bluuebunny/crossref_metadata_2025_split huggingface dataset:
Gastric mucosal adaptation to etodolac and naproxen
Authors: LIPSCOMB G. R. , WALLISt N. , ARMSTRONG† G. , GOODMAN M. J. , REES W. D. W. 
Published: July 2010

SUMMARY Background: Nonsteroidal anti‐inflammatory drugs (NSAIDs) frequently cause damage to the gastroduodenal mucosa, principally by suppressing mucosal prostaglandin synthesis. However, such acute mucosal injury usually resolves, despite continued NSAID administration, by a process known as adaptation. Newer NSAIDs, such as etodolac, have been developed to minimize effects on prostaglandin synthesis. Aim: To determine whether etodolac causes less acute damage than naproxen, and whether the damage produced resolves with continued NSAID administration. Methods: Twenty‐four healthy volunteers were given a 28‐day course of either etodolac 300 mg b.d. or naproxen 500 mg b.d. Gastroduodenal damage was assessed using a modified Lanza scoring system and mucosal blood flow with laser doppler flowmetry at endoscopy before NSAID administration and during days 1, 7 and 28 of continued intake. Results: Maximum gastric damage (median grade and interquartile range, IOR) occurred during the first 24 h of administration, being greater with naproxen (2.0, IOR 1.0–3.0) than etodolac (1.0, IOR 1.0–1.5; P= 0.03). Such damage was associated with a fall in antral blood flow in the naproxen group (mean ± S.E.M.) from 54.5±3.4 to 43.8±3.4 arbitrary units (P= 0.07) and a slight increase in mucosal blood flow in the etodolac group from 43.5 ± 2.24 to 49.5 + 3.6 arbitrary units. With continued intake this damage resolved in all subjects taking etodolac and in eight of 14 subjects on naproxen. Resolution in the naproxen group was associated with a return to normal of antral blood flow. Conclusions: These observations suggest that etodolac causes less mucosal damage than naproxen and that adaptation occurs to both.
Eradication of Helicobacter pylori and prevention of recurrence of duodenal ulcer: a randomized, double‐blind, multi‐centre trial of omeprazole with or without clarithromycin
Authors: LOGAN R. P. H. , BARDHAN K. D. , CELESTIN L. R. , THEODOSSI A. , PALMER K. R. , REED P. I. , BARON J. H. , MISIEWICZ J. J. 
Published: July 2010

SUMMARY Background: Antimicrobial treatment for Helicobacter pylori eradication is currently recommended for all patients with duodenal ulcer disease, but consensus on the best treatment is lacking. Methods: Patients with active duodenal ulcer and H. pylori were enrolled in a double‐blind, randomized, placebo‐controlled multi‐centre study. Patients received omeprazole 40 mg daily for 28 days and either clarithromycin 500 mg t.d.s. or placebo t.d.s. for the first 14 days. Patients underwent endoscopy before starting treatment, at 2 weeks, immediately after stopping treatment if unhealed at 2 weeks, and at 1, 6 and 12 months after the end of treatment, or at the recurrence of symptoms. Eradication of H. pylori, duodenal ulcer healing and ulcer recurrence were measured. Results: One‐hundred and fifty‐four patients were recruited and randomized to omeprazole plus clarithromycin (n= 74) or to omeprazole plus placebo (n= 80). One month after treatment, H. pylori was eradicated in 57 of 69 (83%; 95% CI: 72–91%) patients receiving omeprazole plus clarithromycin, compared with 1 of 75 (1%; 95% CI: 0–7%) receiving omeprazole alone (P < 0.001). In patients receiving omeprazole plus clarithromycin the ulcer healed at 2 weeks in 83% (95% CI: 71–91%) and at 4 weeks in 100% (95% CI: 95–100%), compared with 77% (95% CI: 66–86%) and 97% (95% CI: 91–100%) in those given omeprazole plus placebo (N.S.). Ulcers recurred at 12 months in 6% (95% CI: 1–16%) of patients given omeprazole plus clarithromycin, compared with 76% (95% CI: 63–86%) of patients given omeprazole plus placebo (P < 0.001). The incidence of side‐effects was similar in both treatment groups (38% with clarithromycin dual therapy and 29% with omeprazole plus placebo; P= 0.304). Ninety per cent of patients took at least 90% of their prescribed medication. Conclusions: Omeprazole plus clarithromycin dual therapy eradicated H. pylori in 83% of patients with duodenal ulcer and significantly decreased 12‐month recurrence from 76% to 6%.
Gastric persorption of bismuth from ranitidine bismuth citrate
Authors: ERASER A. G. , LEWIN J. F. , POUNDER R. E. 
Published: July 2010

SUMMARY Aim: To determine whether bismuth penetrates the gastric mucosa after dosing with ranitidine bismuth citrate. Methods: Twelve patients presenting with dyspepsia were randomized to receive either ranitidine bismuth citrate or placebo, 20–40 min prior to endoscopy. Biopsies were taken from four sites during endoscopy: the first and second parts of the duodenum, the antrum, and the body of the stomach. Biopsies were analysed by electron microscopy and X‐ray microanalysis. Results: Bismuth particles were found to be interposed between epithelial cells in the antral mucosa of three of eight patients who were dosed with ranitidine bismuth citrate. Columns of bismuth particles could be tracked down the lamina propria and were seen to be surrounding blood vessels. Bismuth particles were observed in the inter‐ and intra‐cellular channels of the endothelial cells of the blood vessels in the lamina propria and also close to the luminal surface of the endothelial cell. This process of persorption was similar to that described in a previous report of electron microscopy appearances of the gastric antrum after dosing with tripotassium dicitrato bismuthate, but was quantifiably smaller and not observed in all the patients dosed with ranitidine bismuth citrate. No penetration of the mucosa by bismuth particles was seen in the body of the stomach or the duodenum. Conclusion: Penetration of bismuth particles into the gastric mucosa may occur after oral dosing with ranitidine bismuth citrate.
Long term continuous omeprazole treatment of patients with Barrett's oesophagus
Authors: NEUMANN C. S. , IQBAL T. H. , COOPER B. T. 
Published: July 2010

SUMMARY Background: The metaplastic columnar epithelium in Barrett's oesophagus has malignant potential. Aim: To determine whether decreasing acid reflux leads to regression of Barrett's epithelium. Method: Twenty‐four patients with Barrett's oesophagus were treated with omeprazole 20 mg o.m. in an open, prospective study; 11 were treated for 12 months, and 13 for 24 months. Another group of 17 patients with Barrett's oesophagus was treated with an H2‐receptor antagonist in standard dosage for 12‐36 (mean 23) months. Patients were assessed endoscopically. Results: No evidence of significant shortening of the length of Barrett's oesophagus was seen in any patient treated for 12 or 24 months with omeprazole. Similarly, no shortening of the length of Barrett's oesophagus was seen in any patient treated with an H2‐receptor antagonist. However, 6 of 11 patients treated with omeprazole for 12 months, and 7 of 13 treated for 24 months, developed macroscopic squamous islands visible below the squamo‐columnar junction. This was not seen in any patient treated with an H2‐receptor antagonist. Conclusion: Although there can be reappearance of squamous epithelium in Barrett's oesophagus of some patients during treatment with omeprazole 20 mg o.m. over 12–24 months, a significant shortening of the columnar lined segment is not seen.
Treatment of hepatitis B surface antigen carriers in the early stage of the infection using recombinant alpha‐interferon with steroid priming
Authors: GUAN R. , HO K. Y. , YAP I. , KANG J. Y. , TAN C. C. , NG C. , SMITH R. , WEE A. 
Published: July 2010

SUMMARY Background: Alpha‐interferon has been found to inhibit hepatitis B virus (HBV) replication in Chinese patients with chronic HBV infection although a sustained effect was rarely achieved in those with normal pre‐treatment serum alanine amino transferase (ALT) levels. Prednisolone priming has been found to be beneficial over treatment with interferon alone in these subjects. We studied the effect of steroid pre‐treatment followed by recombinant interferon alpha‐2a in the treatment of asymptomatic HBV carriers with positive hepatitis Be antigen (HBeAg), hepatitis B viral DNA (HBV‐DNA) and minimal changes in liver histology. Methods: The treatment regimen included a 6‐week prednisolone priming, a 2 week rest followed by 14 weeks of three times weekly 9 mega units of interferon alpha‐2a injection and 52 weeks of follow‐up. There were seven patients in the treatment group and seven controls. Results: The mean age, pre‐treatment ALT (normal in all except for one in each of the treatment and control groups), HBV‐DNA levels and histological scores were similar in the two groups. Serum HBV‐DNA levels fell in six patients during treatment and became undetectable in two of them by the end. During follow‐up, serum HBV‐DNA returned to pre‐treatment levels in all patients. None of the treated patients had HBeAg sero‐conversion and none of the controls had spontaneous clearance of HBV‐DNA or sero‐conversion of HBeAg. No improvement of liver histology was observed in any of the treated patients. There were only mild flu‐like side‐effects noted and interferon alpha‐2a was well tolerated at the doses given among treated patients. Conclusion: Prednisolone priming followed by interferon alpha‐2a treatment has no beneficial effect on HBV carriers in the early stages of chronic hepatitis B infection.
Lipocortin‐1 autoantibody concentration in children with inflammatory bowel disease
Authors: BEATTIE R. M. , GOULDING N. J. , WALKER‐SMITH J. A. , MACDONALD T. T. 
Published: July 2010

SUMMARY Background: Corticosteroids are widely used to treat children with inflammatory bowel disease although the response is variable, side‐effects are common, and many patients develop a partial or complete steroid resistance. The mechanism underlying these phenomena are unclear. Corticosteroids mediate some of their actions through lipocortin‐l, and the inductic of autoantibodies to lipocortin has been proposed as a possible mechanism by which steroid efficacy is suboptimal in vivo. Patients and methods: We have measured serum lipocortin‐1 antibody concentration by ELISA in 38 children with Crohn's disease, 12 with ulcerative colitis and in 15 controls. Results: IgG and IgA anti‐lipocortin‐1 antibody levels were higher in the Crohn's group than in the ulcerative colitis or control groups. Elevated concentrations did not relate to disease activity, history of steroid therapy or steroid‐responsiveness. Lipocortin IgM antibody status was similar in all three groups. Conclusion: It is therefore unlikely that serum antibodies to lipocortin‐1 have a role in the development of steroid‐resistance in children with inflammatory bowel disease.
The effect of treatment on lymphokine‐secreting cells in the intestinal mucosa of children with Crohn's disease
Authors: BREESE E. J. , MICHIE C. A. , NICHOLLS S. W. , WILLIAMS C. B. , DOMIZIO† P. , WALKER‐SMITH J. A. , MACDONALD T. T. 
Published: July 2010

SUMMARY Background: Recent studies have shown both interleukin 2 (IL‐2) and interferon gamma (IFN) to be elevated in patients with active Crohn's disease compared to ulcerative colitis or non‐inflammatory bowel disease controls. However the effect of treatment on these lymphokines has not been studied. Patients and methods: Using a reverse haemolytic plaque assay the percentage of lymphokine‐secreting cells was determined in the intestinal mucosa of children with Crohn's disease before and after 8 weeks of treatment with either enteral nutrition, cyclosporin or steroids. Results: Before treatment, a high percentage of cells isolated from mucosal biopsies secreted IL‐2 or interferon‐gamma. Eight weeks’treatment with the immunosuppressive agents cyclosporin, or with corticosteroids, produced a significant reduction in the percentage of IL‐2 secreting cells, although only for the former was there also a reduction in interferon‐gamma secreting cells. Enteral nutrition however, produced a reduction in lymphokine‐secreting cells equivalent to cyclosporin and produced the best histological and clinical improvement. Conclusion: Enteral nutrition and cyclosporin can down‐regulate lymphokine secretion in the gut in Crohn's disease.
Patterns of 24‐hour oesophageal acid exposure after acute withdrawal of acid suppression
Authors: ORR W. C. , MELLOW M. H. , GROSSMAN M. R. 
Published: July 2010

SUMMARY Aim: To measure 24‐h ambulatory oesophageal pH data in patients with gastro‐oesophageal reflux disease prior to, during and after acute treatment with comparable doses of omeprazole and ranitidine. Methods: The subjects were 20 adults with at least 8% acid contact time. Ten subjects were treated for 1 week with omeprazole 20 mg q.d.s. and 10 subjects with ranitidine 300 mg t.d.s. All subjects were examined at the end of 1 week of therapy and subsequent to cessation of treatment (1 day for ranitidine and 3 days for omeprazole). Results: Both drugs produced a statistically significant (P < 0.05) decrease in acid contact time with acute treatment. Omeprazole produced a significantly greater decrease in acid contact time when compared to ranitidine. Subsequent to treatment cessation, the total acid contact time for omeprazole remained significantly less than the baseline level, while ranitidine returned to levels which were not significantly different from the baseline. Conclusion: These data provide no evidence for a ‘reflux rebound’ subsequent to the cessation of acute acid secretory suppression.
Do non‐steroidal anti‐inflammatory drugs have an effect on gastric cell turnover?
Authors: SANT S. M. , CAHILL R. J. , GILVARRY J. , O'MORAIN C. A. 
Published: July 2010

SUMMARY Aim: To study the effect of non‐steroidal anti‐inflammatory drugs (NSAIDs) on gastric cell turnover using an in vitro immunohistochemical method of bromodeoxyuridine (BrDU) uptake. Methods: Thirty patients undergoing routine upper gastrointestinal endoscopy were studied. Sixteen had taken NSAIDs daily for more than 3 months and there were 14 age‐matched controls. Endoscopic gastric antral biopsies were obtained and stained immediately using the BrDU technique. Cell proliferation was expressed as a labelling index percentage (LI%) defined as the number of BrDU‐labelled nuclei in 10 gastric glands, expressed as a percentage of the total cells in the gastric gland. Results: Gastric infection with Helicobacter pylori was excluded in all patients. Of the 16 patients on NSAIDs, four had gastritis, four had erosions or ulceration and eight had a normal examination. Endoscopy was normal in all patients in the control group. The LI% (mean ± S.E.M.) in the entire NSAID group was 4.09 ± 0.29 and in the control group 3.57 ± 0.29. No significant difference was observed. In the NSAID patients with gastritis and erosions or ulceration, the LI% was 4.99 ± 0.61 and 3.07 ± 0.32, respectively. There was no significant difference in LI % between the endoscopic subgroups of patients on NSAIDs or between patients on NSAIDs who had normal endoscopy and the control patients. Conclusion: These results provide evidence that refutes the hypothesis that the prevalence of NSAID gastropathy is due to an effect on gastric cell turnover.
Review article Is Helicobacter pylori transmitted by the gastro‐oral route?
Authors: AXON A. T. R. 
Published: July 2010

SUMMARYThe manner in which Helicobacter pylori is transmitted is of fundamental importance when considering strategies for its control, yet to date no satisfactory explanation has been advanced to account for its spread from person to person. This is surprising for a disease that affects 50% of the world's population. Attempts to culture H. pylori from faecal material and saliva have met with difficulty, casting some doubt on the likelihood of a faeco‐oral or oro‐oral route of transfer. The infection is easily passed from person to person by gastric intubation.The hypothesis advanced in this paper is that the natural route of transmission is by gastric juice, specifically as a result of epidemic vomiting in childhood. This theory is supported by literature indicating that acute infection with H. is characterized by vomiting of achlorhydric mucus that may serve as a vehicle for transmission. The hypothesis is consistent with most of the epidemiological data that have been published on H. pylori infection, including its association with childhood overcrowding, the lack of a fixed hot water supply and disadvantaged social conditions.
The effect of polyunsaturated phosphatidyl choline in the treatment of acute viral hepatitis
Authors: GUAN R. , HO K. Y. , KANG J. Y. , YAP I. , GWEE K. A. , TAN C. C. 
Published: July 2010

SUMMARY Background: Polyunsaturated phosphatidyl choline is a preparation often advocated for diseases of the liver. Methods: In a randomized open controlled trial, a preparation of polyunsaturated phosphatidyl choline, at a dose of 900 mg orally daily, was given to 22 patients with acute viral hepatitis. A control group of 25 patients was not treated. Results: Serial serum bilirubin and alanine amino transferase levels were measured up to 12 weeks. The falls in their levels after 2 and 5 weeks, and the lengths of time to their normalization, were not significantly different in the treated group compared to the control group. Conclusion: The results indicated that polyunsaturated phosphatidyl choline had no beneficial effect on the course of acute viral hepatitis.
Drugs for pH control in upper gastrointestinal bleeding
Authors: BRIJNNER G. , LUNA P. , THIESEMANN C. 
Published: July 2010

SUMMARYA few years ago, patients with bleeding peptic ulcers were referred to the surgeon if the bleeding did not stop. Today we have two promising new approaches to prevent emergency surgery. One is endoscopic intervention, the other is the pharmacological approach of blocking the proton pump.The endoscopical techniques of adrenaline injection, fibrin‐‘glue’ injection, polidocanol injection and heat coagulation can stop active bleeding in over 90% of cases. Pharmacologically, proton pump inhibitors can quickly achieve the optimal pH condition for support of the physiological cascade of haemostasis.The aim is to keep the intragastric pH above 6.0 for a few days. For the first time this aim can be achieved quickly and reliably by infusion of proton pump inhibitors. The optimal form of application is continuous infusion. Repeated bolus injections do not give optimal results. The optimal dosing was found to be the continuous infusion of 8 mg/h omeprazole or pantoprazole after an initial loading dose of 40–80 mg.
A prospective study of the effectiveness of low dose omeprazole as initial therapy in Zollinger–Ellison syndrome
Authors: TERMANINI B. , GIBRIL F. , STEWART C. A. , WEBER H. C. , JENSEN R. T. 
Published: July 2010

SUMMARY Background: The proton pump inhibitors (omeprazole and lansoprazole) are the drugs of choice for the medical management of gastric acid hypersecretion in Zollinger–Ellison syndrome (ZES). These drugs are safe for long‐term therapy but are acid‐labile and high doses are expensive. The recommended starting dose of omeprazole is 60 mg/day. However, it has been shown in recent studies that the maintenance dose of omeprazole could be safely reduced to 20 mg once or twice a day in more than two‐thirds of patients with ZES. The purpose of this study is to determine if an initial starting dose of omeprazole 20 mg/day is safe and effective in patients with ZES. Methods: Forty‐nine consecutive patients with ZES being treated with ranitidine for at least 2 weeks were admitted to the NIH. Omeprazole 20 mg was started on day 1 of the admission and ranitidine discontinued 4 h after the first dose. Gastric acid output was measured for 1 h prior to the next omeprazole dose on day 2, then on day 3 if the value was > 10 mmol/h on the previous day. If acid‐peptic symptoms developed or the gastric acid output remained > 10 mmol/h on day 3, the patient was considered to have failed omeprazole 20 mg/day initial therapy and the dose titrated daily to achieve adequate control of acid‐peptic symptoms and gastric secretion. Results: In 33 of the 49 patients (68%) omeprazole 20 mg/day was successful as initial therapy. Sixteen patients (32%) failed this initial omeprazole dose (eight patients owing to persistent peptic symptoms and eight patients owing to inadequate acid control). The final daily omeprazole dose required in these patients was 40 mg in eight patients (16%), 60 mg in one patient (2%) and 80 mg in seven patients (14%). Basal acid output (BAO) was the only clinical or laboratory feature that was significantly different between the two groups in which low dose initial omeprazole therapy was or was not successful: all patients with basal acid output < 20 mmol/h had a successful outcome. Conclusions: Because of the need to rapidly control gastric acid hypersecretion owing to the high risk of complications from peptic ulcer disease, patients with ZES should continue to be started on omeprazole 60 mg/day and the dose adjusted by acute titration methods as is currently recommended. After a maintenance dose is established, attempts should be undertaken to reduce the dose to 20 mg/day once or twice a day. Only the minority of patients with ZES in whom basal acid output is known to be < 20 mmol/h (20% of patients) should be started on a low initial omeprazole dose.
A survey of dyspepsia in Great Britain
Authors: PENSTON J. G. , POUNDER R. E. 
Published: July 2010

SUMMARY Objectives: To determine the prevalence of dyspepsia in the adult population of Great Britain and to describe the clinical features, treatment, effect of dyspepsia on daily lives and perceptions of peptic ulcer disease. Design: Cross‐sectional survey of the adult population using structured questionnaires. Setting: Subjects interviewed at more than 150 sampling points in England, Scotland and Wales in November 1994. Subjects: A representative sample of the adult population comprising 2112 subjects, aged 16 years or more. Main outcome measures: The prevalence of dyspepsia in the adult population and the frequency of various characteristics in dyspeptic subjects. Results: The prevalence of dyspepsia was 40%. Upper abdominal pain and heartburn were the most frequently reported symptoms. Solitary symptoms were uncommon and there was frequent overlap between‘ulcer‐like’and‘reflux‐like’dyspepsia. Forty‐six per cent of dyspeptic subjects reported moderate or severe symptoms. More than half of symptomatic subjects took medication and 22% had visited their GP during the previous year. Overall, 2% of the survey sample had been absent from work due to dyspepsia. Awareness of the factors precipitating or aggravating peptic ulcer disease was poor, particularly in relation to anti‐inflammatory drugs. Conclusions: The present study emphasizes the magnitude of the problem of dyspepsia in the adult population of Great Britain. The survey also shows that the public in general, and patients in particular, require more information if they are to avoid factors known to damage the upper alimentary tract.