bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cure of Helicobacter pylori infection in the elderly: effects of eradication on gastritis and serological markers
Authors: PILOTTO A. , DI MARIO F. , FRANCESCHI M. , LEANDRO G. , SOFFIATI G. , SCAGNELLI M. , BOZZOLA L. , VALERIO G. 
Published: October 2003

Background: Specific data on anti‐H. pylori treatments in elderly people are very scarce. The aim of the study was to evaluate in the elderly the efficacy of different anti‐H. pylori therapies and the behaviour of serum anti‐H. pylori antibodies, pepsinogen A and C, and PGA/PGC ratio induced by the anti‐H. pylori treatment. Methods: One hundred and twenty‐one dyspeptic patients aged >60 years (mean age, 73 years; range, 61–89 years) with H. pylori‐positive gastric ulcers (17 patients), duodenal ulcers (33 patients) or chronic gastritis (71 patients) were treated with one of the following anti‐H. pylori treatments: (A) omeprazole 20 mg/day plus azithromycin 500 mg/day for 3 days; (B) omeprazole 20 mg/day plus azithromycin 500 mg/day for 3 days plus metronidazole 250 mg q.d.s. for 7 days; (C) omeprazole 40 mg/day plus azithromycin 500 mg/day for 3 days plus metronidazole 250 q.d.s. for 7 days; (D) omeprazole 20 mg/day plus clarithromycin 250 b.d. for 7 days; (E) omeprazole 20 mg/day plus clarithromycin 250 b.d. for 7 days plus metronidazole 250 q.d.s. for 7 days; and (F) omeprazole 40 mg/day plus clarithromycin 250 mg b.d. for 7 days plus metronidazole 250 mg q.d.s. for 7 days. At the baseline and 2 months after therapy, endoscopy and serum anti‐H. pylori antibodies, pepsinogen A and C, and PGA/PGC ratio were measured. Results: Ten patients (8.2%) dropped out of the study. Six patients (4.9%) reported side‐effects. The eradication rates of the six regimens, expressed using intention‐to‐treat and per protocol analysis, were, respectively: (A) 39% and 44%; (B) 50% and 56%; (C) 65% and 77%; (D) 47% and 50%; (E) 85% and 90%; and (F) 83% and 87%. The triple therapy for regimens E and F was significantly more effective than dual therapies (regimens A and D; intention‐to‐treat=P<0.007, per protocol=P<0.001) or the triple therapy for regimens B and C (intention‐to‐treat=P<0.009, per protocol=P<0.03). Patients cured of H. pylori infection showed a significant decrease in the activity of gastritis (P<0.0001), a significant drop in IgG anti‐H. pylori (P=0.0004) and pepsinogen C (P<0.0001), and an increase in PGA/PGC ratio (P<0.001), while patients remaining H. pylori‐positive showed no changes in the serum parameters. Conclusions: In the elderly, triple therapy with omeprazole +metronidazole+clarithromycin for 1 week is well tolerated and highly effective; anti‐H. pylori antibody and PGC serum levels decrease soon after anti‐H. pylori therapy only in patients cured of H. pylori infection.
Adverse events in patients treated with 5‐aminosalicyclic acid: 1993–1994 pharmacovigilance report for Pentasa in France
Authors: MARTEAU P. , NELET F. , LE LU M. , DEVAUX C. 
Published: October 2003

Background: The incidence of the side‐effects of 5‐aminosalicylic acid (5‐ASA) in clinical practice is not known. Aim: To present the safety reports on the use of Pentasa in France. Methods: Pentasa‐related adverse events were recorded from 1 January 1993 to 31 December 1994. Spontaneous reports to Ferring S.A. came from physicians or pharmacovigilance regional centres. Results: In 1993 and 1994, 51 and 79 adverse events were reported; the estimated gross incidence was 6.6 and 9.0 per million days of therapy. Detailed information was obtained in 64% of cases in 1993 and 53% in 1994. Adverse events with a high likelihood of causalty included five cases of diarrhoea, 14 cases of pancreatitis, seven cases of liver abnormalities, seven of blood dyscrasias, two cases of renal insufficiency (one of which was in a fetus), and eight of cardiac disorders including three myocarditis. Conclusions: Pentasa seldom has adverse effects. The majority of the adverse events do not seem to be dose‐related. Clinicians should be aware of exceptional but severe adverse events including pancreatitis, cardiac disorders, blood dyscrasias and renal insufficiency.
The effects of cisapride on the topography of oesophageal peristalsis
Authors: STAIANO A. , CLOUSE R. E. 
Published: October 2003

Background: Topographic analysis of oesophageal motility in humans demonstrates sequential pressure regions in the peristaltic wave. This study was designed to see if cisapride preferentially affects any of the topographic regions. Methods: Fifteen asymptomatic volunteers received placebo, 10 mg or 20 mg of cisapride orally in a double‐blind, single‐dose trial. Topographic plots of oesophageal peristalsis through the oesophageal body and lower sphincter were analysed before and after drug administration for each subject. Results: Four sequential contraction segments through the oesophageal body and lower sphincter, separated by amplitude troughs, were again identified on contour plots in normal subjects. Dose‐related increases from cisapride were found in the contraction volume of the first smooth‐muscle segment (P<0.0001), in total contraction volume (P=0.005) and in the amplitude of the trough separating smooth‐muscle segments of the oesophageal body (P=0.005). Within the distal smooth‐muscle segment, significant drug effects were seen only in the cephalad half (P=0.03). Significant effects on conventional manometric parameters could not be demonstrated. Conclusions: Cisapride enhances contraction in the proximal smooth‐muscle segment of the oesophageal body and partially obliterates the pressure trough separating the adjacent smooth‐muscle segment. Considering the known effects of this agent on neural function, our findings support a gradient in cholinergic influence on peristalsis through the human smooth‐muscle oesophagus. Topographic analysis is a novel and sensitive way of examining the effects of pharmacological manipulations on oesophageal peristalsis.
Helicobacter pylori eradication in clinical practice: one‐week low‐dose triple therapy is preferable to classical bismuth based triple therapy
Authors: GODDARD A. F. , SPILLER R. C. 
Published: October 2003

Background: Both classical 2‐week bismuth based triple therapy and the newer 1‐week low‐dose omeprazole based triple therapies achieve high Helicobacter pylori eradication rates in controlled clinical trials and are in widespread use in routine clinical practice. However, their efficacy and acceptability in this setting is unproved. Methods: Over a 1‐year period, the notes for patients attending a dedicated H. pylori treatment clinic were audited. Assessments were made of patient demographics, diagnosis, smoking habits, use of H2‐antagonists, regimen used, efficacy of treatment, compliance and side‐effects experienced. Results: 223 sets of notes were audited. 89 patients received bismuth, tetracycline and metronidazole for two weeks and 111 patients received omeprazole, clarithromycin and either metronidazole (63 patients) or tinidazole (48 patients) for 1 week. Successful eradication was achieved in 75/89 (84.3%), 56/63 (89%) and 42/48 (88%), respectively, (P = N.S.). Severe side‐effects occurred in 11 (12%) of patients receiving bismuth based treatment compared to 1 (0.9%) patient receiving omeprazole based regimens (P<0.02). Treatment failure in patients receiving omeprazole based treatment was associated with smoking (P<0.05). Conclusions: Outside the context of clinical trials, both regimens achieved acceptable eradication rates. However, 1‐week low‐dose therapy is preferable due to the lower incidence of severe side‐effects.
One week triple therapy with omeprazole, clarithromycin and tinidazole for Helicobacter pylori: differing efficacy in previously treated and untreated patients
Authors: MOSHKOWITZ M. , KONIKOFF F. M. , PELED Y. , BRILL S. , HALLAK A. , TIOMNY E. , SANTO M. , BUJANOVER Y. , GILAT T. 
Published: October 2003

Background: Triple therapy with omeprazole, clarithromycin, and tinidazole (OCT) has been found to be highly effective against Helicobacter pylori infection. However, its efficacy as a second line regimen for patients who failed metronidazole‐based triple therapy has not been evaluated. Aim: The aim of this study was to evaluate the efficacy of low‐dose, short‐term OCT therapy in an Israeli population, and to compare results obtained in previously treated and untreated patients. Methods: Patients with duodenal or gastric ulcers and chronic antral gastritis with H. pylori infection as assessed by rapid urease test and/or 14C urea breath test (14C‐UBT), were studied. All patients received omeprazole 20 mg b.d., clarithromycin 250 mg b.d. and tinidazole 500 mg b.d. for 7 days. Eradication was assessed by 14C‐UBT 4 weeks after treatment. Results: One hundred and fourty‐four patients (M/F=81/63) were enrolled (mean age 48.1 years, range 12–78). Eradication of H. pylori was significantly different between patients who were initially treated with this regimen (90/94, 96%) and patients who had previously failed to eradicate H. pylori with standard triple therapy (27/50, 54%). Moreover, the eradication rate was significantly decreased in patients with more than one previous failure (9/22, 41%) compared to that in patients with only one failure (18/29, 62%). No other differences such as age, gastric pathology, ethnic origin, smoking habits, or pre‐treatment urease activity were found to influence the eradication rate. Conclusions: One‐week low‐dose triple therapy with OCT is highly effective as an initial therapy in eradicating H. pylori infection. The efficacy is significantly lower when given as a second line treatment in patients who have previously failed to eradicate H. pylori with bismuth‐based standard triple therapy.
Treatment of left‐sided ulcerative colitis with butyrate enemas: a controlled trial
Authors: STEINHART A. H. , HIRUKI T. , BRZEZINSKI A. , BAKER J. P. 
Published: October 2003

Background: The colonic mucosa is highly dependent upon the presence of luminal nutrients. This dependence is most marked in the distal colon. The major luminal nutrients are short chain fatty acids that are produced as a by‐product of colonic fermentation of carbohydrates. Butyrate appears to be the short chain fatty acid most avidly metabolized by the colonic mucosa. It has been suggested that ulcerative colitis is, at least in part, related to an energy deficiency state of the colonic mucosa which may be secondary to impaired short chain fatty acid production, uptake or utilization. The objective of this study was to determine if butyrate given as enema therapy is effective in the treatment of active distal ulcerative colitis. Methods: Thirty‐eight patients with distal ulcerative colitis were randomly assigned to receive nightly butyrate (n=19) or saline/placebo (n=19) enemas. Butyrate enemas consisted of 60 mL of 80 mm sodium butyrate titrated to a pH of 7.0. Patients were assessed clinically and endoscopically at baseline and at 3 and 6 weeks follow‐up. Pre‐ and post‐treatment mucosal biopsies were assessed histologically. Response to therapy was determined by changes in a 12‐point clinical disease activity index score based on patient symptoms, endoscopic mucosal appearance and physicians' global assessment. Results: Clinical improvement was noted in seven of 19 (37%) butyrate‐treated patients and nine of 19 (47%) placebo‐treated patients (P=0.51). Clinical remission was achieved in three patients in each group (16%). No toxicity was observed in either treatment arm. Conclusions: The results suggests that once nightly 60 mL butyrate enemas (80 mmol/L) are not efficacious in the treatment of distal ulcerative colitis.
Nocturnal intragastric acidity after over‐the‐counter doses of famotidine, ranitidine or placebo
Authors: GRIMLEY C. E. , COTTRELL J. , MANN S. G. , STAUFFER L. , NWOKOLO C. U. 
Published: October 2003

Aim:To compare the inhibitory effects of over‐the‐counter doses of famotidine or ranitidine on nocturnal intragastric acidity in a placebo‐controlled study.Methods:Twelve‐hour intragastric acidity was measured simultaneously in 24 healthy subjects who ate a standard meal at 18.30 h and were dosed (at 19.30 h) with either famotidine 10 mg, ranitidine 75 mg or placebo in a balanced three‐period crossover design. Five‐millilitre aliquots of gastric juice were aspirated half‐hourly 0–3 h post‐dose, and then hourly until the end of the study. pH was measured with a glass electrode. Integrated pH (area under the curve (AUC) of the pH–time curve) was calculated for the intervals 0–12 h and 9–12 h post‐dose. Statistical analysis was by ANOVA.Results:In the 0–12 h post‐dose period, when the 24 subjects were dosed with placebo, mean AUC was 2.12, dosed increasing by 75% to 3.70 with famotidine (P < 0.001) and by 81% to 3.83 with ranitidine (P < 0.001). In the 9–12 h post‐dose period, when the subjects were dosed with placebo, mean AUC was 2.13 increasing by 91% to 4.07 with famotidine (P < 0.001) and by 79% to 3.82 with ranitidine (P < 0.001). There was no significant difference between the pH‐raising effects of famotidine and ranitidine in both periods.Conclusions:Famotidine and ranitidine in over‐the‐counter doses have a similar, sustained, effect on post‐prandial nocturnal intragastric acidity in healthy subjects lasting up to 12 h after oral dosing.
Topical benzocaine anaesthesia lacks analgesic effects in painful non‐acid oesophagitis
Authors: BECKER K. , BECKER C. , FRIELING T. , HÄUSSINGER D. 
Published: October 2003

BackgroundNo established treatment exists for pain relief in symptomatic non‐acid oesophagitis. One of the most common topical anaesthetics is benzocaine which has been demonstrated to produce excellent analgesia on oral mucous membranes.MethodsIn a prospective, placebo‐controlled, balanced, single‐blinded study, 26 patients with retrosternal discomfort or odynophagia due to painful non‐acid oesophagitis were treated either with oral benzocaine 0.75% solution (n = 14) or with benzocaine‐free solvent (placebo, n = 12) at a daily dose of 20–40 mL, for up to 6 consecutive days (median 5.5 days). During the study period patients recorded subjective pain scores for both complaints on visual analogue scales.ResultsBenzocaine did not affect pain scores for any of the two symptoms, nor did it alter global subjective or objective assessment of therapy outcome in treated compared to untreated subjects (P > 0.05). There was a non‐significant tendency for placebo patients to stop prematurely their study medication more often, because of lack of analgesic efficacy (P = 0.098).ConclusionsTopical benzocaine cannot be recommended for routine symptomatic pain relief in non‐acid oesophagitis. By indirect evidence, it is assumed that pain perception of non‐acid oesophagitis is not preferentially mediated by superficially located mucosal nociceptors.
Effect of omeprazole on the bioavailability of unmodified and phospholipid‐complexed aspirin in rats
Authors: GIRAUD M.‐N. , SANDUJA S. K. , FELDER T. B. , ILLICH P. A. , DIAL E. J. , LICHTENBERGER L. M. 
Published: October 2003

Background:Treatment and prevention of non‐steroidal anti‐inflammatory drug‐induced gastropathy involve the concurrent use of antisecretory drugs. Recently, we have shown that the ability of these drugs to increase the intragastric pH to values pKa of NSAIDs compromises their therapeutic activity. In the present study, we evaluated the potential of omeprazole to interfere with the bioavailability of aspirin administered to rats either alone or complexed with the zwitterionic phospholipid, dipalmitoylphosphatidylcholine (DPPC).Methods:Aspirin or aspirin/DPPC was administered intragastrically to rats pre‐dosed with either saline or omeprazole. Concentrations of aspirin and salicylic acid in the blood and the gastric mucosa were assessed by HPLC and the 6‐keto‐PGF1α gastric mucosal concentration by radioimmunoassay.Results:Gastric absorption of aspirin and its relative bioavailability were reduced by an antisecretory dose of omeprazole; its inhibitory effect on gastric prostaglandin synthesis was consequently attenuated. However, these effects could be partly overcome if aspirin was administered as a complex with DPPC.Conclusions:These observations suggest that: (i) DPPC increases the lipid solubility and gastric permeability of NSAIDs; and (ii) neutralization of the gastric pH results in a shift of aspirin absorption toward the intestine where it could be degraded to salicylic acid.
Nicotine enemas for active ulcerative colitis—a pilot study
Authors: GREEN J. T. , THOMAS G. A. O. , RHODES J. , WILLIAMS G. T. , EVANS B. K. , RUSSELL M. A. H. , FEYERABEND C. , RHODES P. , SANDBORN W. J. 
Published: October 2003

BackgroundSince transdermal nicotine is of value in the treatment of active ulcerative colitis but is often associated with side‐effects, an alternative in the form of topical therapy with nicotine enemas has been developed.MethodsIn an open study, 22 patients with active colitis, all non‐smokers, were asked to take a 100 mL enema containing 6 mg of nicotine every night for 4 weeks. Pre‐trial treatment using mesalazine (n=16), oral prednisolone (8), cyclosporin (1) and azathioprine (1) was kept constant for the month prior to assessment and during the study period. Symptoms, with stool frequency, were recorded on a diary card and an endoscopy was performed with rectal biopsy at the beginning of the study and after 4 weeks.ResultsSeventeen of the 22 patients completed 1 month of treatment. Mean duration of relapse was 29 weeks, range 3–94. Sixteen of 17 improved their St Mark's score. Urgency and stool frequency improved in 12 patients, sigmoidoscopic and histological scores in 10. Three patients had a full remission of symptoms with normal sigmoidoscopy. Six of 10 with a partial response continued with the enemas for a second month and five showed further improvement with full remission in two. The enema appeared effective when added to conventional treatment and produced few side‐effects.ConclusionTopical nicotine therapy for ulcerative colitis may have a place in future management, but controlled studies are needed.
Short‐course therapy with amoxycillin–clarithromycin triple therapy for 10 days (ACT‐10) eradicates Helicobacter pylori and heals duodenal ulcer
Authors: WURZER H. , RODRIGO L. , STAMLER D. , ARCHAMBAULT A. , ROKKAS T. , SKANDALIS N. , FEDORAK R. , BAZZOLI F. , HENTSCHEL E. , MORA P. , ARCHIMANDRITIS A. , MEGRAUD F. 
Published: October 2003

Background:Whilst the role of Helicobacter pylori eradication in managing duodenal ulcers has been established, consensus regarding the ideal regimen has not been achieved.Methods:Patients with H. pylori‐positive active duodenal ulcer were randomly assigned to receive triple therapy with amoxycillin 1000 mg b.d. + clarithromycin 500 mg b.d. + omeprazole 20 mg daily for 10 days (ACT‐10) or dual therapy with clarithromycin 500 mg t.d.s. + omeprazole 40 mg daily for 14 days (Dual). No additional acid suppression was provided following eradication therapy. Endoscopy, with biopsy for culture and histology, as well as 13C‐urea breath testing (13C‐UBT) were performed pre‐treatment to assess H. pylori infection. H. pylori eradication was established at 4–6 weeks follow‐up with culture (2 antral, 1 corpus biopsies), histology (2 antral biopsies), and 13C‐UBT. Ulcer healing by endoscopy and change in clinical symptoms were also assessed at 4–6 weeks.Results:Two hundred and sixty‐seven (267) patients were randomized to ACT‐10 (n=137) or Dual therapy (n=130). By per‐protocol and intention‐to‐treat analyses, H. pylori eradication at 4–6 weeks follow‐up was 91% (115/127) and 88% (120/136), respectively, for ACT‐10 patients and 59% (68/115) and 55% (72/130), respectively, for Dual therapy patients (P<0.001 for both analyses). Ulcer healing was high in both treatment groups: ACT‐10, 93% (118/127) and 90% (122/136), respectively; and Dual therapy, 91% (104/114) and 85% (111/130), respectively. Pre‐treatment resistance to clarithromycin was low (4%, 8/214) as compared to metronidazole resistance which was over 40%. Emergence of resistance to clarithromycin was observed in 2% of patients receiving ACT‐10 and in 25% of those receiving Dual therapy. ACT‐10 and Dual therapy patients experienced similar rates of drug‐related adverse events (33% vs. 32%, respectively) and discontinuation from therapy due to an adverse event (1.5% vs. 5%, respectively). More than 90% of patients were compliant with each prescribed medication.Conclusion:In patients with active duodenal ulcer, a 10‐day course of amoxycillin–clarithromycin‐based triple therapy without additional acid suppression is highly effective in eradicating H. pylori and healing duodenal ulcer.
Inhibition of intragastric acidity in healthy subjects dosed with ranitidine 75 mg: a comparative study with cimetidine and placebo
Authors: GRIMLEY C. E. , CONSTANTINIDES S. , SNELL C. C. , MILLS J. G. , NWOKOLO C. U. 
Published: October 2003

BackgroundDespite the widespread use of over‐the‐counter H2‐receptor antagonists little is known about their duration of action on human gastric acid secretion. There are studies reporting inhibitory effects for up to 9 h post‐dose but few data beyond this period.MethodsProfiles of 20‐h intragastric acidity were measured simultaneously in 24 healthy subjects who were dosed (at 12.30 h) with either ranitidine 75 mg, cimetidine 200 mg or placebo in a three‐way crossover study, according to a standard protocol. Five‐millilitre aliquots of gastric juice were aspirated half‐hourly during the day (0–10 h post‐dose) and hourly overnight (10–20 h post‐dose). pH was measured to three decimal places with a glass electrode. Weighted intragastric acidity (AUC/time) was calculated for both day‐ and night‐times using 2.5‐h intervals during the day and 5‐h intervals at night. Statistical analysis was by ANOVA.ResultsThe results are expressed as mean weighted intragastric acidity (mmol/L). (i) Daytime (0–10 h post‐dose): when dosed with placebo the weighted intragastric acidity was 31.03, decreasing to 10.37 (P < 0.001 vs. placebo) and 16.23 (P < 0.001 vs. placebo) when treated with ranitidine and cimetidine, respectively. Ranitidine inhibited weighted intragastric acidity to a greater degree than cimetidine (P < 0.001) during this period. (ii) Night‐time (10–20 h post‐dose): when dosed with placebo the weighted intragastric acidity was 21.36 decreasing to 16.65 (P < 0.001 vs. placebo) when dosed with ranitidine and remaining unchanged at 20.03 (P = 0.886 vs. placebo) when dosed with cimetidine. Ranitidine inhibited weighted intragastric acidity to a greater degree than cimetidine (P = 0.010) during this period. A sub‐analysis of the two 5‐h intervals showed that compared to placebo, ranitidine inhibited weighted intragastric acidity significantly in the 10–15 h period. However, its effect in the 15–20 h period did not differ from placebo.ConclusionsIn healthy subjects, the inhibitory effect of ranitidine 75 mg on intragastric acidity can be detected 10–15 h after an oral dose. By contrast, the inhibitory effect of cimetidine 200 mg seems to be restricted to the first 10 h.