bluuebunny/crossref_metadata_2025_split huggingface dataset:
Non‐absorbable antibiotics for managing intestinal gas production and gas‐related symptoms
Authors: Di Stefano M. , Strocchi A. , Malservisi S. , Veneto G. , Ferrieri A. , Corazza G. R. 
Published: March 2003

Background:Simethicone, activated charcoal and antimicrobial drugs have been used to treat gas‐related symptoms with conflicting results.Aim:To study the relationship between gaseous symptoms and colonic gas production and to test the efficacy of rifaximin, a new non‐absorbable antimicrobial agent, on these symptoms.Methods:Intestinal gas production was measured by hydrogen (H2) and methane (CH4) breath testing after lactulose in 21 healthy volunteers and 34 functional patients. Only the 34 functional patients took part in a double‐blind, double‐dummy controlled trial, receiving, at random, rifaximin (400 mg b.d per 7 days), or activated charcoal (400 mg b.d per 7 days). The following parameters were evaluated at the start of the study and 1 and 10 days after therapy: bloating, abdominal pain, number of flatus episodes, abdominal girth, and cumulative breath H2 excretion.Results:Hydrogen excretion was greater in functional patients than in healthy volunteers. Rifaximin, but not activated charcoal, led to a significant reduction in H2 excretion and overall severity of symptoms. In particular, in patients treated with rifaximin, a significant reduction in the mean number of flatus episodes and of mean abdominal girth was evident.Conclusions:In patients with gas‐related symptoms the colonic production of H2 is increased. Rifaximin significantly reduces this production and the excessive number of flatus episodes.
Endoscopic injection of botulinum toxin in patients with recurrent acute pancreatitis due to pancreatic sphincter of Oddi dysfunction
Authors: Wehrmann T. , Schmitt T. H. , Arndt A. , Lembcke B. , Caspary W. F. , Seifert H. 
Published: March 2003

Aim:To evaluate the technical feasibility, safety, and short‐term efficacy of botulinum toxin injection for pancreatic sphincter of Oddi dysfunction and to analyse whether the symptomatic response to botulinum toxin might be a predictor of outcome for endoscopic sphincterotomy.Methods:Fifteen consecutive patients (nine female, aged 38 ± 12 years) with frequent attacks (median four) of acute pancreatitis within 6 months, and manometrically proven pancreatic sphincter of Oddi dysfunction underwent endoscopic injection of 100 units of botulinum toxin into the major papilla. All patients underwent prospective follow‐up thereafter and in cases of recurrent pancreatitis manometry this was repeated and pancreatic sphincterotomy was performed.Results:No side‐effects occurred after botulinum toxin injection in any patient. Within 3 months after botulinum toxin treatment, 12 out of 15 patients remained asymptomatic (80% primary response). Only one out of three patients without symptomatic benefit showed continued elevated pancreatic sphincter pressure at manometry and only this patient benefited from pancreatic sphincterotomy later on. Eleven of the 12 patients initially responding to botulinum toxin injection developed a symptomatic relapse 6 ± 2 months after botulinum toxin treatment. These patients then achieved long‐term clinical remission from pancreatic or combined (biliary and pancreatic, n=5) sphincterotomy (median follow‐up, 15 months).Conclusion:Endoscopic botulinum toxin injection into the papilla of Vater is a safe procedure for treatment of pancreatic sphincter of Oddi dysfunction that may provide short‐term relief in about 80% of the patients. Those patients who respond to botulinum toxin may subsequently gain definitive cure from sphincterotomy.
Multicentre randomized placebo‐controlled trial of ursodeoxycholic acid with or without colchicine in symptomatic primary biliary cirrhosis
Authors: Almasio P. L. , Floreani A. , Chiaramonte M. , Provenzano G. , Battezzati P. , Crosignani A. , Podda M. , Todros L. , Rosina F. , Saccoccio G. , Manenti F. , Ballardini G. , Bianchi F. P. , Scheuer P. J. , Davies S. E. , Craxì A. 
Published: March 2003

Aim:To establish the efficacy of combination therapy with ursodeoxycholic acid (UDCA) and colchicine in patients with symptomatic primary biliary cirrhosis (PBC), defined by the presence of liver cirrhosis, pruritus or bilirubin exceeding 2 mg/mL.Methods:A total of 90 patients were randomly assigned to ursodeoxycholic acid 500 mg/daily plus placebo (UDCA group, n=44), or ursodeoxycholic acid at the same dosage plus colchicine, 1 mg/daily (UDCA/C group, n=46). The two groups were comparable for age, sex, stage of disease, severity of pruritus, bilirubin, and Mayo score. All patients underwent clinical, ultrasonographic, and biochemical examinations at entry and then every 6 months up to 3 years of follow‐up. Patients with cirrhosis underwent endoscopy every 12 months. In a sub‐group of patients without cirrhosis, who consented, liver biopsy was repeated at the end of the study.Results:The number of treatment failures (i.e. dead, orthotopic liver transplantation (OLT), complications of cirrhosis, doubling of bilirubin, untreatable pruritus) was 11 (25%) in the UDCA group and four (9%) in the UDCA/C group (P < 0.05). No significant differences were observed in terms of improvement of liver enzymes related to cholestasis and cytolysis and of amelioration of pruritus. The Mayo score values increased less above the baseline values at 24 and 36 month‐intervals in the UDCA/C group than in the UDCA group. Histological evaluation at baseline and at the end of the study was available for 15 patients with pre‐cirrhotic stage. A significant reduction in histological grading score was observed in patients from the UDCA/C group, whereas no changes in these histological scores were observed in the UDCA group.Conclusions:The addition of colchicine to ursodeoxycholic acid in patients with symptomatic primary biliary cirrhosis results in a small but significant reduction of disease progress.
Role of antimicrobial susceptibility testing on efficacy of triple therapy in Helicobacter pylori eradication
Authors: Toracchio S. , Cellini L. , Di Campli E. , Cappello G. , Malatesta M. G. , Ferri A. , Ciccaglione A. F. , Grossi L. , Marzio L. 
Published: March 2003

Background: Helicobacter pylori treatment failure may be due to resistance to macrolides and 5‐nitroimidazoles.Aim:To test whether a preliminary in vitro susceptibility test of H. pylori to tinidazole and clarithromycin and a consequent specific regimen could improve the eradication rate.Methods:A total of 109 consecutive H. pylori‐positive patients with dyspeptic symptoms were included. At endoscopy, biopsy from the antrum was obtained for H. pylori culture and antimicrobial susceptibility testing. Fifty‐six patients were treated with omeprazole, tinidazole and clarithromycin for 10 days (group OTC) and 53 patients received therapy on the basis of the susceptibility test (group SUSC). Treatment success was evaluated by the 13C‐urea breath test 1 month after the end of therapy.Results:Eight patients dropped out. Overall primary resistance to clarithromycin, tinidazole and both antibiotics was 13%, 33% and 4%, respectively. In group OTC, H. pylori was eradicated in 81% and 75% of patients by per protocol and intention‐to‐treat analysis, respectively. Per protocol and intention‐to‐treat eradication rates for group SUSC were 98% and 91% (P < 0.05 vs. group OTC).Conclusions:These data show that in H. pylori infection, antibiotic therapy based on the results of culture and susceptibility testing gives, in comparison to standard therapy, a significant improvement in eradication rate.
Efficacy and tolerability of a fixed combination of peppermint oil and caraway oil in patients suffering from functional dyspepsia
Authors: May B. , Köhler S. , Schneider B. 
Published: March 2003

Aim:To assess the efficacy and safety of enteric coated capsules containing a fixed combination of 90 mg peppermint oil and 50 mg caraway oil (PCC; Enteroplant) in patients with functional dyspepsia.Methods:A total of 96 out‐patients received one capsule twice daily of PCC or placebo for 28 days. Primary efficacy variables were the intra‐individual change in (i) pain intensity and (ii) sensation of pressure, heaviness and fullness between days 1 and 29, and the investigators’ rating of (iii) global improvement (Clinical Global Impressions [CGI] item 2) on day 29. A global type I error of α=0.05 was controlled by a priori ordering of hypotheses.Results:All patients were evaluable for efficacy and safety. On day 29, the average intensity of pain was reduced by 40% vs. baseline in the PCC group and by 22% in the placebo group. With regards to pressure, heaviness and fullness, a 43% reduction was observed for PCC vs. 22% for placebo. In CGI item 2, 67% (PCC) vs. 21% (placebo) of the patients were described as much or very much improved. In all three target parameters, the superiority of PCC over placebo was statistically significant. Six patients (PCC: 5; placebo: 1) reported adverse events, either unrelated to the trial, or attributable to an aggravation of the disease under investigation. Eructation with peppermint taste did not occur.Conclusion:These results demonstrate the good tolerability and the favourable risk–benefit ratio of PCC for the treatment of functional dyspepsia.
Rat CXC chemokine GRO/CINC‐1 paradoxically stimulates the growth of gastric epithelial cells
Authors: Suzuki H. , Mori M. , Seto K. , Shibata F. , Nagahashi S. , Kawaguchi C. , Suzuki M. , Matsui H. , Watanabe K. , Miura S. , Ishii H. 
Published: March 2003

Summary Background: CXC chemokines such as interleukin (IL)‐8 are neutrophil chemoattractants, the levels of which increase in Helicobacter pylori‐infected gastric mucosa. Many investigators have focused on the chemotactic aspects of IL‐8; however, CXC chemokines are also reported to have angiogenic activity and to serve as remodelling factors. Rat GRO/CINC‐1 is a rodent counterpart of human GROα, a member of the family of CXC chemokines. Gastric mucosa infected with H. pylori is in a state of hyperproliferation, with increases in the amounts of growth factors such as hepatocyte growth factor (HGF). Aim: To investigate whether rat GRO/CINC‐1 had growth‐stimulating activity for gastric epithelial cells. Methods: The rat gastric epithelial cell line RGM‐1 was incubated in serum‐free medium for 12 h to adjust the cell cycle to the G0 phase, and GRO/CINC‐1 was then added for 24 h. The total cell number was determined by fluorogenic analysis after propidium iodide staining, and cell proliferation was assessed by measuring 5‐bromo‐2′‐deoxyuridine (BrdU) incorporation. The activity of p42/p44 mitogen‐activated protein kinase (MAPK) was measured 5–20 min after the start of GRO/CINC‐1 exposure. Results: Cultures treated with GRO/CINC‐1 showed a significant increase in cell number and BrdU incorporation in a concentration‐dependent fashion. The MAPK activity increased within 5 min after GRO/CINC‐1 application and returned to the control level at 20 min. Conclusion: The growth‐stimulatory effect of GRO/CINC‐1 on rat gastric epithelial cells suggests a dual function of this chemokine: proinflammatory action and induction of epithelial proliferation.
Induction of signal transduction pathways in rat gastric epithelial cells stimulated with interleukin‐1β
Authors: Tominaga K. , Higuchi K. , Tsuno M. , Watanabe T. , Fujiwara Y. , Kim S. , Arakawa T. , Iwao H. , Kuroki T. 
Published: March 2003

Summary Background: Interleukin‐1β (IL‐1β) participates in cell growth, differentiation and apoptosis via activation of several kinases in a variety of cells. Mitogen‐activated protein (MAP) kinases are important intermediates of the signal transduction pathway from the cell surface to the nucleus, leading to activation of transcription factors. There are no reports on the effect of IL‐1β on these pathways in gastric epithelial cells. Aim: To investigate whether IL‐1β activates MAP kinases [extracellular signal‐regulated kinases (ERKs), c‐Jun NH2‐terminal kinases (JNKs) and p38 MAP kinase (p38 MAPK)] and nuclear factor (NF)‐κB, a transcription factor, in gastric epithelial cells (RGM1). Methods: The activities of ERKs and JNKs were estimated by in‐gel kinase assay, and p38 MAPK activity was measured by in vitro kinase assay at various time points (0–40 min) after addition of IL‐1β (100 pg/mL) for 20 min. The activity of NF‐κB was analysed using gel mobility shift assay at times from 0 to 4 h after addition of IL‐1β. Results: Activity of ERKs was detectable at 10 min, peaked at 20 min, and continued at increased levels until 40 min. Activity of both JNKs and p38 MAPK were detectable during 5–20 min, and then decreased within 40 min. Activation of NF‐κB occurred at 30 min, and increased activity continued for 6 h. Interleukin‐1β activated MAP kinases and NF‐κB in RGM1 cells. Conclusion: The activation induced by this cytokine may play an important role in the initiation of the inflammatory process in gastric mucosa.
Mechanism of prevention by capsaicin of ethanol‐induced gastric mucosal injury – a study in the rat using intravital microscopy
Authors: Saeki T. , Ohno T. , Boku K. , Saigenji K. , Katori M. , Majima M. 
Published: March 2003

Summary Background: Capsaicin acts specifically on primary afferent neurones to release neuropeptides, including calcitonin gene‐related peptide (CGRP), and prevents ethanol‐induced mucosal injury. Aim: To investigate the microvascular changes in the gastric mucosa in response to ethanol using intravital microscopy to elucidate the mechanism of capsaicin‐induced gastroprotection. Methods: The posterior gastric wall in the rat was secured in an observation chamber and perfused with Tyrode's solution. The microcirculation was observed through a window made by removing a limited area of smooth muscle. Results: Ethanol (50%) applied to the mucosa constricted the collecting venules and venules but dilated arterioles. The constriction of the collecting venules resulted in mucosal congestion, which caused mucosal injury. Application of capsaicin to the mucosa dilated the arterioles but not the collecting venules or venules. Arteriolar dilation was inhibited by a CGRP antagonist, CGRP‐(8–37). Prior application of capsaicin prevented ethanol‐induced constriction of the collecting venules, and the action of capsaicin was inhibited by prior application of CGRP‐(8–37). Conclusions: The results suggest that the inhibition of ethanol‐induced gastric injury by capsaicin is attributable to the suppression of collecting venule constriction, via CGRP release.
Review: low caloric intake and gall‐bladder motor function
Authors: Festi D. , Colecchia A. , Larocca A. , Villanova N. , Mazzella G. , Petroni M. L. , Romano F. , Roda E. 
Published: March 2003

SummaryCholelithiasis is the primary expression of obesity in the hepatobiliary system. In obese subjects the risk of developing gallstones is increased due to a higher cholesterol saturation of gall‐bladder bile. During weight reduction with very low calorie diets (VLCD) the incidence of gallstones increases, but the mechanism for gallstone formation is not completely understood and several pathogenetic mechanisms have been suggested: increased saturation of bile, increased gall‐bladder secretion of mucin and calcium, increased presence of prostaglandins and arachidonic acid. Alterations in gall‐bladder motility may contribute to gallstone formation, but few studies have addressed the issue of gall‐bladder motility during rapid weight loss and its possible role in gallstone formation. VLCD have been associated with a gall‐bladder stasis, as a consequence of reduced gall‐bladder stimulation by low fat content of the diets. A threshold quantity of fat (10 g) has been documented to obtain efficient gall‐bladder emptying. Ursodeoxycholic acid administered during VLCD seems to have a protective role in developing a biliary cholesterol crystals. Gall‐bladder emptying was lower in response to low fat meals with respect to relative higher fat meals, before as well as during the VLCD. This may account the possibility of an adaptative response of the gall‐bladder motility to a given diet regimen. Adequate fat content of the VLCD may prevent gallstone formation, maintaining adequate gall‐bladder motility and may be more economic and physiologically acceptable than administration of a pharmacological agent.
Helicobacter pylori: where are we and where are we going?
Authors: Tytgat G. N. J. 
Published: March 2003

SummaryThis paper contains a personal view on what has been achieved in Helicobacter pylori research and what the expectations might be for further developments. Knowledge about the organism is already extensive. Particularly intriguing are the differences in genetic make‐up in the various geographical regions. Sadly, detailed knowledge on how the organism spreads is still lacking. The clinical spectrum of the disease in man is largely known, but as H. pylori is disappearing worldwide, the relative frequency of H. pylori‐negative ulcer disease is increasing. To what extent H. pylori disappearance and eradication is responsible for the decreasing incidence of gastric cancer remains uncertain. Antimicrobial therapy is dominated by proton pump inhibitor triple therapy as first line with quadruple therapy as second‐line therapy. The long‐term consequences of the rising resistance to the ‘key’ antimicrobials are so far unknown and speculative.
Helicobacter pylori effects on gastritis, gastrin and enterochromaffin‐like cells in Zollinger–Ellison syndrome and non‐Zollinger–Ellison syndrome acid hypersecretors treated long‐term with lansoprazole
Authors: Hirschowitz B. I. , Haber M. M. 
Published: March 2003

Background: Helicobacter pylori is said to cause atrophy of the gastric corpus and enterochromaffin‐like cell proliferation in gastro‐oesophageal reflux disease (GERD) patients treated long‐term with a proton pump inhibitor.Aims:To determine the effect of H. pylori infection on gastritis, enterochromaffin‐like cell density and hyperplasia, mucosal atrophy and serum gastrin in patients with gastric hypersecretion (basal acid output gt; 15 mmol/h) with either hypergastrinemia (Zollinger–Ellison syndrome) or normal gastrin (non‐Zollinger–Ellison syndrome) before and during long‐term treatment with lansoprazole.Methods:Lansoprazole was individually titrated to reduce basal acid output to < 5 mmol/h (< 1 mmol/h in post‐surgical Zollinger–Ellison syndrome). Gastric corpus biopsies were obtained every 6 months before treatment and up to 8 years later.Results: H. pylori was present in corpus biopsies in ≈ 50%, causing active gastritis which resolved rapidly in 15 subjects after elimination of H. pylori. Patchy mild/moderate corpus atrophy was present at entry in two and at the end in four out of 60 patients, one being H. pylori‐positive. Intestinal metaplasia (< 10%) was seen in six isolated biopsies (1% of total). H. pylori did not affect serum gastrin, enterochromaffin‐like cell density or hyperplasia. Enterochromaffin‐like cell density was twice as high in Zollinger–Ellison syndrome as in non‐Zollinger–Ellison syndrome patients (241 vs. 126 cells/mm2, P < 0.001). Enterochromaffin‐like cells remained normal in the non‐Zollinger–Ellison syndrome hypersecretors regardless of H. pylori status.Conclusion:Corpus enterochromaffin‐like cell increases were related to serum gastrin elevation, but neither H. pylori nor long‐term treatment with lansoprazole alone or together had any effect on enterochromaffin‐like cell density or hyperplasia. Corpus acute gastritis resulted from H. pylori infection, but did not result in mucosal atrophy despite long‐term proton pump inhibitor treatment and promptly resolved with loss of H. pylori.
Non‐Helicobacter pylori bacterial flora during acid‐suppressive therapy: differential findings in gastric juice and gastric mucosa
Authors: Sanduleanu S. , Jonkers D. , De Bruine A. , Hameeteman W. , Stockbrügger R. W. 
Published: March 2003

Background:Intragastric growth of non‐Helicobacter pylori bacteria commonly occurs during acid‐suppressive therapy. The long‐term clinical consequences are still unclear.Aim:To investigate the luminal and mucosal bacterial growth during gastric acid inhibition, in relation to the type and duration of acid‐inhibitory treatment, as well as to concomitant H. pylori infection.Methods:A total of 145 patients on continuous acid inhibition with either proton pump inhibitors (n=109) or histamine2‐receptor antagonists (H2RAs, n=36) for gastro‐oesophageal reflux disease, and 75 dyspeptic patients without acid inhibition (control group) were included. At endoscopy, fasting gastric juice was obtained for pH measurement and bacteriological culture. Gastric biopsy specimens were examined for detection of H. pylori (immunohistochemistry) and of non‐H. pylori bacteria (modified Giemsa stain‐positive and immunohistochemistry‐negative at the same location).Results:Non‐H. pylori flora was detected in the gastric juice of 92 (41.8%) patients and in the gastric mucosa of 109 (49.6%) patients. In gastric juice, prevalence rate for non‐H. pylori bacteria was higher in patients taking proton pump inhibitors than controls and those taking H2RAs (58.7% vs. 22.6% and vs. 30.6%, P < 0.0001 and P < 0.003, respectively), but did not differ statistically between H2RAs and controls. In gastric mucosa, prevalence rates for non‐H. pylori bacteria were higher in patients taking proton pump inhibitors and H2RAs than in the controls (antrum: 46.9% and 48.6% vs. 25%, P < 0.05 for both; corpus: 52.2% and 56.8% vs. 23.7%, P < 0.001 for both), but did not differ between proton pump inhibitors and H2RAs. Both luminal and mucosal growth of non‐H. pylori bacteria were significantly greater in H. pylori‐positive than ‐negative patients taking proton pump inhibitors (P < 0.05 for both). Luminal growth of non‐H. pylori flora increased with the intragastric pH level, whilst mucosal bacterial growth increased with the duration of acid inhibition.Conclusions:Non‐H. pylori flora not only contaminates the gastric juice but also colonizes the gastric mucosa of a large proportion of patients treated long‐term with acid inhibition. The relationship between H. pylori and non‐H. pylori bacteria in the pathogenesis of atrophic gastritis and gastric cancer needs further elucidation.
Combination therapy with ribavirin and alpha interferon for the treatment of chronic hepatitis C refractory to interferon
Authors: Cozzolongo R. , Cuppone R. , Giannuzzi V. , Amati L. , Caradonna L. , Tamborrino V. , Jirillo E. , Manghisi O. G. 
Published: March 2003

Background:Up to 80% of hepatitis C patients are refractory to treatment with interferon‐α. These patients are not likely to benefit from higher dosages or longer duration of interferon alone. The addition of ribavirin has been shown to improve the response rate in patients resistant to a previous course of interferon‐α alone.Aim:To evaluate whether a sustained hepatitis C virus (HCV) RNA response could be obtained with combination therapy of interferon‐α and ribavirin in patients who did not respond to or relapsed after a standard interferon‐α treatment.Methods:A total of 73 patients, 59 non‐responders and 14 relapsers after interferon‐α alone, were treated with a combination of ribavirin (1000–1200 mg/day) and interferon‐α (3 MU three times a week) for 24 weeks. Alanine aminotransferase levels and HCV RNA were checked for 24 weeks after completion of therapy.Results:At the end of the combination therapy, 36 patients (49%) showed alanine aminotransferase normalization and in 20 patients (27%), HCV RNA was undetectable in serum. At the end of the 24 weeks follow‐up period, only 12 patients (16%) had a sustained response with serum negativity of HCV RNA. This response was significantly higher in relapsers than in non‐responders: five (36%) vs. seven (12%) patients (P=0.03), respectively. Adverse effects were restricted to flu‐like symptoms and moderate haemolytic anaemia.Conclusions:Combination of interferon‐α and ribavirin is quite limited, both in scope and efficacy, in HCV patients who had a non‐response to monotherapy with interferon. Better results may be expected in relapsers, but larger studies are necessary.