bluuebunny/crossref_metadata_2025_split huggingface dataset:
Short report: the effect of omeprazole on Helicobacter pylori and associated gastritis
Authors: DAW M. A. , DEEGAN P. , LEEN E. , O'MORÁIN C. 
Published: July 2010

SUMMARYTwenty‐one patients with endoscopically confirmed duodenal ulceration, who had failed to heal with an H2‐antagonist, were given omeprazole 20 mg o.m. for four weeks. Four antral biopsies from each patient were taken at endoscopy before, at the end of, and four weeks after treatment. Rapid urease test, culture, histopathology and transmission electron microscopy were carried out on these biopsies to determine the presence of Helicobacter pylori and improvement of gastritis. After four weeks of treatment, duodenal ulceration was healed in 16 (79%) of the patients; H. pylori was not detected by culture in 11 (50%) of the patients, and the associated gastritis improved in 12 (54%) patients. Four weeks after cessation of treatment the organism was cultured from antral biopsies of 18 (86%) of the patients and all of these had gastritis. Omeprazole treatment healed duodenal ulceration, improved gastritis temporarily, and suppressed but did not eradicate H. pylori.
Effects on bowel motility of misoprostol administered before and after meals
Authors: RUTGEERTS P. , VANTRAPPEN G. , HIELE M. , GHOOS Y. , ONKELINX C. 
Published: July 2010

SUMMARYProstaglandin analogues, used in the treatment of duodenal and benign gastric ulcer and in the prevention of gastric ulceration caused by nonsteroidal anti‐inflammatory drugs, are frequently associated with gastrointestinal side effects, particularly diarrhoea and abdominal cramps. We investigated the effects of misoprostol, a prostaglandin E1 derivative, on bowel motility and faecal loss of fat, water and bile acids in relation to its postprandial vs. preprandial administration. Twelve healthy subjects participated in a double‐blind crossover study comparing three 5‐day courses of therapy with a washout period of 1‐2 weeks between courses. Following a Latin Square design, the dosing regimens were (a) 400 μ misoprostol b.d. after meals and placebo b.d. before meals; (b) 400 μ misoprostol b.d. before meals and placebo b.d. after meals; (c) placebo before and after meals. Orocaecal transit time measured by H2 breath tests following lactulose administration, was shortest during pre‐prandial dosing but was also significantly decreased during post‐prandial dosing. The overall treatment difference was highly significant (P < 0.001), and the difference between each pair of treatments was also statistically significant. Whole bowel transit time studied by means of 3H‐PEG 4000 determination in stools, was shorter for the two misoprostol regimens but statistical significance was borderline. The number of stools passed per day was similar in the three groups. During both misoprostol dosing periods, stools were less formed and their content of water, fat and bile acids was higher. There was also more urgency, flatulence, abdominal pain and nausea. It is concluded that the gastrointestinal side effects caused by misoprostol are mainly based on an increased orocaecal transit time. The effects are more important when the drug is administered before meals than after meals.
Short report: plasma aluminium concentration and 24‐hour urinary aluminium excretion before, during and after treatment with sucralfate
Authors: MISTRY P. , VARGHESE Z. , POUNDER R. E. 
Published: July 2010

SUMMARYTen dyspeptic patients were treated with 1 g sucralfate q.d.s. for six weeks. The plasma aluminium concentration and 24‐h urinary aluminium excretion were measured at 3‐weekly intervals before, during and after treatment with sucralfate. Compared with before treatment, there were significant rises in the median plasma aluminium concentration at 3 and 6 weeks during treatment with sucralfate (6 μ/L to 13 and 12 μ/L). The median 24‐h urinary aluminium excretion rose significantly from a pretreatment level of 20 μ to 71 and 78 μ after 3 and 6 weeks of treatment; the significant increase of urinary aluminium excretion persisted for three weeks after cessation of treatment (52 μ/24 hours), but thereafter urinary excretion was not significantly different from pretreatment. The results are consistent with significant absorption and tissue accumulation of aluminium during standard treatment with sucralfate in individuals with normal renal function.
Review article: the histamine H3‐receptor: a novel prejunctional receptor regulating gastrointestinal function
Authors: BERTACCINI G. , CORUZZI G. , POLI E. 
Published: July 2010

SUMMARYThis review examines the evidence for the existence in the gastrointestinal tract of a new subtype (H3) of histamine receptors, previously described in the central nervous system. Study of these receptors is facilitated by the availability of the highly selective agonist (R)α‐methylhistamine and the selective antagonist, thioperamide. H3‐receptors seem to exert negative control on gastric acid secretion evoked by indirect cholinergic stimuli: their localization is unclear but it seems to be outside the parietal cell. H3‐receptors also seem to be located on cholinergic and non‐adrenergic non‐cholinergic (NANC) neurones of the myenteric plexus, where they negatively control the release of neurotransmitters.
The effect of bile acids on the growth and adherence of Helicobacter pylori
Authors: MATHAI E. , ARORA A. , CAFFERKEY M. , KEANE C. T. , O'MORAIN C. 
Published: July 2010

SUMMARYBile reflux gastritis occurs in the absence of Helicobacter pylori (H. pylori). The aim of this study was to see if the bile acids cheno or ursodeoxycholic acid affected the growth or adherence of H. pylori in vitro. Twenty‐seven strains growth were inhibited by 0.1% chenodeoxycholic acid whereas only 11 out of the 27 were inhibited by 0.1% ursodeoxycholic acid. Growth was totally inhibited by a combination of 0.05 % chenodeoxycholic acid + 0.05 % ursodeoxycholic acid. Chenodeoxycholic acid was a more effective inhibitor of adherence in that the number inhibited and percentage inhibition were greater than with ursodeoxycholic acid. Bile salts might be useful in the treatment of H. pylori infection.
Short report: plasma somatostatin concentrations in the irritable bowel syndrome
Authors: O'DONNELL L. J. D. , DAVIDSON K. , CAMERON D. , WASS J. A. H. , FARTHING M. J. G. 
Published: July 2010

SUMMARYThe description of a patient with the irritable bowel syndrome whose symptoms were completely relieved by the administration of somatostatin raised the possibility that a deficiency of somatostatin may be involved in the pathogenesis of the disorder. We have examined this possibility by studying 11 healthy controls (35 ± 12 years; mean ± S.D. 8 female) and 10 irritable bowel syndrome patients (39 ± 14 years; 7 female) complaining of frequency of defaecation of 4 or more times a day. Plasma somatostatin concentrations were determined by specific radioimmunoassay, fasting and at 15, 30, 45, 60, 90, 120 and 180 min after a standard breakfast. Irritable bowel syndrome patients and controls had similar fasting (27.4 ± 5.1 vs. 35.2 ± 4.3 pg/ml; mean ± S.E.M. and integrated increment of post‐prandial (5105 ± 858 vs. 3885 ± 793 pg. min/L) plasma concentrations of somatostatin, as assessed by student's t‐test. These observations do not support the idea that a state of somatostatin deficiency exists in the irritable bowel syndrome.
Idiopathic gastric acid hypersecretion: treatment implications for refractory acid/peptic disorders
Authors: LEWIS J.H. 
Published: July 2010

SUMMARYAlthough in most patients with duodenal ulcer disease the ulcer heals after 8 weeks of treatment with standard doses of H2 blockers or other agents, in about 10% the ulcer does not heal. These patients are considered ‘refractory’to treatment. Reasons often cited for non‐healing include poor patient compliance, cigarette smoking, and non‐steroidal anti‐inflammatory drug (NSAID) use. Gastric acid hypersecretion also appears to be an important factor in non‐healing with standard doses of antisecretory agents. We have defined idiopathic gastric acid hypersecretion as a basal acid output of > 10 mmol/h in the absence of an elevated fasting serum gastrin level (or a negative secretin test if gastrin level > 100 pg/ml) to exclude persons with Zollinger‐Ellison syndrome. Among the acid/peptic‐related disorders in which idiopathic gastric acid hypersecretion should be considered are refractory duodenal ulcer, refractory gastro‐oesophageal reflux disease (especially patients with oesophagitis), postbleeding duodenal ulcer, and certain rare disorders such as hereditary angioedema. Some children with atypical abdominal pain may also be hypersecretors of gastric acid.Once identified, patients with refractory duodenal ulcer or gastrooesophageal reflux disease are treated with incremental doses of ranitidine titrated against the level of gastric acid secretion that remains during therapy. Ranitidine was selected to avoid the dose‐related antiandrogenic effects and potential hepatic cytochrome P450 system‐related drug interactions that may occur with cimetidine. In most cases of refractory duodenal ulcer, doubling the standard dose of ranitidine (to 300 mg b.d.) is sufficient to achieve symptomatic relief and mucosal healing. Higher doses appear to be necessary for refractory oesophagitis. To date, no side effects have been associated with high doses of ranitidine (up to 1800 mg/day) for periods of longer than 6 months. Idiopathic gastric acid hypersecretion is an important factor in explaining why not all patients respond to a ‘standard’ulcer‐healing dose of H2 blocker, and it provides a rationale for use of higher‐dose therapy as a safe and effective alternative to omeprazole or to combination drug therapy in refractory acid/peptic disease.
Pathophysiology of NSAID‐induced gastroduodenal damage: epidemiology and mechanisms of action of therapeutic agents
Authors: IVEY K. J. 
Published: July 2010

SUMMARYAll NSAIDs cause gastroduodenal mucosal damage. The mechanisms by which NSAIDs damage the mucosa are not fully understood. Peptic ulcers appear to be caused by an imbalance between acid output and mucosal resistance; therapeutic agents that act favourably on either variable will heal NSAID‐induced ulcers, particularly if the NSAID is discontinued. Inhibition of acid secretion and/or stimulation of prostaglandin secretion are also believed to have a protective effect against NSAID‐induced mucosal damage. Thus, antisecretory agents, such as the H2 blockers, and prostaglandin analogues, such as misoprostol, can provide protection against NSAID‐induced gastroduodenal damage.
Drug interactions with antisecretory agents
Authors: HANSTEN P. D. 
Published: July 2010

SUMMARYAntisecretory agents may affect the absorption, metabolism, and renal excretion of other drugs. Inhibition of gastric acid secretion may decrease the gastrointestinal absorption of drugs such as ketoconazole that dissolve poorly in the absence of adequate acid. With anti‐secretory agents, the drug interaction mechanism most likely to result in adverse effects is the inhibition of hepatic oxidative drug metabolism, primarily a problem with cimetidine. Omeprazole also appears to inhibit the hepatic metabolism of some drugs, but available evidence indicates that it interacts with fewer drugs than cimetidine and the magnitude of the inhibition is lower. Cimetidine decreases the renal clearance of procainamide and its active metabolite, N‐acetylprocainamide, probably through interference with active renal tubular secretion. In therapeutic doses, other H2‐receptor antagonists probably have minimal effects on renal procainamide elimination.
Pharmacokinetics and absolute rectal bioavailability of hydrocortisone acetate in distal colitis
Authors: PETITJEAN O. , WENDLING J. L. , TOD M. , LOUCHAHI K. , NICOLAS P. , PERRET G. , ASTIER A. 
Published: July 2010

SUMMARYThe hydrocortisone pharmacokinetic profiles of hydrocortisone acetate foam (Proctocort) administered rectally was assessed in healthy volunteers and patients with ulcerative colitis or X‐irradiation colitis. Endogenous production of hydrocortisone was suppressed by dexamethasone. Comparison of these data with those obtained after intravenous administration enabled assessment of absolute bioavailability, which was 30.0 ± 15.1% in healthy volunteers vs. 16.4 ± 14.8% in patients (P= 0.09). Maximal concentrations of hydrocortisone were also decreased in patients, 277 ± 215 nmol/L vs. 610 ± 334 mmol/L (P= 0.03). There was a nonsignificant tendency to faster absorption of hydrocortisone in patients vs. healthy volunteers, as the times to peak concentration were, respectively, 2.5 ± 1.2 h vs. 2.8 ± 0.8 h (P= 0.64), and the mean absorption times were 1.96 ± 1.45 h vs. 2.54 ± 1.62 h (P= 0.46). Thus, rectal inflammation resulted in a lower absorption of hydrocortisone. In addition systemic plasma levels remained in the physiological range, so that only minor side effects are to be expected.
Effects of oral pantoprazole on 24‐hour intragastric acidity and plasma gastrin profiles
Authors: HANNAN A. , WEIL J. , BROOM C. , WALT R. P. 
Published: July 2010

SUMMARYPantoprazole selectively blocks gastric parietal cell H+,K+‐ATPase. To define a dosage regimen for clinical trials we compared the effect of pantoprazole 40 and 60 mg daily on 24‐h intragastric acidity and plasma gastrin concentrations using a double‐blind, randomized, cross‐over design. Eleven men took each of the three regimens (placebo, 40, 60 mg) for 5 days. On Day 5, 24‐h pHmetry and plasma gastrin profile were performed. A consistent decrease in intragastric acidity with each dosage regimen was shown by a rise in 24‐h median pH from 1.4 (1.2–1.8, IQR) on placebo to 2.3 (1.8–4.4, P= 0.0022) during pantoprazole 40 mg and to 3.5 (2.6–4.9, P= 0.0017) during 60 mg. Pantoprazole 40 and 60 mg maintained the intragastric pH above 3 for 33% and 58% of time, respectively, compared with 15% time with placebo. Twenty‐four‐hour integrated plasma gastrin concentration rose from 478 to 1798 and 1962 pmol.h/L, respectively. The drug was well tolerated. The decrease of acidity was dose related and should result in clinical efficacy similar to other antisecretory drugs. It is not known whether higher doses might abolish acid secretion. The optimal dose of pantoprazole is yet to be established.
Helicobacter pylori lipopolysaccharide stimulates gastric mucosal pepsinogen secretion
Authors: YOUNG G. O. , STEMMET N. , LASTOVICA A. , MERWE E. L. VAN DER , LOUW J. A. , MODLIN I. M. , MARKS I. N. 
Published: July 2010

SUMMARYThe effect of Helicobacter pylori lipopolysaccharide on guinea pig gastric mucosal pepsinogen secretion has been examined using an Ussing chamber technique. Luminal addition of H. pylori lipopolysaccharide resulted in a fifty‐fold stimulation of pepsinogen secretion compared to a twelve‐fold increase with E. coil lipopolysaccharide. Electron microscopy showed marked degranulation of zymogen granules but no evidence of chief cell disruption.
Circadian differences in pharmacological blockade of meal‐stimulated gastric acid secretion
Authors: SANDERS S. W. , MOORE J. G. , DAY G. M. , TOLMAN K. G. 
Published: July 2010

SUMMARYThe effects of identical morning (08.05 hours) and evening (20.05 hours) meals on intragastric pH were compared in 12 healthy volunteers receiving gastric antisecretory medication. Dosing included continuous intravenous infusion ranitidine (50 mg bolus followed by 12.5 mg/h) or a matching placebo which were randomly administered prior to and following 7 days of treatment with oral omeprazole (40 mg mane). Intragastric pH was monitored continuously using a tethered indwelling pH probe. Subjects were divided into groups, one of which began the pH monitoring session in the morning, the other in the evening. The median 24‐h intragastric pH was significantly increased by all active dosing regimens (P < 0.05). Combined omeprazole and ranitidine produced the highest median pH, 5.92. However, a breakthrough drop in intragastric pH occurred during the evening after all active dosing. Intragastric pH fell prior to and after consumption of the evening meal with median pH values less than 4 during all sessions. The evening meal led to significantly lower intragastric pH compared to the morning meal for omeprazole and the combined omeprazole and ranitidine dosing periods (P < 0.05). There was no difference between morning and evening pH during the placebo or ranitidine periods. Ranitidine and omeprazole, either alone or in combination, were unable to prevent the mealstimulated decline in intragastric pH during the evening time period.
Effect of acute and chronic acid suppression on plasma gastrin release in the rat
Authors: SCHUERER‐MALY C.‐C. , KROMER W. , FLOGERZP B. , VARGA L , POSTIUS S. , HALTER F. 
Published: July 2010

SUMMARYThe mechanisms by which administration of the H+, K+‐ATPase inhibitor B 831–78 or intragastric perfusion with NaHCO3 induces plasma gastrin release were studied in the rat. Experiments were performed after a washout of residual intragastric contents in fasted animals provided with chronic gastric fistulae. Acute and chronic administration of B 831–78 elevated plasma gastrin dose‐dependently up to 5–6 times above control levels, while the increase was only twofold with intragastric NaHCO3 infusion despite similar neutralization of gastric acidity.The profound hypergastrinaemia induced by the H+, K+‐ATPase inhibitor, after both acute and chronic treatment, was completely prevented or reversed by intragastric perfusion with physiological amounts of acid (0.15 N HCl, 2.5 ml/h). The hypergastrinaemia was, however, largely resistant to high doses of atropine (4.3 μ mol/kg) and of the M1 selective muscarinic antagonist telenzepine (10 μ mol/kg). In contrast, the modest increase in plasma gastrin induced by gastric perfusion with NaHCO3 was completely suppressed by the high atropine dose and was attenuated by small doses of atropine or telenzepine (0.01 μ mol/kg and 1 μ mol/kg).These results demonstrate that, in the rat, blockade of the H+, K+‐ATPase can potently induce gastrin release in the absence of a meal. Moreover, they suggest that interruption of the negative feedback between acid and gastrin release is the main mechanism through which this class of drugs releases gastrin in the rat. Since a similar degree of gastrin release cannot be achieved by alkalinization of gastric contents, additional hormonal or neural regulatory factors may contribute to the drug‐induced hypergastrinaemia.
Comparison of plasma bismuth levels after oral dosing with basic bismuth carbonate or tripotassium dicitrato bismuthate
Authors: MADAUS S. , SCHULTE‐FROHLINDE E. , SCHERER C. , KÄMMEREI? A. , SCHUSDZIARRA V. , CLASSEN M. 
Published: July 2010

SUMMARYIn 20 healthy subjects plasma bismuth concentration was measured after single oral doses of basic bismuth carbonate or tripotassium dicitrato bismuthate. The drugs were administered in the fasted state or immediately after ingestion of a standard breakfast. After basic bismuth carbonate, plasma bismuth rose to concentrations between 0.7 and 2.6, μg/L in the fasted state, while after the meal the maximal level was only 1.3, μg/L. In contrast to these very low levels after basic bismuth carbonate, the administration of tripotassium dicitrato bismuthate was paralleled by an increase of plasma bismuth to concentrations between 15 and 232 μg/L with a mean peak value of 64 ± 15.3 (S.E.M.), μg/L in the fasted state. Postprandial ingestion of tripotassium dicitrato bismuthate attenuated the peak concentrations to 10.9 ± 6.3, μg/L. One subject, however, had a value of 120 μg/L. This study demonstrates that basic bismuth carbonate leads to very low plasma bismuth concentrations, which are far below the critical range that might eventually be associated with bismuth neurotoxicity. Therefore this compound can be considered potentially useful for bismuth therapy of gastrointestinal disorders.
Sucralfate diminishes basal acid output without affecting gastrin, H. pylori or gastritis in duodenal ulcer patients
Authors: MOSS S. F. , THOMAS D. M. , AYESU K. , LEVI S. , CALAM J. 
Published: July 2010

SUMMARYTwelve patients with active duodenal ulcer disease and Helicobacter pylori infection were treated with 1 g sucralfate q.d.s. for 1 month. Ulcers healed in 8 of the 12 patients without an alteration in the H. pylori‐associated antral gastritis. Sucralfate produced a significant fall in basal acid output in all the patients, from a median of 4.8 (range 2.1–12.1) to 1.6 (0.4–8) mmol/h, P < 0.01, whereas peak acid output was unchanged from 41 (21–59) before to 38 (24–55) mmol/h after treatment. Basal plasma gastrin concentrations and the meal‐stimulated integrated gastrin response were not altered significantly by sucralfate : 8 (2–17) pmol/L and 732 (188–1045) pmol. min/L pre‐treatment and 6 (2–17) pmol/L and 600 (140–1302) pmol. min/L post‐treatment, respectively. The fall in basal acid output observed may contribute to prolonged duodenal ulcer remission after treatment with sucralfate.
An Eudragit‐coated prednisolone preparation for ulcerative colitis: pharmacokinetics and preliminary therapeutic use
Authors: FORD G. A. , OLIVER P. S. , SHEPHERD N. A. , WILKINSON S. P. 
Published: July 2010

SUMMARYPrednisolone metasulphabenzoate, a steroid with poor colonic absorption, was coated with the pH‐dependent acrylic resin Eudragit S, as a means of delivering an orally administered preparation to the proximal colon. The therapeutic potential of delivering this steroid with potentially less systemic side‐effects to the proximal colon was assessed in extensive ulcerative colitis. Plasma and urine prednisolone profiles in 6 healthy volunteers confirmed minimal absorption from Eudragit S‐coated prednisolone metasulphabenzoate compared to prednisolone acetate: peak plasma prednisolone concentrations 29 ± 21 ng/ml vs. 570 ± 185 ng/ml (P < 0.01), area under curve measurements 204 ± 214 vs. 2724 ± 1236 ng.h/ml (P < 0.01). Prednisolone metasulphabenzoate coated with Eudragit S (30–60 mg daily) was then administered for 12 weeks to 12 patients with colonoscopically proven extensive ulcerative colitis in relapse. Symptoms, sigmoidoscopic appearances and rectal histological abnormalities all improved during therapy. Complete clinical remission occurred in 7 patients, a partial response in 2 patients and no response in 3 patients. Cortisol responses to tetracosactrin demonstrated no significant adrenal suppression following treatment. Eudragit S‐coated prednisolone metasulphabenzoate may be a useful treatment for extensive ulcerative colitis, without risk of systemic steroid side‐effects.
The in‐vitro mucosal conjugation of ethinyloestradiol and the bioavailability of oral contraceptive steroids in patients with treated and untreated coeliac disease
Authors: GRIMMER S. F. M. , BACK D. J. , ORME M. L'E. , TJIA J. F. , GILMORE I. T. , ELLIS A. 
Published: July 2010

SUMMARYThe ethinyloestradiol (EO2) component of oral contraceptive steroids is extensively conjugated with sulphate by the gut wall. The ability of gastrointestinal mucosa to conjugate EO2 has been examined in vitro in samples of mucosa taken from normal women as well as from women with coeliac disease. The percentage conjugation per mg dry weight for normal tissue (n= 11) was 17.1 ± 6.4 (mean ± s.d.) while in untreated coeliac tissue (n= 6) the figure was 6.3 ± 3.6% (P < 0.01). In tissue from patients with treated coeliac disease (n= 5) the figure was 12.1 ± 3.2%.Thus the ability of intestinal mucosa to conjugate ethinyloestradiol was significantly reduced in patients with coeliac disease, and restored towards normal following treatment. However, in patients with coeliac disease the pharmacokinetics of ethinyloestradiol were not significantly different from normal controls.