bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chemotactic properties of ICAM‐1 and PECAM‐1 on neutrophil granulocytes in ulcerative colitis: effects of prednisolone and mesalazine
Authors: Vainer B. , Nielsen O. H. 
Published: March 2003

Background:ICAM‐1 seems to exhibit effects other than passive leucocyte/endothelial interaction.Aim:To investigate the attracting properties of selected adhesion molecules, assessing the influence of the two major anti‐inflammatory drugs in ulcerative colitis, prednisolone and mesalazine.Methods:Circulating neutrophils (11 ulcerative colitis, 15 controls) were assessed in microchemotaxis chambers by the leading front technique, using physiologically relevant concentrations of ICAM‐1 (0.005–5000 p M), PECAM‐1 (0.001–1000 n
M), and P‐selectin (0.01–100 n
M). Neutrophils pre‐incubated with prednisolone (10–8–10–4 M) or mesalazine (0.65–10.4 n
M) were assessed towards ICAM‐1.Results:Migration of neutrophils towards ICAM‐1 showed a bell‐shaped curve with a maximum at 5 p M (migration: 37.7 μm; P < 0.001), whereas PECAM‐1 attracted neutrophils equally in the range of 0.1–10 n
M (25.0 μm; P < 0.001). P‐selectin had no cell‐attracting effect. No differences were detected between cells from ulcerative colitis patients and controls. Pre‐treatment with prednisolone decreased the cell attracting effect of ICAM‐1 in a dose‐dependent manner to 72% of the basal migration (P < 0.001). Conversely, prednisolone showed a pro‐chemokinetic effect by increasing the spontaneous locomotion of neutrophils by 40% (P < 0.001).Conclusions:Specific chemotactic properties were observed for ICAM‐1 and PECAM‐1. Prednisolone exhibited a dual effect in inhibiting the ICAM‐1‐mediated migration and stimulating the general locomotion of neutrophils.
Parkinsonism: differential age‐trend in Helicobacter pylori antibody
Authors: Dobbs  , Charlett  , Dobbs  , Weller  , Peterson  
Published: March 2003

Background:Parkinsonism is associated with prodromal peptic ulceration. Dopamine antagonists provoke experimental ulcer, dopaminergic agents protect, and might inhibit growth of Helicobacter pylori.Objective:To describe the relationship between H. pylori serology and parkinsonism.Methods:Serum H. pylori anti‐urease‐IgG antibody was measured in 105 people with (idiopathic) parkinsonism, 210 without, from same locality. None had received specific eradication therapy.Results:Controls showed a birth‐cohort effect: antibody titre rose from 30 to 90 years (P < 0.001). Parkinsonism obliterated this (disease status · age interaction, P < 0.05), the differential age trend not being attributable to social class. Those with diagnosed parkinsonism were more likely to be seropositive (odds ratio 2.04 (95% CI: 1.04, 4.22) P < 0.04) before 72.5 years. Overall, titre fell (P=0.01) by 5 (1, 9)% per unit increase in a global, 30‐point rating (median 14 (interquartile range 10.5, 17)) of disease severity. No individual category of anti‐parkinsonian medication (92% taking) had a differential lowering effect.Conclusions:Higher prevalence of seropositivity in parkinsonism, before 8th decade, may be due to host susceptibility/reaction, or, conversely, infection with particular H. pylori strain(s) lowering dopaminergic status. Absence of a birth cohort effect in parkinsonism, despite similar social class representation, may be consequent on eradication, spontaneous (gastric atrophy) or by anti‐parkinsonian medication.
Allopurinol in addition to 5‐aminosalicylic acid based drugs for the maintenance treatment of ulcerative colitis
Authors: Järnerot  , Ström  , Danielsson  , Kilander  , Lööf  , Hultcrantz  , Löfberg  , Florén  , Nilsson  , Broström  ,   FOR THE SWEDISH ORGANISATION FOR STUDY OF INFLAMMATORY BOWEL DISEASES (SOIBD)
Published: March 2003

Background:To investigate the value of combined treatment with allopurinol and 5‐aminosalicylic (5‐ASA) based drugs as maintenance treatment for ulcerative colitis (UC).Methods:199 patients with UC in remission but with active disease during the preceding 3 years were included. Allopurinol 100 mg twice daily or placebo was added to the 5‐ASA based maintenance treatment. Clinical and endoscopic follow up was performed after 1, 6 and 12 months.Results:Intention‐to‐treat analysis after 6 and 12 months showed similar results in both groups. A log‐rank test showed that 77% in the allopurinol compared to 59% in the placebo group were still in remission after 6 months (P=0.0083) and 62% and 53% after 12 months, respectively (P=0.0936). This was mainly due to a higher than expected number of relapses during the first 3 months in the placebo group. After the first 3 months, the rate of relapse in each group was similar.Conclusions:It appears possible that allopurinol in combination with 5‐ASA is better than 5‐ASA alone for a 6‐month, but not a 12‐month period. This has to be verified in further dose‐ranging studies.
Role of inducible nitric oxide synthase in dextran sulphate sodium‐induced colitis
Authors: Yoshida Y. , Iwai A. , Itoh K. , Tanaka M. , Kato S. , Hokari R. , Miyahara T. , Koyama H. , Miura S. , Kobayashi M. 
Published: March 2003

Summary Background: Different authors have postulated both toxic and protective effects for nitric oxide (NO) in the pathophysiology of active inflammation. Aim: To examine the role of NO, especially that produced by the inducible form of nitric oxide synthase (iNOS), by investigating the effects of NOS inhibitors and NO donors on inflammation in experimental acute colitis. Methods: Acute colitis was induced in rats by dextran sulphate sodium (DSS). White blood cell counts and levels of thiobarbituric acid reactants in the portal blood were determined, as were histological changes in the colonic mucosa. We then evaluated the effects of NG‐nitro‐
l‐arginine methyl ester (
l‐NAME), aminoguanidine (AG) and an NO donor on DSS‐induced changes in these inflammatory parameters. Results and Conclusions: Inhibition of NO production by either
l‐NAME or AG worsened DSS‐induced inflammation, suggesting a protective role for NO in acute colitis. On the other hand, a NO donor also exaggerated DSS‐induced inflammatory parameters, suggesting that acute colitis may be aggravated by either too much or too little NO. These results suggest that medical treatment of ulcerative colitis must aim for maintenance of appropriate NO levels in the intestinal mucosa.
The incidence of reflux oesophagitis after cure of Helicobacter pylori in a Japanese population
Authors: Murai T. , Miwa H. , Ohkura R. , Iwazaki R. , Nagahara A. , Sato K. , Yamada T. , Ota K. , Tanaka H. , Kawabe M. , Minowa T. , Takei Y. , Miyazaki A. , Sato N. 
Published: March 2003

Summary Aim: To investigate the incidence of reflux oesophagitis after antibacterial therapy for Helicobacter pylori infection in our patient population. Methods: Subjects were 451 H. pylori‐infected patients (primary symptom: peptic ulcer disease in 347, nonulcer dyspepsia in 100, and reflux oesophagitis in four); 11 of these patients had reflux oesophagitis on study entry. H. pylori infection was treated by a proton pump inhibitor/amoxycillin‐clarithromycin regimen for either 7 or 14 days. Each patient was examined by endoscopy before treatment and more than 6 months after treatment to compare oesophageal findings. In addition, 227 patients were interviewed regarding reflux symptoms, using symptom questionnaires, before and more than 6 months after treatment. Results: Among 440 patients who did not have reflux oesophagitis prior to antibacterial treatment (340 peptic ulcer patients and 100 nonulcer dyspepsia patients), 23 patients whose infection was eradicated developed reflux oesophagitis (5.4%). The 11 patients who had reflux oesophagitis prior to treatment were all successfully cured of infection. Six of these patients showed no change in their oesophagitis, while the condition improved in three and worsened in two. Symptom scores improved in 34 of the 36 patients who reported reflux symptoms. Among 19 patients who showed persistent infection, only one developed reflux oesophagitis (5.2%), while none complained of newly developed symptoms following treatment. Conclusions: Development of reflux oesophagitis after treatment of H. pylori infection was observed in a Japanese population. However, the incidence of this condition was comparable between those with persistent H. pylori infection and those in whom the infection was eradicated.
Pharmacokinetics of clarithromycin in Helicobacter pylori eradication therapy in patients with liver cirrhosis
Authors: Azuma T. , Ito S. , Suto H. , Ito Y. , Miyaji H. , Yamazaki Y. , Kato T. , Kuriyama M. 
Published: March 2003

Summary Background: Proton pump inhibitor triple therapy with clarithromycin and metronidazole has been widely used for Helicobacter pylori eradication. However, the efficacy and the safety of this therapy in patients with liver cirrhosis have not been established. Aim: To evaluate the effect of hepatic dysfunction on metabolism of clarithromycin as it is used for H. pylori eradication therapy in patients with liver cirrhosis, and the efficacy of eradication therapy in those patients. Methods: Serum levels of clarithromycin and its meta‐bolite, 14‐(R)‐hydroxyclarithromycin, were examined in 18 subjects (five normal controls and 13 hospitalized patients with liver cirrhosis) on a selected day between days 7 and 10 of a 2‐week course of eradication therapy. This therapy consisted of lansoprazole (30 mg, once a day) together with clarithromycin (200 mg, twice a day) and metronidazole (250 mg, twice a day). In addition, 118 H. pylori‐positive out‐patients, 88 with peptic ulcer and 30 with liver cirrhosis, underwent the same eradication therapy. Results: Values for the area under the 0–6 h concentration–time curve (AUC) for clarithromycin were not significantly different among the groups. However, the AUC (0–6 h) values of 14‐(R)‐hydroxyclarithromycin were significantly lower in the Child‐Pugh C group than in either the normal controls or the Child‐Pugh A/B group. The cure rate for the peptic ulcer patients was 84% on a per protocol analysis (95% CI: 80%−88%) and 81% on an intention‐to‐treat analysis (95% CI: 77%−85%), while in the liver cirrhosis patients it was 89% in a per protocol analysis (95% CI: 78%−99%) and 83% in an intention‐to‐treat analysis (95% CI: 70%−97%). Mild adverse effects were observed in 10% of the peptic ulcer patients and 13% of the liver cirrhosis patients, with none leading to premature withdrawal from the study. Conclusion: The 2‐week low‐dose lansoprazole‐based triple therapy tested is a simple, effective and well‐tolerated regimen for H. pylori eradication in patients with liver cirrhosis.
Review article: defects in gall‐bladder motor function – role in gallstone formation and recurrence
Authors: Pauletzki J. , Paumgartner G. 
Published: March 2003

SummaryThe pathogenesis of cholesterol gallstones is now recognized as a multifactorial process, including saturation of bile with cholesterol, destabilization of bile leading to cholesterol crystals and hypomotility permitting crystal growth, and agglomeration and retention of microstones which then grow to macroscopic gallstones. In the last 15 years meticulous research has demonstrated convincing evidence that many patients with cholesterol gallstone disease have a distinct defect in gall‐bladder motor function that is induced by bile saturated with cholesterol.
Expression and cellular localization of COX‐1 and ‐2 in Helicobacter pylori gastritis
Authors: Chan F. K. L. , To K. F. , Ng Y. P. , Lee T. L. , Cheng A. S. L. , Leung W. K. , Sung J. J. Y. 
Published: March 2003

Background:There are conflicting reports on the expression of cyclooxygenase in Helicobacter pylori infection.Aim:To evaluate the expression of COX‐1 and COX‐2 in H. pylori gastritis at messenger RNA (mRNA) and protein levels.Methods:Endoscopic gastric biopsies were obtained from patients with non‐ulcer dyspepsia. The levels of COX‐1 and COX‐2 mRNA were compared between H. pylori‐infected and uninfected specimens using reverse transcription‐polymerase chain reaction. The immunohistochemical findings were correlated with the cellular localization of cyclooxygenase mRNA using in situ hybridization.Results:A total of 40 H. pylori‐infected and 40 uninfected specimens were studied. mRNA of COX‐2 but not COX‐1 was elevated in H. pylori‐infected mucosa. COX‐1 was localized to the mononuclear inflammatory, endothelial and smooth muscle cells in the lamina propria. COX‐2 was barely detectable in uninfected mucosa but was strongly expressed in the foveolar and glandular epithelia in H. pylori gastritis.Conclusion:Cyclooxygenase‐1 is expressed in the mononuclear inflammatory, endothelial and smooth muscle cells in the lamina propria irrespective of the H. pylori status. By contrast, H. pylori induces COX‐2 expression in the foveolar and glandular epithelia.
One‐week ranitidine bismuth citrate‐based triple therapy for the eradication of Helicobacter pylori in Hong Kong with high prevalence of metronidazole resistance
Authors: Wong B. C. Y. , Wong W. M. , Wang W. H. , Fung F. M. Y. , Lai K. C. , Chu K. M. , Yuen S. T. , Leung S. Y. , Hu W. H. C. , Yuen M. F. , Lau G. K. K. , Chan C. K. , Lam S. K. 
Published: March 2003

Aim:To compare 1‐week ranitidine bismuth citrate‐based (RBC) triple therapy vs. omeprazole‐based (O) triple therapy for the eradication of Helicobacter pylori infection in Hong Kong with high prevalence of metronidazole resistance.Methods:Patients with non‐ulcer dyspepsia and H. pylori infection were randomized to receive either: (i) RBCCM: ranitidine bismuth citrate (pylorid) 400 mg, clarithromycin 250 mg and metronidazole 400 mg; or (ii) OCM: omeprazole 20 mg, clarithromycin 250 mg and metronidazole 400 mg, each given twice daily for 1 week. Endoscopy (CLO test, histology and culture) and 13C‐urea breath test were performed before randomization and 6 weeks after drug treatment.Results:A total of 180 patients were randomized. H. pylori eradication rates (intention‐to‐treat, n=180/per protocol, n=166) were 83%/92% for RBCCM and 66%/70% for OCM (P=0.01, intention‐to‐treat and P=0.001, per protocol, respectively). RBCCM treatment was unaffected by metronidazole susceptibility and achieved a significantly higher eradication rate in metronidazole‐resistant cases (89%) than the OCM group (45%, P=0.0064).Conclusion:One‐week ranitidine bismuth citrate‐based triple therapy is significantly better than omeprazole‐based triple therapy for the eradication of H. pylori infection, especially in metronidazole‐resistant cases. It is an effective regimen for the eradication of H. pylori infection in regions with a high prevalence of metronidazole resistance.
Impact of Helicobacter pylori resistance to clarithromycin on the efficacy of the omeprazole–amoxicillin–clarithromycin therapy
Authors: Tankovic J. , Lamarque D. , Lascols C. , Soussy C. J. , Delchier J. C. 
Published: March 2003

Background: Helicobacter pylori resistance to clarithromycin is relatively frequent in France and is assumed to be the main cause of failure of the proton pump inhibitor–amoxicillin–clarithromycin (proton pump inhibitor–AC) therapy, which is the first‐line regimen in France.Aim:To determine the respective effects of clarithromycin primary and secondary resistances on efficacy of the proton pump inhibitor–AC regimen and to determine whether failures are associated with persistence of the same strain or with emergence of a new one.Methods:A total of 123 H. pylori‐infected patients were treated for 7 days with omeprazole 20 mg b.d., amoxicillin 1 g b.d., and clarithromycin 500 mg b.d. Eradication was assessed by breath test in 102 patients. Minimal inhibitory concentrations of clarithromycin were determined by E‐test. Strain genotyping was performed by random amplified polymorphic DNA.Results:The pre‐treatment and post‐treatment prevalences of clarithromycin resistance were 19% (23 out of 123) and 69% (nine out of 13), respectively. The rates of eradication were 68% (69 out of 102), 79% (67 out of 85), and 12% (two out of 17) for all, susceptible and resistant strains, respectively. The post‐treatment isolate was available for six patients with a susceptible pre‐treatment isolate and a persistent infection. Resistance emerged in two patients and was associated with persistence of the pre‐treatment strain in one and with selection of a new strain in the other.Conclusions:In our hospital, failures of the proton pump inhibitor–AC therapy are related to both clarithromycin primary and secondary resistances, but the emergence of secondary resistance does not explain all of the failures in the initial clarithromycin‐susceptible group. In that group a new strain can emerge after failure.
Increased gastric acid secretion after Helicobacter pylori eradication may be a factor for developing reflux oesophagitis
Authors: Koike T. , Ohara S. , Sekine H. , Iijima K. , Kato K. , Toyota T. , Shimosegawa T. 
Published: March 2003

Background:The role of acid secretion in reflux oesophagitis which may develop after H. pylori eradication is not well known.Aim:To investigate the participation of altered gastric acid secretion and the presence of hiatal hernia in the development of reflux oesophagitis after eradication therapy for H. pylori.Subjects and Methods:A total of 105 patients with H. pylori infection, but without reflux oesophagitis at the time of eradication therapy, were followed prospectively for 7 months after the clearance of this microorganism. Gastric acid secretion was assessed by endoscopic gastrin test, and the presence of hiatal hernia by endoscopy.Results:Reflux oesophagitis developed in 11 out of 105 (10.5%) patients when examined at 7 months after the eradication therapy. The incidence was correlated significantly with the increase in gastric acid secretion after the eradication of H. pylori, and was significantly higher in the patients with hiatal hernia (20%) than in those without it (0%).Conclusions:Increased acid secretion after H. pylori eradication is an important risk factor of reflux oesophagitis, especially in patients with hiatal hernia.
Photodynamic therapy and the alimentary tract
Authors: Selvasekar C. R. , Birbeck N. , Mcmillan T. , Wainwright M. , Walker S. J. 
Published: March 2003

Photodynamic therapy offers the possibility of relatively selective tumour necrosis and normal tissue healing. It has many potential applications but as yet no clear role. Articles, editorials and case reports published primarily in English and listed in Medline/ISI up to April 2000 or identified by a manual search have been reviewed in an attempt to provide a comprehensive overview of the use of photodynamic therapy in the alimentary tract.It is concluded that photodynamic therapy can be an effective treatment for superficial pre‐malignant mucosal lesions and early cancers, especially in diffuse disease. Suitable patients include those wishing to avoid surgery, high risk subjects or those in whom other forms of treatment have failed. Superiority over other methods of ablation has not so far been demonstrated. Cheaper and more effective photosensitizers and improved techniques of light delivery are likely to increase the application of photodynamic therapy.
Predictors of failure of Helicobacter pylori eradication with the standard ‘Maastricht triple therapy’
Authors: Perri F. , Villani M. R. , Festa V. , Quitadamo M. , Andriulli A. 
Published: March 2003

Background:Triple therapy with proton pump inhibitor, clarithromycin and amoxicillin has recently been proposed in Maastricht as first‐line treatment for H. pylori infection.Aim:To determine predictors of unsuccessful eradication.Methods:Two hundred and forty‐eight patients underwent endoscopy with biopsies for rapid urease test, histology and culture with antibiotic susceptibility tests, and 13C‐UBT. All infected patients were given pantoprazole (40 mg b.d.), clarithromycin (500 mg b.d.) and amoxicillin (1 g b.d.) for 1 week. Eradication was assessed by UBT at 4–6 weeks after therapy.Results:One hundred and sixty‐two of 248 patients (65%) were infected. Culture was positive in 144 (89%). Prevalence rates of metronidazole, clarithromycin and amoxicillin resistance were 14, 8 and 3%, respectively. Eradication rates (95% CI) were 63% (54.7–70.6) by intention‐to‐treat analysis and 67% (59.4–75.4) by per protocol analysis. Drug compliance was excellent and side‐effects were mild. Age ≥ 45 years (OR: 2.35, CI: 1.30–4.25), smoking (OR: 1.37, CI 1.01–1.87) and high pre‐treatment UBT results (OR: 1.36, CI: 1.08–1.72) were independent predictors of eradication failure. Gender, endoscopic findings, alcohol intake, and clarithromycin and amoxicillin resistance did not predict treatment failure.Conclusion:Despite the low prevalence of primary antibiotic resistance in our geographical area, triple therapy with pantoprazole, amoxicillin and clarithromycin achieves low eradication rates. Smoking, age and pre‐treatment UBT results are predictors of potential eradication failure.
Interleukin‐8 increases acetylcholine response of rat intestinal segments
Authors: Plattner V. , Leray V. , Leclair M.‐D. , Aubé A.‐C. , Cherbut C. , Galmiche J. P. 
Published: March 2003

Background: Interleukin‐8 (IL‐8) is a pro‐inflammatory cytokine highly expressed in inflammatory bowel diseases, but whose effects on intestinal motility are unknown.Aim: To characterize the role of IL‐8 in the contraction of rat intestinal segments.Methods: Contractile response to acetylcholine (ACh 10−6 M) in terminal ileal segments (including mucosa) from Wistar rats was measured before and after incubation (15, 30, 60 or 90 min) with IL‐8 (1 ng/mL), and after 60 min of incubation with different doses of IL‐8 (0, 0.1, 0.5, 1, 10 and 100 ng/mL). The effects of blocking neural transmission with tetrodotoxin (TTX) and inhibiting protein synthesis (cycloheximide) were tested. The contractile response of longitudinal muscle–myenteric plexus preparations (i.e. without mucosa) was measured after 60 min of incubation with 0.1 and 1 ng/mL of IL‐8.Results: IL‐8 increased ileal contraction induced by ACh 10−6 M. This augmentation was significant after 60 min of incubation (58%, P=0.01) and persisted after 90 min (18%, P=0.04). A 60‐min incubation period showed a dose‐related effect, beginning at 0.5 ng/mL (30%, P=0.003) and reaching a peak at 1 ng/mL (58%, P=0.01). The same effect was also observed on colonic segments. TTX did not affect the IL‐8 increase of ACh‐induced contractions, which was completely abolished by cycloheximide. IL‐8 had no significant effect on longitudinal muscle–myenteric plexus preparations.Conclusion: In vitro, IL‐8 increases contractile response of the ileum to ACh in a dose‐dependent manner. This effect is not neurally mediated, but seems to involve protein synthesis by intestinal mucosa.