bluuebunny/crossref_metadata_2025_split huggingface dataset:
Impact on the composition of the faecal flora by a new probiotic preparation: preliminary data on maintenance treatment of patients with ulcerative colitis
Authors: Venturi  , Gionchetti  , Rizzello  , Johansson  , Zucconi  , Brigidi  , Matteuzzi  , Campieri  
Published: March 2003

Background: Although 5‐aminosalicylic acid (5‐ASA) oral compounds are the standard maintenance treatment for ulcerative colitis in remission, some patients cannot use them because of side‐effects. Clinical and experimental observations have suggested the potential role of probiotics in inflammatory bowel disease therapy.Aim: To evaluate the effects on intestinal microflora and the clinical efficacy of a new probiotic preparation in patients with ulcerative colitis in remission.Patients and methods: Twenty patients with ulcerative colitis, intolerant or allergic to 5‐ASA, have been treated with a new probiotic preparation (VSL # 3, CSL, Milan, Italy) containing 5 × 1011 cells/g of 3 strains of bifidobacteria, 4 strains of lactobacilli and 1 strain of Streptococcus salivarius ssp. thermophilus. Two doses of 3 g were administered o.d. for 12 months. Faecal samples for stool culture were obtained from the patients at the beginning of the trial and after 10, 20, 40, 60, 75, 90 days, 12 months and at 15 days after the end of the treatment. The following bacterial groups have been evaluated in the faeces: total aerobic and anaerobic bacteria, enterococci, Streptococcus thermophilus, lactobacilli, bifidobacteria, Bacteroides, clostridia, coliforms. Patients were assessed clinically every two months, and assessed endoscopically at 6 and 12 months or in relapse.Results: Faecal concentrations of Streptococcus salivarius ssp. thermophilus, lactobacilli and bifidobacteria increased significantly in all patients, compared to their basal level, from the 20th day of treatment (P < 0.05) and remained stable throughout the study. Concentrations of Bacteroides, clostridia, coliforms, total aerobic and anaerobic bacteria did not change significantly during treatment (P = N.S.). Fifteen of 20 treated patients remained in remission during the study, one patient was lost to follow up, while the remaining relapsed. No significant side‐effects have been reported.Conclusions: These results show that this probiotic preparation is able to colonize the intestine, and suggest that it may be useful in maintaining the remission in ulcerative colitis patients intolerant or allergic to 5‐ASA. Controlled trials are warranted to confirm these preliminary results.
Seroprevalence of cytotoxin‐associated gene A positive Helicobacter pylori strains in Changle, an area with very high prevalence of gastric cancer in South China
Authors: Wong  , Lam  , Ching  , Hu  , Ong  , Chen  , Gao  , Chen  , Jiang  , Hou  , Lu  , Wang  , Ho  , Yuen  , Lai  , Kwok  , Hui  , Covacci  ,   THE CHINA GASTRIC CANCER STUDY GROUP
Published: March 2003

Background: Helicobacter pylori, especially the CagA‐positive strains, are closely associated with peptic ulcers and gastric cancers. We performed a large scale gastric cancer screening project and examined the prevalence of H. pylori and CagA‐positive strains in Changle, China, an area with one of the World’s highest gastric cancer mortality. We also compared the prevalence with that in Hong Kong which has one‐tenth of the gastric cancer mortality of that in Changle.Methods: A total of 2424 subjects in Changle and 523 subjects in Hong Kong had endoscopic examination and venesection. Sera were tested for anti‐H. pylori antibody and anti‐CagA antibody and correlated with endoscopic findings.Results: In Changle, 80.9% of the subjects were H. pylori carriers. Out of 551 carriers, 408 (74%) were positive for anti‐CagA antibody. A total of 76% and 87% of the asymptomatic and gastric cancer patients were positive for anti‐CagA antibody, respectively (P > 0.05). Compared to Hong Kong, there was a significantly (P < 0.0001) higher prevalence of CagA‐positive strains in asymptomatic subjects in Changle (76%) than in Hong Kong (28%), but not in peptic ulcers or gastric cancers.Conclusions: Subjects in Changle had a high prevalence of H. pylori infection and a high prevalence of the CagA‐positive strains. The contrast in the prevalence of CagA‐positive strains, in asymptomatic subjects in two areas with differing gastric cancer mortality, supports the pathogenic role of CagA‐positive strains in gastric carcinogenesis.
Invasive and non‐invasive tests for Helicobacter pylori infection
Authors: Vaira D. , Holton J. , Menegatti M. , Ricci C. , Gatta L. , Geminiani A. , Miglioli M. 
Published: March 2003

SummaryThere are two general ways in which a diagnosis of infection by Helicobacter pylori can be made: by using either an invasive or non‐invasive procedure. The invasive procedures involve an endoscopy and biopsy. A biopsy is essential because often the mucosa may appear macroscopically normal but nevertheless be inflamed. A biopsy is obtained by histological examination, culture, polymerase chain reaction or detection of the presence of urease activity in biopsy material.The non‐invasive tests that can be used to diagnose the infection are serology, detection of labelled metabolic products of urea hydrolysis in the breath (13CO2, 14CO2), the urine or the blood, and detection of H, pylori antigen in a stool specimen. At present no single test can be relied upon to detect definitely colonization by H. pylori, and a combination of two is recommended if this is feasible. The choice of the test to be used is not straightforward and may vary according to the clinical condition and local expertise.
Comparison of lansoprazole‐based triple and dual therapy for treatment of Helicobacter pylori‐related duodenal ulcer: an Asian multicentre double‐blind randomized placebo controlled study
Authors: Wong  , Xiao  , Hu  , Qian  , Huang  , Li  , Hu  ,   DALDIYONO, Manan  , Lesmana  , Carpio  , Perez  , Fock  , Kachintorn  , Phornphutkul  , Kullavanijaya  , Ho  , Lam  
Published: March 2003

Bakcground: In Asian countries with limited resources, clarithromycin‐based triple therapy may not be readily available. There are also few direct comparisons of different regimens in Asia.Aim: To compare two lansoprazole‐based non‐clarithromycin triple therapies and one dual therapy in a prospective double‐blind placebo‐controlled study of Helicobacter pylori eradication and duodenal ulcer healing.Methods: Fourteen centres in Asia participated in this study. Patients with acute duodenal ulcer who were H. pylori‐positive were recruited. They were randomized to receive: (a) lansoprazole 30 mg b.d., amoxycillin 1 g b.d. and metronidazole 500 mg b.d. for 2 weeks (LAM‐2 W), or (b) LAM for 1 week and placebo (LAM‐1 W), or (c) lansoprazole 30 mg b.d., amoxycillin 1 g b.d. and placebo for 2 weeks (LA‐2 W). Upper endoscopy was repeated at week 6 to check for duodenal ulcer healing. Symptoms and side‐effects were recorded.Results: A total of 228 patients were recruited, and two patients took less than 50% of the drugs. H. pylori eradication rates (intention‐to‐treat) were 68 out of 82 (83%) with LAM‐2 W, 55 out of 71 (78%) with LAM‐1 W and 43 out of 75 (57%) with LA‐2 W. There were significant differences (P=0.001) in eradication rates when comparing either LAM‐2 W or LAM‐1 W with LA‐2 W. The eradication rate in patients with metronidazole resistant H. pylori strains were significantly lower than those with metronidazole sensitive strains (P=0.0001). The duodenal ulcer healing rates at week 6 were 85%, 85% and 72% in LAM‐2 W, LAM‐1 W and LA‐2 W, respectively (P=0.065). Side‐effects occurred in 13%, 11% and 9% in LAM‐2 W, LAM‐1 W and LA‐2 W, respectively. H. pylori eradication and initial ulcer size were factors affecting duodenal ulcer healing.Conclusions: This Asian multicentre study showed that 1‐week lansoprazole‐based triple therapy without clarithromycin has similar efficacy in H. pylori eradication and ulcer healing compared with a 2‐week regimen. Both triple therapies were significantly better than dual therapy in H. pylori eradication. Therefore, 1‐week lansoprazole‐based triple therapy is as safe and effective as 2‐week therapy in eradication of H. pylori infection and healing of duodenal ulcer in these Asian centres.
Cyclosporin in the treatment of adults with refractory coeliac disease—an open pilot study
Authors: Wahab  , Crusius  , Meijer  , Uil  , Mulder  
Published: March 2003

Aim:To evaluate the effect of cyclosporin treatment on clinical and histological parameters in adult patients with refractory coeliac disease.Methods:Thirteen patients were treated with oral cyclosporin for 2 months, aiming at serum levels of 100–200 ng/mL. Seven extended medication intake up to a maximum of 12 months. Before and after treatment, clinical parameters were monitored and small intestinal biopsies taken. Ten of 13 patients were typed for HLA‐DQA1 and ‐DQB1 alleles.Results:Eight of 13 patients responded histologically to cyclosporin treatment. Normalization of villi was demonstrated in five patients, three after prolonged treatment. Eight patients reported a clinical response, of whom six had concomitant histological improvement. No serious side‐effects of cyclosporin were noticed. Nine of 10 patients who were immunogenetically typed carried the coeliac disease associated serologic DQ2 markers, one carried neither DQ2 nor DQ8 markers.Conclusion:In our study group of 13 adult refractory coeliac disease patients, cyclosporin in therapeutic doses induced a histological improvement in eight patients (61%), in five of whom (38%) normalization of villi was demonstrated. Thus, we believe that cyclosporin is a therapeutic option in refractory coeliac disease, although we could not confirm earlier reports of unconditional successful treatment.
Interaction of Helicobacter pylori eradication and non‐steroidal anti‐inflammatory drugs on gastric epithelial apoptosis and proliferation: implications on ulcerogenesis
Authors: Leung  , To  , Chan  , Lee  , Chung  , Sung  
Published: March 2003

Background:Apoptosis is associated with loss of gastric mucosal integrity and may play an important role in ulcer development.Aim:To examine how Helicobacter pylori and NSAIDs interact to effect apoptosis and proliferation of the gastric mucosa.Methods:Patients presenting with musculoskeletal pain requiring NSAID treatment and without previous exposure to NSAID or pre‐existing ulcers were recruited. Patients were divided into three groups: (A) H. pylori‐infected; (B) H. pylori‐eradicated; and (C) non‐infected patients. They were given naproxen for 8 weeks. Patients with non‐ulcer dyspepsia and H. pylori infection who were given anti‐Helicobacter therapy were recruited as controls (D). Endoscopy was performed at baseline and 8‐weeks after receiving naproxen. Gastric antral biopsies were obtained to assess apoptosis by terminal uridine deoxynucleotidyl nick end‐labelling (TUNEL) and proliferation by Ki67 immunostaining.Results:A total of 55 patients were studied. H. pylori‐positive patients had a higher apoptosis and proliferation index at baseline than non‐infected patients (P < 0.0001), and eradication of H. pylori resulted in a significant reduction in these parameters. The NSAID induced apoptosis in non‐infected subjects (P=0.03) whilst apoptosis was reduced in H. pylori‐positive patients receiving NSAID (P=0.02). After 8 weeks of NSAID, post‐treatment apoptosis was significantly higher in patients with persistent H. pylori infection than in non‐infected patients (P=0.01).Conclusions:Eradication of H. pylori prior to NSAID therapy significantly reduces the level of apoptosis in the gastric mucosa, which may contribute to maintaining mucosa integrity and preventing ulcer development.
Sedation with propofol plus midazolam versus propofol alone for interventional endoscopic procedures: a prospective, randomized study
Authors: Seifert  , Schmitt  , Gültekin  , Caspary  , Wehrmann  
Published: March 2003

Aim:Adequate patient sedation is mandatory for most interventional endoscopic procedures. Recent anaesthesiologic studies indicates that propofol and midazolam act synergistically in combination and therefore may be superior to sedation with propofol alone in terms of sedation efficacy, recovery and costs (due to a presumed lower total dose of propofol needed).Methods:A total of 239 consecutive patients undergoing therapeutic EGD or ERCP (EGD/ERCP‐ratio, 1:1) randomly received either propofol alone (n=120, group A, loading dose 40–60 mg intravenously, followed by repeated doses of 20 mg) or propofol plus midazolam (n=119, group B, initial midazolam dose of 2.5–3.5 mg intravenously, followed by repeated doses of 20 mg of propofol) for sedation. Vital signs (heart rate, blood pressure, oxygen saturation, electrocardiogram) were continuously monitored. Procedure‐related parameters, the recovery time and quality (post‐anaesthesia recovery score) as well as the patient’s co‐operation and tolerance to the procedure (visual analogue scale) were prospectively assessed.Results:Patients of group A and B were well matched with respect to demographic and clinical data, endoscopic findings, and the type of associated procedures. In group A, a mean dose of 0.25 ± 0.13 mg·min/kg propofol was used compared to 0.20 ± 0.09 mg·min/kg of propofol in group B (P < 0.01, plus additional 2.9 ± 0.5 mg of midazolam). Clinically relevant changes in vital signs were observed at comparable frequencies with a lowering of the systolic blood pressure < 90 mmHg in six out of 119 patients in group B and one out of 120 patients in group A (P=0.07). The sedation efficacy was rated similarly in both groups, whereas the mean recovery time (group A, 19 ± 7 min vs. group B, 25 ± 8 min, P <  0.05) as well as the recovery score (post‐anaesthesia recovery score group A, 8.0 ± 1.1 vs. post‐anaesthesia recovery score group B, 7.3 ± 1.2, P <  0.001) were significantly better with propofol alone than with propofol plus midazolam.Conclusion:During therapeutic endoscopy, sedation with propofol and midazolam requires a lower total dose of propofol, but otherwise has no superior sedation efficacy and is associated with a slower post‐procedure recovery than sedation with propofol alone.
Helicobacter pylori eradication: proton pump inhibitor vs. ranitidine bismuth citrate plus two antibiotics for 1 week—a meta‐analysis of efficacy
Authors: Gisbert  , González  , Calvet  , Roqué  , Gabriel  , Pajares  
Published: March 2003

Objective:To compare the efficacy of proton pump inhibitor vs. ranitidine bismuth citrate (RBC) with two antibiotics for 1 week in Helicobacter pylori eradication.Methods:Randomized trials comparing 1‐week regimens with (i) proton pump inhibitor plus two antibiotics [clarithromycin (C) and amoxycillin (A) or a nitroimidazole (N)]; or (ii) RBC plus the same antibiotics. Eradication was confirmed by histology or 13C‐urea breath test at least 4 weeks after therapy. Data sources included PubMed database and abstracts from congresses until October 1999. Statistical analysis was by meta‐analysis combining the odds ratios (OR) of the individual studies in a global OR (Peto method).Results:Twelve studies met the selection criteria. Nine compared proton pump inhibitor vs. RBC plus C and A, and five compared proton pump inhibitor vs. RBC plus C and N. With RBC, C and A, mean H. pylori eradication efficacy by intention‐to‐treat analysis (pooled data) was 76.6% (95% CI: 72–81%) and 73.7% (95% CI: 69–78%) with proton pump inhibitor, C and A. The OR for the effect of RBC vs. proton pump inhibitor (plus C and A) on H. pylori eradication was 1.15 (95% CI: 0.8–1.64%). Mean H. pylori eradication with RBC, C and N was 87.2% (95% CI: 83–91%), and 74.9% (95% CI: 74–84%) with proton pump inhibitor plus these two antibiotics. The OR for the effect of RBC vs. proton pump inhibitor (plus C and N) on H. pylori eradication was 1.76 (95% CI: 1.08–2.85%).Conclusion:RBC and proton pump inhibitor have similar efficacy for H. pylori eradication when given with C and A for 1 week, but RBC seems to have a higher efficacy than proton pump inhibitor when C and N are the co‐prescribed antibiotics.
Inhibition of platelet activation by 5‐aminosalicylic acid in inflammatory bowel disease
Authors: Carty  , Macey  , Rampton  
Published: March 2003

Background:Platelets play an important role in inflammation and are activated in inflammatory bowel disease. Micro‐vascular thrombosis in the gut wall leading to intestinal micro‐infarction may be a pathogenic feature of Crohn’s disease. 5‐Aminosalicylic acid is an effective treatment for patients with inflammatory bowel disease.Aims:To assess the effects of 5‐aminosalicylic acid on platelet activation, when taken orally and in vitro by patients with inflammatory bowel disease.Methods:Spontaneous and thrombin‐induced platelet activation were studied using fluorescent antibodies to the activated platelet surface glycoprotein P‐selectin and flow cytometry.Results:Baseline platelet activation in inflammatory bowel disease was significantly greater than that in controls (P=0.0003). Independent of diagnosis or disease activity, spontaneous ex‐vivo platelet activation was 50% lower in patients with inflammatory bowel disease taking 5‐aminosalicylic acid orally than in those not on such treatment (P < 0.05). In vitro, 5‐aminosalicylic acid significantly reduced both spontaneous (P < 0.03 for ≥1 μM 5‐aminosalicylic acid) and thrombin‐induced platelet activation (P < 0.02 for ≥ 1 μM 5‐aminosalicylic acid).Conclusions:5‐Aminosalicylic acid given either orally or in vitro inhibits platelet activation. If this effect reflects an in vivo action in the gut, it could contribute to the beneficial actions of 5‐aminosalicylic acid in inflammatory bowel disease.
CYP2C19 genotype status and intragastric pH during dosing with lansoprazole or rabeprazole
Authors: Adachi K. , Katsube T. , Kawamura A. , Takashima T. , Yuki M. , Amano K. , Ishihara S. , Fukuda R. , Watanabe M. , Kinoshita Y. 
Published: March 2003

Background:CYP2C19 has an important role in the catabolism of several proton pump inhibitors. However, the relative contribution of CYP2C19‐mediated metabolism varies among the different proton pump inhibitors.Aim:To determine the effect of CYP2C19 genotype status on intragastric pH during dosing with lansoprazole or rabeprazole.Subjects and methods:The subjects were 20 male volunteers without Helicobacter pylori infection. Their CYP2C19 genotype status was determined by a polymerase chain reaction‐restriction fragment length polymorphism method. Twenty‐four‐hour monitoring of intragastric acidity was performed three times: once without medication, once on the last day of a 7‐day course of rabeprazole, and once on the last day of a 7‐day course of lansoprazole.Results:Subjects were divided into three groups on the basis of their CYP2C19 genotype status: homozygous extensive metabolizers (homo‐EMs, n=7), heterozygous extensive metabolizers (hetero‐EMs, n=9), and poor metabolizers (PMs, n=4). The median pH during rabeprazole administration was not influenced by CYP2C19 genotype. On the other hand, the median pH in PMs during lansoprazole dosing was higher than in homo‐EMs and hetero‐EMs. The percentage of time with pH < 4.0 had a similar tendency to that of median pH.Conclusion:CYP2C19 genotype status influences gastric acid suppression by lansoprazole, but not by rabeprazole.
A new quadruple therapy for Helicobacter pylori using tripotassium dicitrato bismuthate, furazolidone, josamycin and famotidine
Authors: Liu Wen‐Zhong , Xiao Shu‐Dong , Hu Pin‐Jin , Lu Hong , Cui Yi , Tytgat Guido N. J. 
Published: March 2003

Background:In our previous study, a triple therapy using tripotassium dicitrato bismuthate (TDB), josamycin and furazolidone achieved a suboptimal cure rate of Helicobacter pylori infection.Aim:To investigate whether the addition of an antisecretory agent raises the cure rate using this regimen.Methods:One hundred and twenty H. pylori positive patients with peptic ulcer disease or functional dyspepsia were randomly assigned to receive 1‐week quadruple therapy of TDB 240 mg b.d., furazolidone 100 mg b.d., josamycin 1000 mg b.d. and famotidine 20 mg b.d. (BFJF group), or triple therapy of TDB 240 mg b.d., furazolidone 100 mg b.d. and clarithromycin 250 mg b.d. (BFC group). H. pylori status was assessed by histology and culture of gastric biopsy specimens before and at least 4 weeks after completion of therapy.Results:Seven patients (three in the BFJF group and four in the BFC group) dropped out. Eradication rates (intention‐to‐treat/per protocol) were 90%/95% in the BFJF group and 82%/88% in the BFC group, respectively (P > 0.05). Duodenal ulcer healing rates were 94% (16/17) in the BFJF group and 80% (20/25) in the BFC group, respectively (P > 0.05). Mild side‐effects occurred in 11 (18%) patients in the BFJF group and 10 (17%) in the BFC group (P > 0.05).Conclusions:One‐week quadruple therapy consisting of TDB, furazolidone, josamycin and famotidine achieves a high cure rate of H. pylori infection.
The use of 6‐mercaptopurine in patients with inflammatory bowel disease after failure of azathioprine therapy
Authors: Boulton‐Jones J. R. , Pritchard K. , Mahmoud A. A. 
Published: March 2003

Introduction:Azathioprine is a useful therapy in patients with inflammatory bowel disease that is difficult to control. However, 10% of patients are unable to tolerate azathioprine, and the best form of treatment for this group of patients is unknown. The azathioprine metabolite 6‐mercaptopurine may be a useful therapy for these patients.Aim:To review our clinical experience of the use of the 6‐mercaptopurine in inflammatory bowel disease patients who are intolerant of azathioprine.Methods:All patients who were prescribed 6‐mercaptopurine in a 2‐year period were identified from pharmacy records. The case notes were reviewed and those who had previously been intolerant of azathioprine were included.Results:A total of 19 with either ulcerative colitis and Crohn’s disease were included. The reasons for discontinuing azathioprine were side‐effects (13 patients), failure of efficacy (four patients) and leucopenia (two patients). Eleven of the 19 patients (68%) tolerated 6‐mercaptopurine, including seven out of 13 patients (54%) who discontinued azathioprine due to side‐effects. The length of follow‐up of patients on 6‐mercaptopurine was between 126 and 780 days (median 390 days).Discussion:6‐mercaptopurine should be considered in patients with inflammatory bowel disease who require continuing immunosuppressive therapy, but are intolerant of azathioprine.
Review article: agents affecting gall‐bladder motility – role in treatment and prevention of gallstones
Authors: Van Erpecum K. J. , Venneman N. G. , Portincasa P. , Vanberge‐Henegouwen G. P. 
Published: March 2003

SummaryVarious agents may either enhance or impair post‐prandial gall‐bladder motility, and they are identified in this review. When studying the impact of medication on gall‐bladder motility, the effects on interdigestive gall‐bladder and intestinal motility should also be taken into account. Patients at high risk of gallstone disease, and patients who are treated chronically with gall‐bladder motility inhibiting drugs, may benefit from improved gall‐bladder motility using a prokinetic agent. However, there are no long‐term studies to prove that such a strategy prevents gallstone formation.