bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of omeprazole on gastro‐oesophageal reflux and symptoms during strenuous exercise
Authors: Peters  , De Kort A. F. C. C. , Van Krevelen H. , Akkermans  , Van Berge Henegouwen G. P. , Bol  , Mosterd  , De Vries W. R. 
Published: March 2003

Background: Strenuous exercise exacerbates gastro‐oesophageal reflux and symptoms and this may be diminished by antisecretory medication with omeprazole.Methods: Fourteen well‐trained athletes (13 men, one woman), who indicated suffering from either heartburn, regurgitation or chest pain during competition running, performed two experimental trials at 2‐week intervals using a randomized, double‐blind, placebo‐controlled crossover design. During the 6 days preceding the trial and on the trial day itself either 20 mg of omeprazole or a placebo was administered. Two hours after a low‐fat breakfast and 1 h after the last study dose, the trial started with five successive 50‐min periods: rest, three running periods on a treadmill, and recovery. Reflux (percentage time and number of periods oesophageal pH < 4) was measured with an ambulant pH system during these periods.Results: Compared to rest, reflux lasted significantly longer and occurred more frequently during the first running period, irrespective of the intervention, whereas during the second running period this effect was only observed with the placebo. Reflux occurred for longer and more frequently with the placebo than with omeprazole, but this was significant during the first two running periods only. Seven subjects reported heartburn, regurgitation and/or chest pain during exercise, irrespective of the intervention. Only a minority of the symptom periods was actually associated with acid reflux and in all cases this concerned periods with heartburn.Conclusions: Running‐induced acid reflux, but not symptoms, were decreased by omeprazole, probably because most symptoms were not related to acid reflux.
Effect of ursodeoxycholic acid administration in patients with acute viral hepatitis: a pilot study
Authors: Fabris  , Tositti  , Mazzella  , Zanetti  , Nicolin  , Pellizzer  , Benedetti  , De Lalla F. 
Published: March 2003

Background: Ursodeoxycholic acid (UDCA) is able to improve biochemical markers of cholestasis, with a parallel decrease in transaminases, in various cholestatic liver diseases.Aim: To evaluate the effects of UDCA administration on acute viral hepatitis‐related cholestasis and the course of acute viral hepatitis.Methods: Seventy‐nine consecutive patients with acute viral hepatitis (HBV: 43, HCV: 11, HAV: 15, HEV: 3, Non A‐E: 7) were randomized to receive either UDCA for 3 weeks or no treatment. Liver biochemistry and serum bile acid determinations were run at weekly intervals.Results: No significant differences were observed in mean percentage decreases in transaminases between treated and untreated patients. By contrast, cholestatic indexes decreased significantly more quickly in patients treated with UDCA than in controls, and this effect was more evident in patients with increasing alanine transaminase levels at admission. After a peak at the end of the first week of therapy, serum levels of conjugated ursodeoxycholic acid (CUDCA) showed a gradual decrease. Conjugated cholic acid (CCA) and chenodeoxycholic acid (CCDCA) showed a progressive decrease with the resolution of viral hepatitis, but no influence of UDCA administration was observed.Conclusions: Our study demonstrates that UDCA significantly improves cholestatic indices in patients with acute viral hepatitis, but this effect does not seem to affect the course of the illness.
Regression of columnar‐lined (Barrett’s) oesophagus with omeprazole 40 mg daily: results of 5 years of continuous therapy
Authors: Wilkinson  , Biddlestone  , Gore  , Shepherd  
Published: March 2003

Background: We have previously reported the effect of 2 years of omeprazole 40 mg daily on columnar‐lined (Barrett’s) oesophagus (CLO).Aims: In the present study, follow‐up has been extended to 5 years to assess the macroscopic and microscopic effects of continuing therapy.Patients and methods: The 23 patients have been followed for up to a further 3 years. Endoscopy with multiple biopsies was performed at the end of years 3, 4 and 5.Results: Although there had been a statistically significant regression in the length of CLO after 2 years, there was no overall further measurable change after 5 years. However, one patient showed complete macroscopic and microscopic regression. The number and size of macroscopic squamous islands within the CLO continued to increase, and there was a further increase in microscopic squamous re‐epithelialization of surface mucosa, gland ducts and Barrett’s gland tissue. Low‐grade dysplasia was found consistently in one patient in biopsies taken up to the end of year 3 but it could not be detected thereafter.Conclusions: Omeprazole 40 mg daily appears to have beneficial effects on CLO, although it rarely induces a complete regression. Whether the benefits will reduce the risk of malignant transformation is unknown.
The effect of dosing with omeprazole on the accuracy of the 13C‐urea breath test in Helicobacter pylori‐infected subjects
Authors: Connor  , Seow  , Ngu  , Katelaris  
Published: March 2003

Background: The 13C‐urea breath test (13C‐UBT) is an accurate means of Helicobacter pylori diagnosis. However, proton pump inhibitors may suppress H. pylori and cause false negative results.Aim: To study the kinetics of H. pylori suppression by omeprazole during and after short‐term use.Methods: Volunteers underwent a baseline 13C‐UBT (13C‐urea 100 mg). H. pylori‐positive subjects took omeprazole 20 mg daily for 14 days. Those who remained 13C‐UBT positive (δ13CO2 ≥ 5) continued omeprazole for a further 14 days. 13C‐UBTs were performed weekly on omeprazole and then every second day after it was stopped. False negatives occurred when δ13CO2 fell to < 5.Results: In 25 H. pylori‐positive subjects (mean age 43.9 ± 2.4 years; 21 females, 4 males) the mean baseline δ13CO2 was 28.1 ± 3.4. False negative breath tests occurred in three subjects after 7 days of omeprazole and in a further four subjects after 14 days. A further six subjects developed negative tests between Days 14 and 28. Following cessation of omeprazole, the 13C‐UBT became positive again in 12/13 subjects within 4 days and in all within 6 days, with a mean recovery to 99.9 ± 18.6% of baseline δ13CO2.Conclusions: False negative 13C‐UBTs are common during treatment with omeprazole and occur after as little as 7 days. Return to positive test results is rapid after cessation of omeprazole. These findings are relevant to the timing of testing in clinical practice.
Ibuprofen augments gastrointestinal symptoms in lactose maldigesters during a lactose tolerance test
Authors: Peuhkuri  , Nevala  , Vapaatalo  , Moilanen  , Korpela  
Published: March 2003

Background: Clinical symptoms during lactose tolerance test mimic those seen after therapeutic administration of prostaglandins, and resemble inflammatory processes.Aim: To investigate the possibility that lactose‐induced gastrointestinal symptoms are associated with prostaglandins and/or nitric oxide.Methods: After an overnight fast, nine maldigesters ingested lactose or sucrose with or without an inhibitor of prostaglandin synthesis (ibuprofen), in a randomised double‐blind crossover trial. Gastrointestinal symptoms, concentrations of PGE2‐M in blood and urine, and urinary 6‐keto PGF1α (as indicators of prostaglandin synthesis), and urinary nitrate and nitrite as well as cyclic GMP excretions (as indicators of nitric oxide formation), were measured.Results: Ibuprofen increased the first 3‐h symptom scores (flatulence + borborygmi + abdominal bloating + pain) caused by lactose (P=0.008) but not sucrose. The concentrations of PGE2‐M in the plasma and in the urine were unaffected. Lactose increased the urinary excretion of 6‐keto PGF1α by about 30% (P=0.17), which was inhibited by ibuprofen (P=0.02). The production of nitric oxide was unaffected by lactose or ibuprofen.Conclusion: The inhibition of prostaglandin synthesis intensified gastrointestinal symptoms in lactose maldigesters, suggesting a negligible role for prostanoids in lactose‐induced symptoms.
5‐HT4 receptor antagonism in irritable bowel syndrome: effect of SB‐207266‐A on rectal sensitivity and small bowel transit
Authors: Houghton  , Jackson  , Whorwell  , Cooper  
Published: March 2003

Background: Pre‐clinical studies indicate that the 5‐hydroxytryptamine (5‐HT)4 receptor may be involved in the pathophysiology of irritable bowel syndrome and that antagonism of this receptor may be an effective therapeutic strategy.Aim: To investigate the effects of SB‐207266‐A, a selective 5‐HT4 receptor antagonist on rectal sensitivity and small bowel transit in patients with irritable bowel syndrome.Methods: Eighteen patients with diarrhoea‐predominant irritable bowel syndrome and a history of increased rectal sensitivity were randomized to receive either SB‐207266‐A (20 mg) or placebo for 10 days. Following a washout period, patients were then crossed over to receive the alternative therapy for 10 days. Rectal sensitivity and orocaecal transit time were assessed on day 10 of each treatment period. In addition, patients were asked whether they had experienced any changes in their symptoms.Results: Fifteen patients completed the study. SB‐207266‐A significantly increased orocaecal transit time towards normal (placebo: 5.3 h (4.0–7.2 h), mean (IQR) vs. SB‐207266‐A: 6.5 h (4.8–8.0 h); P=0.027) and tended to decrease rectal sensitivity (volume to discomfort 89 mL (60–150 mL), geometric mean (IQR) vs. 107 mL (75–150 mL); P=0.134). Eleven out of 15 patients reported symptomatic improvements with SB‐207266‐A but none with placebo. SB‐207266‐A was well tolerated.Conclusion: Our results support a role for the 5‐HT4 receptor in the pathophysiology of irritable bowel syndrome and suggest that the selective 5‐HT4 antagonist, SB‐207266‐A, is worthy of further evaluation in this disorder.
Eradication of Helicobacter pylori does not decrease the long‐term use of acid‐suppressive medication
Authors: Tan  , Hartog G. Den , Mulder  
Published: March 2003

Background: Many patients are not symptom‐free after eradication therapy for Helicobacter pylori and continue to use proton pump inhibitors or H2‐receptor antagonists (H2‐RAs).Aim: To ascertain whether a cohort of patients treated for H. pylori were still taking either proton pump inhibitors or H2‐RAs more than 4 years after H. pylori eradication therapy.Methods: In 1993–94, a cohort of 167 patients were given eradication therapy for their H. pylori infection. By means of questionnaires to the patient, general practitioner and pharmacist we were able to retrieve data from 151 patients. The use (at the time of questionnaire) of proton pump inhibitors or H2‐RAs was noted.Results: Indications for eradication therapy were peptic ulcer disease: 28 patients (19%) or functional dyspepsia: 123 patients (82%). Mean time of follow‐up was 1466 ± 21 days. In this group, 77 patients (51%) still used acid‐suppressive medication (proton pump inhibitors 44% and H2‐RAs 7%) at the time of the survey (mean follow‐up more than 4 years after eradication). In the group treated for peptic ulcer disease (n=28), only nine patients still used proton pump inhibitors or H2‐RAs. In contrast, 68 patients who were treated for functional dyspepsia (total number 123) still used proton pump inhibitors or H2‐RAs (55%) (P < 0.05).Conclusion: Even after successful H. pylori eradication, < 50% of patients stop acid‐suppressive therapy. This contributes significantly to economic cost and raises doubts about the practice of routinely eradicating H. pylori in patients with functional dyspepsia. In contrast, the majority of peptic ulcer patients are able to stop acid‐suppressive medication.
Use of a dried plasma collection card for simplified diagnosis of Helicobacter pylori infection
Authors: Kearney  , Boes  , Peacock  
Published: March 2003

Objectives: To compare testing for Helicobacter pylori IgG antibodies using a dried plasma collection card device with specimens obtained by venepuncture.Methods: Eighty‐four patients underwent testing for H. pylori IgG antibodies by venepuncture and by fingerstick using a single drop of blood placed on each of two dried plasma collection card devices. The correlation of venepuncture results to dried plasma card results was assessed.Results: There was a high degree of correlation of EIA results between venepuncture and dried plasma card specimens (r=0.98). The qualitative result of the first dried plasma card and venepuncture specimen testing differed in 7 of 84 patients and for the second dried plasma card differed in 7 of 82 patients. The first dried plasma card was 93% sensitive and 100% specific and the second was 93% sensitive and 98% specific as compared to the venepuncture result. There was a high degree of correlation between the first and second dried plasma cards (r=0.996).Conclusions: The dried plasma collection card has adequate sensitivity and excellent specificity as compared to venepuncture specimens and is a feasible alternative for H. pylori IgG antibody testing.
Omeprazole, clarithromycin and furazolidone for the eradication of Helicobacter pylori in patients with duodenal ulcer
Authors: Dani  , Queiroz  , Dias  , Franco  , Magalhães  , Mendes  , Moreira  , De Castro  , Toppa  , Rocha  , Cabral  , Salles  
Published: March 2003

Aim:To evaluate the efficacy of omeprazole plus clarithromycin and furazolidone in Helicobacter pylori eradication and duodenal ulcer healing in Brazilian patients.Methods:Forty H. pylori‐positive patients with duodenal ulcer were randomized to receive 20 mg omeprazole o.m. or b.d. for 1 month plus 500 mg clarithromycin (b.d.) and 200 mg furazolidone (b.d.) for 1 week.Results:Three months after the end of the treatment the eradication rates were 90% by intention‐to‐treat analysis, and 97% by per protocol analysis. Mild side‐effects were observed in 25 patients, none of whom abandoned the protocol. No difference was observed between the 20 mg and 40 mg omeprazole daily doses. Cure or significant improvement of the symptoms and of the histological alterations were observed after H. pylori eradication.Conclusion:Our results demonstrate that clarithromycin and furazolidone in combination with omeprazole are a good alternative for H. pylori eradication in Brazilian patients with duodenal ulcer.
Impact of advertisement and clinic populations in symptoms and perception of irritable bowel syndrome
Authors: Lee  , Fitzgerald  , Naliboff  , Schmulson  , Liu  , Fullerton  , Mayer  , Chang  
Published: March 2003

Background:This study assessed the impact of recruitment on irritable bowel syndrome clinical trials, by determining whether irritable bowel syndrome patients recruited from advertisement or a specialty clinic differ in clinical and physiologic measures.Methods:We prospectively surveyed 657 irritable bowel syndrome patients who either: (i) were referred from a functional bowel disease clinic (52%); or (ii) responded to advertisement for clinical trials (48%), using questionnaires about bowel and psychological symptoms, and quality of life. In a subset of 42 irritable bowel syndrome patients (29 advertisement and 15 clinic patients), rectal discomfort thresholds were measured before and after repetitive sigmoid stimulation.Results:While the advertisement population more commonly consulted primary care physicians, the clinic population more commonly consulted gastroenterologists. The clinic population reported more prevalent and severe abdominal pain, and higher psychological symptom scores, while the advertisement population had greater quality of life. In the visceral perception studies, both subgroups were hypersensitive to rectal distension.Conclusion:Compared to the clinic population, the advertisement population had less severe abdominal pain and psychological symptoms, better quality of life but similar visceral perception. The differences in clinical self‐reports may have consequences for enrolment of these different patient populations into clinical trials.
Ursodeoxycholic acid has no influence on function after restorative proctocolectomy in ulcerative colitis
Authors: Tan  , Morton  , Bain  , Keighley  
Published: March 2003

Background:Poor pouch function is associated with impaired bile acid absorption and increased faecal loss of bile acids. Bile acid replacement therapy might therefore be of clinical benefit, provided that diarrhoea is not aggravated by therapy.Aim:To investigate the role of exogenous bile acid therapy in patients with poor pouch function after restorative proctocolectomy for ulcerative colitis.Patients and methods:Twenty ulcerative colitis patients with poor pouch function (score > 4 on a 12‐point score) were recruited for inclusion to a prospective, randomized, double‐blind crossover, placebo‐controlled trial of ursodeoxycholic acid (10 mg/kg per day in two divided doses for 1 month).Results:A total of 16 patients completed the study. There was no significant difference in the functional score or bowel frequency following treatment irrespective of whether the active treatment was given before or after placebo.Conclusions:We conclude that ursodeoxycholic acid given over 4 weeks had no influence on functional score or bowel frequency after restorative proctocolectomy for U.C.
Non‐steroidal anti‐inflammatory drugs inhibit Helicobacter pylori‐induced human neutrophil reactive oxygen metabolite production in vitro
Authors: Jones‐Blackett  , Hull  , Davies  , Crabtree  
Published: March 2003

Background: Helicobacter pylori infection is associated with increased production of gastric mucosal reactive oxygen metabolites which have been implicated in mucosal damage and carcinogenesis. In vitro, neutrophils produce reactive oxygen metabolites following activation by H. pylori. Non‐steroidal anti‐inflammatory drugs (NSAIDs) inhibit neutrophil activation by several factors, e.g. N‐formyl‐methionyl‐leucyl‐phenyalanine (f‐MLP).Aim:To examine the effect of NSAIDs on H. pylori‐induced reactive oxygen metabolite production by human peripheral blood neutrophils.Methods:Neutrophils were stimulated by H. pylori (NCTC 11637) water extract or f‐MLP in the presence or absence of NSAIDs. Reactive oxygen metabolite activity was measured by luminol‐enhanced chemiluminescence.Results: H. pylori water extract stimulated a sevenfold increase in chemiluminescence which was inhibited dose‐dependently by diclofenac. All six NSAIDs studied (at 10–4 M) significantly inhibited H. pylori‐and f‐MLP‐stimulated neutrophil reactive oxygen metabolite production. Meclofenamic acid and diclofenac had the greatest inhibitory effects on both H. pylori and f‐MLP‐stimulated neutrophil reactive oxygen metabolite production. The inhibitory effects of other NSAIDs varied with the activation stimulus. NSAIDs did not quench reactive oxygen metabolites generated in a cell‐free xanthine:xanthine oxidase assay.Conclusion:Several NSAIDs attenuate H. pylori‐induced neutrophil reactive oxygen metabolites production in vitro. This may be relevant to a potential chemopreventative role in gastric cancer and to a possible lack of synergy between H. pylori and NSAID use regarding peptic ulceration.
Is Helicobacter pylori status relevant in the management of GORD?
Authors: Vigneri S. , Termini R. , Savarino V. , Pace F. 
Published: March 2003

SummaryThere is growing interest in the relationship between H. pylori infection and gastro‐oesophageal reflux disease (GORD). However, this relationship is complex, as yet not fully elucidated, and probably based on a multiplicity of factors. The prevalence of H. pylori infection in patients with GORD is similar, more often lower than in matched controls. There is a negative correlation between H. pylori infection and the severity of GORD. There are many hypothetical mechanisms by which H. pylori infection may protect from the development of GORD. Conversely, there are many possible mechanisms by which H. pylori infection could theoretically foster the GORD. Patients after H. pylori eradication may develop GORD, and this seems to suggest a protective role of H. pylori infection, but other possible explanations include weight gain after H. pylori eradication, changes in dietary habits and smoking, and pre‐existing GORD. H. pylori infected patients treated by various acid‐inhibiting therapies such as proton pump inhibitors (PPIs), H2‐receptors antagonists (H2‐RA) or vagotomy, have an increase of their corpus gastritis severity, both in the activity of inflammation and in the density of organisms. Long‐term therapy of GORD in H. pylori infected may lead to rapid progression of atrophic gastritis intestinal metaplasia and dysplasia, and increase the risk of developing gastric cancer. More recently it has been shown that H. pylori infection may interfere with the acid suppressive therapies used for treating GORD.In our opinion the progression of gastritis depends on the threshold of acid output at which H. pylori can ‘flourish’. Recently interest is growing on gastric transitional zones and Helicobacter ecology. Any decrease of acid secretion changes the behaviour of H. pylori: the activity of gastritis improves in the antrum, but it deteriorates in the body. During proton pump inhibitor treatment, H. pylori redistribution occurs within the stomach, from an antral to a corpus or fundus prevalent pattern; corpus‐fundus gastritis, exacerbated by PPI therapy, may result both in a diminished acid secretion and gastro‐oesophageal reflux.The interest in Barrett's oesophagus is growing due to the associated risk of adenocarcinoma. The literature seems to demonstrate that the prevalence of H. pylori infection of the stomach in Barrett's oesophagus patients is not different from that exhibited by controls, roughly one‐third of the subjects. Intestinal metaplasia of the gastric cardia seems to be equally frequent in patients with and without GORD. Finally, it appears unlikely that a causal relationship exists between H. pylori infection and Barrett's‐associated adenocarcinoma.
A retrospective study of the usefulness of acid secretory testing
Authors: Metz  , Starr  
Published: March 2003

Background:Gastric analysis is useful for diagnosing and monitoring the control of hypersecretory conditions and to distinguish appropriate from inappropriate causes of hypergastrinaemia. Pentagastrin, used to measure maximal acid output (MAO), is no longer available in the USA.Methods:We examined the University of Pennsylvania Health System gastric analysis database, which includes demographic data, study indications, gastric analysis, and serum gastrin and secretin testing results according to referral indications, paying specific attention to discordant basal acid output (BAO) and MAO measurements.Results:One hundred and twenty‐four gastric analyses were performed in 103 patients (42 males, mean age 47.5 years, 14 with prior acid‐decreasing surgery). Recurrent ulceration or pain unresponsive to antisecretory therapy was the indication in 42 patients. Twelve were hypersecretory, including three each with isolated elevations of BAO or MAO. Hypergastrinaemia was the indication in 35 patients. Five were hypersecretory (four with Zollinger–Ellison syndrome), three had isolated MAO elevations and 16 were hypo‐ or achlorhydric, indicating appropriate hypergastrinaemia. Of the seven patients with isolated MAO elevations, two had clear benefit from the stimulated portion of the study (four additional patients had equivocal benefit).Conclusions:Gastrin concentrations cannot be interpreted without knowledge of acid secretory capacity. MAO measurement has a small but significant benefit over measuring BAO alone.