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K Vetvik

Publications and source records attributed to K Vetvik.

At least 19 recordsLinked to original sources

Esomeprazole 20 mg and lansoprazole 15 mg in maintaining healed reflux oesophagitis: Metropole study results.

AIM: To compare the efficacy of esomeprazole, 20 mg once daily, vs. lansoprazole, 15 mg once daily, for the maintenance treatment of patients with healed reflux oesophagitis. METHODS: During the initial open healing phase, 1391 patients with endoscopically verified reflux oesophagitis and a history of heartburn, with or without acid regurgitation, received esomeprazole 40 mg for 4-8 weeks. Patients who were healed (identified by endoscopy at 4 or 8 weeks) and symptom free were then randomized to receive 6 months of treatment with esomeprazole, 20 mg once daily, or lansoprazole, 15 mg once daily. RESULTS: Esomeprazole, 20 mg once daily, maintained a significantly higher proportion of patients in remission than lansoprazole, 15 mg once daily, over 6 months [83% (95% CI, 80-86%) of esomeprazole recipients compared with 74% (95% CI, 70-78%) of lansoprazole recipients; P < 0.0001; life table estimates]. When data were analysed according to baseline Los Angeles grade classification, esomeprazole, 20 mg once daily, achieved consistently higher remission rates across all grades of disease severity, whereas the efficacy of lansoprazole decreased to a greater extent with increasing severity of reflux oesophagitis. CONCLUSION: Esomeprazole, 20 mg once daily, is more effective than lansoprazole, 15 mg once daily, in maintaining remission in patients with healed reflux oesophagitis.

2-Pyridinylmethylsulfinylbenzimidazoles↗

Esomeprazole 20 mg and lansoprazole 15 mg in maintaining healed reflux oesophagitis: Metropole study results.

INTRODUCTION: Esomeprazole, the first proton pump inhibitor to be developed as an optical isomer, has demonstrated more effective healing vs. omeprazole and lansoprazole in patients with reflux oesophagitis (RO). However, RO recurs in a high proportion (approximately 80%) of these patients within 12 months of initial therapy, highlighting the importance of maintenance treatment. Previous studies have shown esomeprazole to be effective as maintenance therapy in healed RO patients. AIM: This study was conducted to compare esomeprazole 20 mg once daily (o.d.) with lansoprazole 15 mg o.d. for the prevention of recurrence of RO. METHODS: 1391 patients with endoscopically verified RO (LA classification) were enrolled in this randomized, double-blind, parallel-group, multicentre trial. During the initial healing phase of the study, all patients received 4-8 weeks' open treatment with esomeprazole 40 mg: 1236 healed (identified by endoscopy at 4 and 8 weeks) and symptom-free (i.e. no heartburn or acid regurgitation) patients were randomized to 6 months' maintenance treatment with esomeprazole 20 mg o.d. or lansoprazole 15 mg o.d. Time to relapse (relapse of RO and/or discontinuation due to symptom recurrence) was analysed using a log-rank test. RESULTS: Esomeprazole maintained a significantly higher proportion of patients in remission than lansoprazole over the 6-month course of treatment (P < 0.0001, intention-to-treat analysis). After 6 months' treatment, 83% of esomeprazole recipients were in remission compared with 74% of lansoprazole recipients (life-table estimates). Esomeprazole gave a longer time to relapse than lansoprazole irrespective of baseline LA Grade, significantly so for baseline LA Grades B, C and D (P < 0.05 for each comparison). Significantly more patients were free from heartburn in the esomeprazole group compared with the lansoprazole group at 1, 3 and 6 months (P < 0.05). Significant differences at 6 months between esomeprazole 20 mg o.d. and lansoprazole 15 mg o.d. were also observed for control of epigastric pain and acid regurgitation (P < 0.05 and P < 0.001, respectively). Both treatment regimens were well tolerated. CONCLUSION: Esomeprazole 20 mg o.d. is a more effective maintenance treatment than lansoprazole 15 mg o.d. for symptom-free patients with healed RO.

2-Pyridinylmethylsulfinylbenzimidazoles↗

[Acid-related disease in the population of two Norwegian municipalities--diagnosis and drug therapy].

BACKGROUND: The introduction of acid suppressant, cytoprotective and prokinetic drugs represented major progress in the treatment of acid-related diseases. In Norway, these drugs were reimbursed by the National Insurance System (NIS) from 1986. However, even if the distribution of the various diagnostic indications for prescribing were lacking, this reimbursement was stopped in 1995. The aim of this study was to describe prescriptions for presumed licensed diagnostic indications of these drugs for a defined population, and analyse them with regard to patients characteristics, verified (endoscopic) diagnoses, and therapeutic guidelines. MATERIAL AND METHODS: All prescriptions issued in 1994 to inhabitants of Lindesnes and Mandal Municipalities (17,105 inhabitants) were retrospectively retrieved from the pharmacies and the NIS. The medical records of the local endoscopy units and roentgen laboratories were subsequently searched for information on diagnostic procedures and final diagnosis leading to the prescriptions for these patients. RESULTS: A total number of 1,128 prescriptions (87,905 DDDs) were issued to 441 patients (3% of the population at risk; mean age 63 years; 55% men), and more commonly for the elderly (for 11% of those aged 80 years or more). Diagnostic procedures were documented for 93% of the patients (upper endoscopy in 404, 92%). Diagnostic indications for prescribing were reflux oesophagitis (48%), duodenal ulcer (24%), gastric ulcer (13%), and dyspepsia with normal endoscopic findings (12%). The drugs issued were H2-receptor antagonists (59%), proton pump inhibitors (31%), and cisapride (10%). 8% of the patients were long-term users of an NSAID. Of the 441 patients, drug treatment was issued to 38 with normal endoscopic findings and to 31 patients in whom we could not document examination by endoscopy or X-ray. INTERPRETATION: This study supports that the prevalence of dyspeptic complaints calling for drug treatment increases with patient age. With minor exceptions we found that the prescribing practice for the different diagnoses is in accordance with established therapeutic guidelines.

Adolescent↗

Bone density reduction in patients with Crohn disease and associations with demographic and disease variables: cross-sectional data from a population-based study.

BACKGROUND: The extent of bone density reduction in patients with Crohn disease is still being debated. The aim of this study was to examine bone mineral density (BMD) and factors associated with reduced BMD in a representative population of patients with Crohn disease aged between 20 and 70 years. METHODS: BMD (using dual energy X-ray absorptiometry) was measured in spine and hip in 55 patients with Crohn disease recruited from the entire Crohn population (n = 96) in a defined area of southern Norway. Demographic and clinical data were also collected. The patients were compared with 52 age- and gender-matched healthy controls. Potential demographic and disease-related factors associated with BMD reduction were statistically tested with bi- and multivariate analyses. RESULTS: The BMD reduction in patients with Crohn disease was 7.1% (P = 0.02) in spine L1-4, 6.1% (P = 0.08) in femoral neck and 8.4% (P = 0.02) in total hip as compared with the controls. In total hip and femoral neck, age, body weight and gender were independently associated with reduced BMD, but in the spine only body weight. Among the disease-related variables, only ever use of prednisolone was independently associated with reduction in BMD but this only in the femoral neck. CONCLUSIONS: The spine and hip BMD reduction of 6%-8% is similar to that found in a comparable population-based study performed in another area in Norway. Among the disease-related variables tested for, only the use of prednisolone was independently associated with BMD reduction. However, the BMD reduction measured in this study indicates that disease-related mechanisms are involved.

Absorptiometry, Photon↗

Effects of omeprazole and eradication of Helicobacter pylori on gastric and duodenal mucosal enzyme activities and DNA in duodenal ulcer patients.

BACKGROUND: Duodenal and gastric content of mucosal enzymes in duodenal ulcer (DU) patients differs from that of controls. The purpose of this study has been to examine the effect of omeprazole and eradication of Helicobacter pylori on mucosal enzymes in DU patients. METHODS: The enzyme activities of seven gastric and duodenal mucosal marker enzymes from the brush border, lysosomes, and mitochondria have been studied. In study I the measurements were made in 29 patients with an active DU before and after 14 days of omeprazole treatment. In study II 22 duodenal ulcer patients were given bismuth subnitrate, oxytetracycline, and metronidazole (triple therapy) for 2 weeks to eradicate H. pylori. Biopsy specimens were taken from the duodenum and the stomach for enzyme measurements and histologic assessment. In study II additional specimens were obtained from the prepyloric region for urease tests and culture of H. pylori. RESULTS: The ulcer healing rates were more than 90% after both omeprazole and triple therapy. H. pylori was eradicated in 86% after triple therapy. The activities of the brush-border enzymes lactase, neutral-alpha-glucosidase, alkaline phosphatase, leucyl-beta-naphthylamidase, and gamma-glutamyltransferase (gamma-GT) increased significantly in the duodenal bulb and the descending duodenum during treatment with omeprazole. No changes in duodenal enzyme activity were detected after triple therapy, whereas a significant fall in gamma-GT and acid phosphatase activities was seen in the stomach. The mucosal DNA in the gastric antrum decreased both after treatment with omeprazole and after triple therapy. CONCLUSIONS: A similar decrease in mucosal DNA of the gastric antrum was demonstrated after both omeprazole and triple therapy with bismuth subnitrate, oxytetracycline, and metronidazole. Omeprazole also affects the content of duodenal mucosal enzymes, whereas triple therapy particularly affects the gastric mucosal enzyme activity.

Antacids↗

Helicobacter-associated duodenitis and gastric metaplasia in duodenal ulcer patients.

Biopsy specimens were taken from the duodenal bulb and the distal duodenum in 45 duodenal ulcer patients before and after treatment with histamine-2 antagonists, prostaglandin analogues or antacids. After four weeks of treatment, the ulcer had healed in 31 patients. The treatment did not lead to a reduced frequency of helicobacter-associated duodenitis or gastric metaplasia of the duodenal epithelium. We found gastric metaplasia in 52.3% of all biopsy specimens from the duodenal bulb, chronic active duodenitis in 71.9% and helicobacter-like structures in 15.9%. The helicobacter organisms were found only in areas of gastric metaplasia, and an accompanying chronic active duodenitis was found in 94.1%. In the distal duodenum, we observed chronic active duodenitis in 15.0% of the specimens. Here the inflammation was not associated with gastric metaplasia or helicobacter-like structures. These observations support the hypothesis that Helicobacter pylori colonizes the duodenal mucosa only in areas of gastric metaplasia, and that such colonization may lead to an active duodenitis.

Antacids↗

Effect of misoprostol and antacids on gastric and duodenal mucosal enzyme activities in duodenal ulcer patients.

The activities of 11 marker enzymes from the gastric and duodenal mucosa were determined in 15 patients with active duodenal ulcer disease before therapy, after 4 weeks of therapy with the prostaglandin E1 analogue misoprostol, 400 micrograms twice daily, and after another 4 weeks without any therapy. Another 15 patients were given a high-dose liquid antacid regimen. The activities were measured in homogenized material obtained with forceps through an endoscope. The healing rates of the two groups at 4 weeks were 53% and 80%, respectively. No changes in mucosal inflammation were noted during therapy. During treatment with misoprostol the activities in the descending duodenum of the membrane enzymes alkaline phosphatase, leucyl-beta-naphthylamidase, gamma-glutamyltransferase, and 5'-nucleotidase increased towards the values seen in normal controls. Despite a higher healing rate, no changes in the enzyme activities occurred in the group given high-dose antacid therapy. Four weeks after cessation of therapy the enzyme activities in the misoprostol group were not significantly different from the pretreatment values. In the biopsy specimens from the duodenal bulb the activities of monoamine oxidase fell during treatment with misoprostol and were restored to the pretreatment activity when therapy was stopped. In the stomach mucosa the enzyme activities were largely unchanged during treatment with both misoprostol and antacids. These results indicate that misoprostol and antacids have different mechanisms of action but may also suggest that the demonstrated enzymic changes are unrelated to the healing process.

Alprostadil↗

Helicobacter pylori and chronic active inflammation of the duodenum and stomach in duodenal ulcer patients treated with ranitidine, misoprostol, or an acid-neutralizing agent.

Biopsy specimens from the stomach and duodenum of 45 duodenal ulcer patients treated with ranitidine, misoprostol, or an antacid were examined. During 4 weeks of treatment the duodenal ulcer healed in 31 patients. The treatment regimens showed no significant effect on the amount of Helicobacter-like structures (HLS) or the presence of active inflammation, either in the stomach or in the duodenum. All patients had chronic active antral gastritis before and after treatment. HLS were found histologically in 91.7% of all antral specimens, in 94.2% of the gastric corpus specimens, in 15.9% of the duodenal bulb specimens, and in 0.9% from the lower duodenal knee. The frequency of chronic active gastritis was clearly lower in the gastric corpus than in the antrum, whereas the occurrence of HLS was about the same. This may indicate a higher resistance of the gastric corpus mucosa to H. pylori.

Adult↗

Effect of ranitidine on gastric and duodenal mucosal enzyme activities in duodenal ulcer patients.

The activities of 11 marker enzymes from the gastric and duodenal mucosa were determined in 19 patients with active duodenal ulcer disease (DU) before therapy, after 4 weeks of therapy with ranitidine, 300 mg/day, and after another 4 weeks without treatment. The activities were measured in homogenized material obtained with forceps through an endoscope. The healing rate at 4 weeks was 68%. In the descending duodenum the activities of the membrane enzymes increased during the treatment period compared with pre-treatment activities. Although not as extensive as in the descending duodenum, an increase of membrane enzyme activities was also noted in the duodenal bulb during treatment. In the gastric mucosa only minor enzymic activity changes were seen. The altered enzyme activities in duodenum and stomach during treatment were independent of ulcer healing, smoking, antacids, and mucosal inflammation. Previously, significant differences in mucosal enzyme activities have been demonstrated between DU patients and controls. During ranitidine treatment the enzyme activities in the duodenal mucosa of the same DU patients tended to normalize, whereas they were mostly unchanged in the gastric mucosa. Four weeks after treatment the mucosal enzyme activities in the duodenum were as before treatment started, without occurrence of ulcer relapse. The altered enzymic activities of the duodenal mucosa in DU patients therefore seem to be largely independent of the presence of active ulcer.

Adult↗

Enzyme activities in the gastric mucosa in duodenal ulcer patients.

In a series of 45 consecutive duodenal ulcer patients (DU) the activities of 10 marker enzymes from the brush border, basolateral membrane, mitochondria, and lysosomes were determined by analysis of homogenized material taken with biopsy forceps through an endoscope from the antral and body part of the stomach. They were compared with the enzyme activities determined in controls with similar types of gastritis but without any evidence of peptic ulcer disease. All the DU patients had gastritis in the antral mucosa. In the body part, about 30% had gastritis. In the antral mucosa of DU patients the activities of the membrane and lysosomal enzymes were mostly increased when compared with the controls. In the gastric body mucosa of DU patients the activities of the lysosomal enzymes were mostly increased, whereas most of the membrane enzymes showed unchanged activities when compared with the corresponding controls. Monoamine oxidase activities were decreased or unaltered in both regions in these patients. The finding of enzymatic changes in the gastric mucosa of DU patients gives further support to an altered mucosal metabolism in these patients.

Adolescent↗

Enzyme activities in the duodenal mucosa in duodenal ulcer patients.

The mucosal enzyme activities of 11 marker enzymes from the brush border, basolateral membrane, and lysosomes of 45 patients with an active duodenal ulcer (DU) were determined by analysis of homogenized biopsy specimens obtained from the duodenal bulb and descending duodenum at endoscopy. They were compared with activities measured in 22 controls. In the duodenal bulb lactase (p less than 0.005), neutral-alpha-glucosidase (p less than 0.0005), and monoamine oxidase (p less than 0.0005) were significantly decreased in DU patients. In the descending duodenum all the brush border enzymes except sucrase were significantly decreased when compared with controls. DU patients with inflammation in the biopsy specimens from the duodenal bulb had decreased levels of lactase (p less than 0.05), sucrase (p less than 0.05), neutral-alpha-glucosidase (p less than 0.05), leucyl-beta-naphthylamidase (p less than 0.05), and acid phosphatases (p less than 0.05) when compared with DU patients with normal histology in this region. In the descending duodenum the activities of leucyl-beta-naphthylamidase (p less than 0.05) were decreased in patients with inflammation compared with those without such histologic changes. DU patients who had taken antacids before the investigation had decreased activities of lactase (p less than 0.05) in the descending duodenum when compared with those who had not taken antacids. Activities of lactase (p less than 0.005), sucrase (p less than 0.005), neutral-alpha-glucosidase (p less than 0.05), and acid beta-glucuronidase (p less than 0.0005) in the descending duodenum were significantly lower in smokers than in non-smokers with active DU.

Adolescent↗

Influence of remote cancer and obesity on, and distribution of mucosal enzymes in, the upper small intestine.

A series of mucosal enzymes were estimated by analysis of homogenized biopsy specimens from the lower duodenal flexure, obtained from 10 large-bowel carcinoma patients, 15 patients with morbid obesity, and 15 controls. In 11 subjects the distribution along the upper small intestine was determined. The activities of the brush border enzymes lactase (p less than 0.01), neutral-alpha-glucosidase (p less than 0.01), and alkaline phosphatase (p less than 0.05) were significantly lower in the large-bowel carcinoma patients than in the controls. In obese subjects significantly lower activities (p less than 0.05) were demonstrated for the basolateral membrane enzyme 5'-nucleotidase and the lysosomal enzymes N-acetyl-beta-D-glucosaminidase and acid beta-glucuronidase, when compared with those in controls. Compared with the enzyme levels of the duodenal bulb, significantly higher activities of a series of enzymes were demonstrated at both the lower duodenal flexure and the angle of Treitz.

Adenocarcinoma↗

Chronic pancreatitis in patients with sclerosing cholangitis and ulcerative colitis.

In the 4-year period 1980-83 sclerosing cholangitis was demonstrated in 7 out of 151 patients with ulcerative colitis hospitalized in our department. Total ulcerative colitis was demonstrated in all patients with sclerosing cholangitis, whereas abnormal pancreatograms compatible with chronic pancreatitis were seen in four of these patients. According to the criteria of Kasugai, one had minimal, two moderate, and one advanced changes of chronic pancreatitis. Although three of four patients had been treated with drugs known to induce pancreatitis (sulfasalazine and corticosteroids), it is tempting to assume that ulcerative colitis, sclerosing cholangitis, and pancreatitis, when seen in combination, are manifestations of autoimmune diseases with a genetic predisposition. A mechanical mechanism for the development of chronic pancreatitis in sclerosing cholangitis must also be considered.

Adolescent↗

Screening for occult faecal blood loss in a community by means of Hemoccult II slides and a tetramethylbenzidine test.

A total of 754 persons statistically selected from the age group 54-64 years were asked by letter to provide faecal samples for screening of occult blood during dietary restrictions. A total of 413 persons (55%) returned an average of 5.8 (range, 1-6) faecal samples each. All the faecal specimens were analysed with Hemoccult II slides and the 3,3',5,5'-tetramethylbenzidine (TMB) test 0.10%. For technical reasons, however, the Hemoccult test could not be evaluated. The TMB test showed faecal blood in 50 persons. A case history was obtained in 49 persons, of whom 47 agreed to further clinical, radiological, and endoscopic investigations. The most important findings in these examinations were resectable colonic carcinoma (Dukes's stage B) in 1 subject, a gastric ulcer in 1, haemorrhagic gastritis in 1, duodenal ulcers in 2, and colorectal polyps in 11 persons. The cost of the study was estimated to be NOK 114,000 (about USD 16,000).

Benzidines↗