELICOBACTER‐STUDY GROUP
Published: March 2003

Background: In vitroω‐3‐fatty acids (Eicosapen) are bacteriostatic to Helicobacter pylori and have a variety of immuno‐modulating effects.Aim:To investigate the efficacy and tolerability of eicosapen (E) as an antibiotic‐sparing component of a triple H. pylori eradication regimen in non‐ulcer dyspepsia patients in a randomized, double‐blind trial.Methods:Non‐ulcer dyspepsia patients (n=199), with a normal upper endoscopy and a positive 13C‐urea breath test (UBT) were randomly assigned to either pantoprazole, clarithromycin and metronidazole (PCM) or pantoprazole, clarithromycin and eicosapen (PCE) for 7 days. Four weeks after treatment, H. pylori eradication was determined by UBT. Symptoms were followed up to 16 months.Results:In the intention‐to‐treat population, PCM eradicated infection in 78% but PCE was successful in only 34% (P < 0.001). Symptomatic improvement occurred in both groups, and was not related to H. pylori eradication.Conclusion:Eicosapen is unlikely to be useful in H. pylori eradication regimens.
The pharmacology of the internal anal sphincter and new treatments of ano‐rectal disorders
Authors: Cook T. A. , Brading A. F. , Mortensen N. J. McC. 
Published: March 2003

Surgical options for faecal incontinence in the presence of intact sphincters are limited. Furthermore, in patients with fissures, lateral sphincterotomy reduces anal sphincter hypertonia but there has been concern about complications. A greater understanding of the basic pharmacology of the internal anal sphincter has led to the development of novel treatments for both these disorders. A Medline review was undertaken for internal anal sphincter pharmacology, anal fissures and faecal incontinence. This review is based on these articles and those found by further cross‐referencing.  Nitric oxide released from non‐adrenergic non‐cholinergic nerves is the main inhibitory agent in the internal anal sphincter. Relaxations are also mediated through β‐adrenoceptors and muscarinic receptors. Stimulation of α‐receptors results in contraction. Calcium and its entry through L‐type calcium channels is important for the maintenance of tone. Nitric oxide donors produce reductions in resting anal tone and heal fissures but are associated with side‐effects. Muscarinic agents and calcium channel antagonists show promise as low side‐effect alternatives. Botulinum toxin appears more efficacious than other agents in healing fissures. To date, α‐receptor agonists have been disappointing at improving incontinence.Further understanding of the pharmacology of the internal anal sphincter may permit the development of new agents to selectively target the tissue with greater efficacy and fewer side‐effects.
Abnormal bone turnover in long‐standing Crohn’s disease in remission
Authors: Schoon E. J. , Geerling B. G. , Van Dooren I. M. A. , Schurgers L. J. , Vermeer C. , Brummer R.‐J. M. , Stockbrügger R. W. 
Published: March 2003

Background:A high prevalence of osteoporosis is found in patients with Crohn’s disease. The pathogenesis of this condition seems to be multifactorial and its pathophysiology is still not completely understood.Aim:To elucidate the pathophysiology of osteopenia in quiescent Crohn’s disease.Methods:Bone turnover was studied in 26 patients (13 males and 13 females) with long‐standing quiescent Crohn’s disease and small bowel involvement. Bone mineral density was assessed by dual energy X‐ray absorptiometry. Biochemical markers for bone formation (osteocalcin and bone‐specific alkaline phosphatase) and for bone resorption (deoxypyridinoline and collagen type I C‐terminal crosslinks) were measured. Urinary calcium excretion was determined.Results:Markers for bone formation were significantly lower in patients than in controls (osteocalcin: P= 0.027, bone‐specific alkaline phosphatase: P < 0.001), but both bone resorption markers were not significantly different. Urine calcium excretion was significantly decreased in patients (P=0.002) compared to controls. Bone mineral density of the lumbar spine was significantly and inversely correlated with bone‐specific alkaline phosphatase and collagen type I C‐terminal crosslinks.Conclusions:Bone turnover in long‐standing Crohn’s disease in clinical remission is characterized by suppressed bone formation and normal bone resorption. Urine calcium excretion is decreased. Hence, interventions and therapy should be directed towards the improvement of bone formation.
Ranitidine bismuth citrate‐based triple therapies after failure of the standard ‘Maastricht triple therapy’: a promising alternative to the quadruple therapy?
Authors: Perri F. , Villani M. R. , Quitadamo M. , Annese V. , Niro G. A. , Andriulli A. 
Published: March 2003

Background:Triple therapy with proton pump inhibitor, clarythromycin, and amoxicillin has been proposed in Maastricht as the first‐line treatment of H. pylori infection.Aim:To determine whether ranitidine bismuth citrate (RBC) based regimens may be used as second‐line treatments after ‘Maastricht therapy’ failure.Methods:A total of 285 patients with H. pylori infection were given a 7‐day treatment with pantoprazole 40 mg b.d., clarythromycin 500 mg b.d., and amoxicillin 1 g b.d. Patients who were still infected were randomly given one of the following 14‐day treatments: RBC 400 mg b.d. plus amoxicillin 1 g b.d. and tinidazole 500 mg b.d. (RAT group), RBC 400 mg b.d. plus amoxicillin 1 g b.d. and clarythromycin 500 mg b.d. (RAC group), and RBC 400 mg b.d. plus clarythromycin 500 mg b.d. and tinidazole 500 mg b.d. (RCT group).Results:The ‘Maastricht therapy’ achieved an eradication rate of 59% (95% CI: 54–65) on intention‐to‐treat analysis. The RAT, RAC, and RCT regimens achieved eradication rates of 81% (95% CI: 67–94), 43% (95% CI: 26–60), and 62% (95% CI: 44–80), respectively, on intention‐to‐treat analysis. Patient compliance was optimal in RAT and RAC groups.Conclusion:RBC plus tinidazole and either amoxicillin or clarythromycin can be used as second‐line therapies after failure of the Maastricht triple therapy.