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Biomedical subjects

P Snel

Publications and source records attributed to P Snel.

At least 19 recordsLinked to original sources
PubMed1999

Omeprazole versus high-dose ranitidine in mild gastroesophageal reflux disease: short- and long-term treatment. The Dutch Reflux Study Group.

OBJECTIVE: Patients with reflux esophagitis suffer from a chronic condition that may cause considerable discomfort because of recurrent symptoms and diminished quality of life. This study was designed to evaluate acute and long-term treatment comparing standard doses of omeprazole and high-dose ranitidine. METHODS: Patients with endoscopically verified symptomatic esophagitis grade I or II were initially treated with omeprazole 20 mg daily or ranitidine 300 mg twice daily for 4-8 wk. Patients who were symptom free were randomized to maintenance treatment with omeprazole 10 mg daily or ranitidine 150 mg twice daily. Patients were seen every 3 months or at symptomatic relapse. RESULTS: The percentage of asymptomatic patients after 4 and 8 wk treatment were 61% and 74%, respectively, for omeprazole and 31% and 50%, respectively, for ranitidine. Of 446 patients treated initially, 277 were asymptomatic, of whom 263 entered the maintenance study. The estimated proportion of patients in remission after 12 months of maintenance treatment with omeprazole 10 mg daily (n = 134) and ranitidine 150 mg twice daily (n = 129) were 68% and 39%, respectively (p < 0.0001). CONCLUSIONS: Omeprazole 20 mg daily is superior to high-dose ranitidine in the symptomatic treatment of reflux esophagitis grade I and II. Furthermore, omeprazole at half the standard dose is more effective than ranitidine in a standard dose in keeping patients in remission for a period of 12 months.

Double-Blind Method↗
PubMed1999

Validation of the Rockall risk scoring system in upper gastrointestinal bleeding.

BACKGROUND: Several scoring systems have been developed to predict the risk of rebleeding or death in patients with upper gastrointestinal bleeding (UGIB). These risk scoring systems have not been validated in a new patient population outside the clinical context of the original study. AIMS: To assess internal and external validity of a simple risk scoring system recently developed by Rockall and coworkers. METHODS: Calibration and discrimination were assessed as measures of validity of the scoring system. Internal validity was assessed using an independent, but similar patient sample studied by Rockall and coworkers, after developing the scoring system (Rockall's validation sample). External validity was assessed using patients admitted to several hospitals in Amsterdam (Vreeburg's validation sample). Calibration was evaluated by a chi2 goodness of fit test, and discrimination was evaluated by calculating the area under the receiver operating characteristic (ROC) curve. RESULTS: Calibration indicated a poor fit in both validation samples for the prediction of rebleeding (p<0.0001, Vreeburg; p=0.007, Rockall), but a better fit for the prediction of mortality in both validation samples (p=0.2, Vreeburg; p=0.3, Rockall). The areas under the ROC curves were rather low in both validation samples for the prediction of rebleeding (0.61, Vreeburg; 0.70, Rockall), but higher for the prediction of mortality (0.73, Vreeburg; 0.81, Rockall). CONCLUSIONS: The risk scoring system developed by Rockall and coworkers is a clinically useful scoring system for stratifying patients with acute UGIB into high and low risk categories for mortality. For the prediction of rebleeding, however, the performance of this scoring system was unsatisfactory.

Adolescent↗
PubMed1997

Previous use of non-steroidal anti-inflammatory drugs and anticoagulants: the influence on clinical outcome of bleeding gastroduodenal ulcers.

OBJECTIVE: To evaluate the relationship between prior non-steroidal anti-inflammatory drug (NSAID) or anticoagulant use and clinical outcome in bleeding gastric and duodenal ulcer patients. DESIGN: Prospective cohort-study. PARTICIPANTS: All patients (n = 132) admitted because of upper gastrointestinal bleeding during 3 months in the Amsterdam area. METHODS: We compared clinical outcome (blood transfusion, rebleeding, surgery and mortality) between ulcer patients who used NSAIDs or anticoagulants and patients who did not use these drugs before the bleeding-episode. RESULTS: Of the 132 patients admitted, 56 patients had gastric or duodenal ulcers. NSAIDs were used significantly more often before the bleeding episode in these ulcer patients than in the non-ulcer patients (n = 76), 21/56 (37.5%) vs. 15/76 (19.7%), respectively (P < 0.05), relative risk = 2.57, 95% confidence interval: 1.04-5.77). Stigmata of recent haemorrhage were found in 16/21 (76.2%) patients in the NSAID ulcer group, in 2/9 (22.2%) in the coumarin-ulcer patients, and in 12/24 (50%) in the no-medication ulcer group (not significant). Prior NSAID usage increased the in-hospital rebleeding rate from 16.7% to 42.9% (P = 0.05), leading to an increased need for surgical intervention from 16.7% to 42.9% (P = 0.05). In contrast prior usage of anticoagulants, which could be antagonized, did not affect the clinical outcome of the bleeding. Mortality was 9.5% in the NSAID group, 0% in the coumarin group, and 4.2% in the no-medication group. CONCLUSION: Prior use of NSAIDs increases the risk of rebleeding in bleeding ulcer patients, and leads to a higher need for urgent surgery. In contrast, prior anticoagulant therapy does not raise the rebleeding risk.

Adolescent↗
PubMed1997

Effect of omeprazole on the outcome of endoscopically treated bleeding peptic ulcers. Randomized double-blind placebo-controlled multicentre study.

BACKGROUND: Haemostasis is highly pH-dependent and severely impaired at low pH. However, there is no clear evidence that acid-suppressing drugs have beneficial effects in peptic ulcer haemorrhage. Endoscopic haemostatic treatment provides important reduction in morbidity and may be more efficient when a neutral intragastric pH is maintained. METHODS: We conducted a double-blind, placebo-controlled multicentre study of intravenous infusion of omeprazole (80 mg as bolus, followed by 8 mg/h) or placebo for 72 h. All patients received 20 mg omeprazole orally from day 3 until follow-up on day 21. Only patients with ulcer haemorrhage, endoscoped within 12 h after admission, and with a history or signs of circulatory failure and spurting bleeding, oozing bleeding, visible vessel, or clot, were included. Endoscopic intervention was aimed at when spurting bleeding, oozing bleeding, or a visible vessel was observed. The primary efficacy measure was the worst ranking on an overall outcome scale (5 = death, 4 = surgery, 3 = additional endoscopic treatment, 2 = more than 3 units of blood, and 1 = no more than 3 units of blood transfused). Base-line prognostic factors of treatment success by day 3 and of other binary outcomes were considered in a logistic regression model. RESULTS: Two hundred and seventy-four patients were randomly assigned to omeprazole (134 patients) or placebo (140 patients). The number of patients included in the 'intention-to-treat' analysis was 130 in the omeprazole group and 135 in the placebo group. The primary variable, the overall outcome at 72 h, showed a difference (P = 0.004) between the two treatments in favour of omeprazole. Treatment success by 72 h defined as no death, no operation, or no additional endoscopic treatment was 91.0% in the omeprazole group and 79.7% in the placebo group (therapeutic gain, 11.3 percentage units; 95% confidence interval, 2.3 to 20.4 percentage units). Significant differences in favour of omeprazole were also found for secondary variables such as number of blood transfusions, duration and degree of bleeding, and the need for surgery and additional endoscopic treatments on day 3 and day 21. However, the numbers of deaths by day 3, 21, or 35 were very similar. CONCLUSIONS: We found a beneficial effect of intravenous omeprazole in severe ulcer haemorrhage, with a reduction in the number of operations, in endoscopic treatments, and in the duration and severity of bleeding.

Aged↗
PubMed1997

Lack of effect of omeprazole in oral acenocoumarol anticoagulant therapy.

BACKGROUND: Omeprazole is eliminated almost completely by hepatic metabolism within the cytochrome P-450 system and might inhibit the oxidative metabolism of other drugs. This is particularly relevant for compounds with a narrow therapeutic range, such as acenocoumarol. In this study we evaluated the effect of omeprazole use in patients receiving continuous acenocoumarol therapy. METHODS: One thousand and fifty-seven patients receiving long-term oral acenocoumarol combined with omeprazole were selected retrospectively. In 118 of these patients omeprazole was considered the only factor of possible influence on anticoagulant therapy. The control group consisted of 299 age- and sex-matched patients taking acenocoumarol without interfering medication. Dose adjustment of acenocoumarol on starting omeprazole therapy was indicated by clinically relevant changes in coagulation time. RESULTS: No adaptation of the anticoagulant dose was necessary in 74 of 118 omeprazole patients (62.7%), compared with 169 of 299 controls (56.5%). A higher dose was necessary in 30 of 118 omeprazole patients (25.4%), compared with 84 of 299 controls (28.0%). In 14 of 118 omeprazole patients (11.9%) a lowering of the anticoagulant dose was required, compared with 46 of 299 controls (15.4%). CONCLUSIONS: We found no evidence of any interaction between omeprazole and acenocoumarol. It seems likely that omeprazole can be administered safely to patients treated with acenocoumarol.

Acenocoumarol↗
PubMed1997

Malabsorption syndrome associated with ulceration of the stomach and small bowel caused by chronic intestinal ischemia in a patient with hyperhomocysteinemia.

We describe a 39-year-old woman with an 8-month history of abdominal pain, diarrhea, and weight loss. Clinical and laboratory evaluation indicated the presence of a malabsorption syndrome. Endoscopy revealed multiple gastric ulcerations and an abnormal "picture" of the duodenal mucosa. At duodenal biopsy, necrosis confined to the distal parts of the enteric villi and a polymorphonuclear leukocyte response were found. Further evaluation revealed intestinal ischemia as a result of mesenteric atherosclerosis. After a revascularization procedure was performed, the symptoms disappeared. The macroscopic and microscopic picture of the bowel normalized. In our search for risk factors of atherosclerosis, we found a substantially increased basal plasma homocysteine concentration. This case suggests that hyperhomocysteinemia may have a causal role in the development of symptomatic, premature atherosclerosis of the mesenteric circulation.

Adult↗
PubMed1997

Acute upper gastrointestinal bleeding in the Amsterdam area: incidence, diagnosis, and clinical outcome.

OBJECTIVES: In the United States of America and the United Kingdom several epidemiological upper gastrointestinal bleeding (UGIB) surveys have been done. However, information about the current epidemiology of acute UGIB in continental Western Europe is sparse. METHODS: From July of 1993 to July of 1994, 951 patients with acute UGIB were prospectively included in 12 hospitals in the Amsterdam area. Data were collected prospectively with a standard questionnaire and included demographic as well as specific data relating to UGIB. RESULTS: The overall incidence was 45 per 100,000 persons/yr. Patients had an advanced age (median, 71 yr), and shock was found in 63%. Coexisting illnesses were present in 85%. Twenty percent had a history of previous ulcer disease, of whom 33% used acid suppressive therapy. Endoscopy was performed within 24 h in 78%, and in 42% a gastroduodenal ulcer was found. In 24%, no diagnosis could be made at the initial endoscopy, in these patients endoscopy was done significantly later than in those in whom a diagnosis was readily made. Rebleeding occurred in 16.4%, and 7% had surgery. Mortality rate was 13.9%, which was considered in one-third to be directly related to the bleeding. CONCLUSIONS: The incidence and diagnostic profile of UGIB is similar to other large European studies, but different from those for the United States. Bleeding could perhaps have been prevented in the patients with a history of previous ulcer disease. The 24-h endoscopy service was not as fast, accurate, and widespread as we assumed. Mortality seems to be more related to advanced age, shock, and coexisting illnesses.

Acute Disease↗
PubMed1996

Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication.

BACKGROUND: Helicobacter pylori infection plays an important part in the development of atrophic gastritis and intestinal metaplasia, conditions that predispose patients gastric cancer. Profound suppression of gastric acid is associated with increased severity of gastritis caused by H. pylori, but it is not known whether acid suppression increases the risk of atrophic gastritis. METHODS: We studied patients from two separate cohorts who were being treated for reflux esophagitis: 72 patients treated with fundoplication in Sweden and 105 treated with omeprazole (20 to 40 mg once daily) in the Netherlands. In both cohorts, the patients were followed for an average of five years (range, three to eight). After fundoplication, the patients did not receive acid-suppressive therapy. The presence of H. pylori was assessed at the first visit by histologic evaluation in the fundoplication group and by histologic and serologic evaluation in the omeprazole group. The patients were not treated for H. pylori infection. Before treatment and during follow-up, the patients underwent repeated gastroscopy, with biopsy sampling for histologic evaluation. RESULTS: Among the patients treated with fundoplication, atrophic gastritis did not develop in any of the 31 who were infected with H. pylori at base line or the 41 who were not infected; 1 patient infected with H. pylori had atrophic gastritis before treatment that persisted after treatment. Among the patients treated with omeprazole, none of whom had atrophic gastritis at base line, atrophic gastritis developed in 18 of the 59 infected with H. pylori(P<0.001) and 2 of the 46 who were not infected (P=0.62). CONCLUSIONS: Patients with reflux esophagitis and H. pylori infection who are treated with omeprazole are at increased risk of atrophic gastritis.

Adolescent↗
PubMed1995

Molecular, cytogenetic, and phenotypic studies of a constitutional reciprocal translocation t(5;10)(q22;q25) responsible for familial adenomatous polyposis in a Dutch pedigree.

Familial adenomatous polyposis (FAP) is an inherited predisposition to colorectal cancer caused by germline mutations in the adenomatous polyposis coli (APC) gene located on chromosome segment 5q21-q22. We detected a germline rearrangement of the APC gene in a Dutch FAP family by screening genomic DNA samples with APC cDNA probes. Subsequent molecular and cytogenetic studies revealed a constitutional reciprocal translocation t(5;10)(q22;q25) that resulted in the disruption of the APC gene. Southern blot and polymorphic marker analysis indicated that part of the APC gene had been deleted. Analysis of the APC protein product indicated that the translocation breakpoint did not lead to the formation of a detectable truncated APC protein but apparently resulted in a null allele. Evaluation of the clinical phenotypes in the patients suggested that they exhibited features of an unusual form of FAP characterized by a slightly delayed age of onset of colorectal cancer and a reduced number of colorectal polyps. The latter were mainly sessile and were located predominantly in the proximal colon. To our knowledge, this is the first description of FAP caused by a reciprocal translocation disrupting the APC gene.

Adenomatous Polyposis Coli↗
PubMed1994

[Upper digestive tract hemorrhage; an assessment in the Amsterdam region].

OBJECTIVE: To inventory diagnostic and therapeutic strategies and the value of endoscopy in upper gastrointestinal haemorrhage in Amsterdam and environs. DESIGN: Descriptive. SETTING: Eight hospitals in and around Amsterdam. METHOD: For 3 months all patients with upper gastrointestinal haemorrhage were recorded. The total group consisted of 132 patients. RESULTS: The group included 81 men and 51 women, the mean age was 63 years. Prior to the symptoms, 44% had used acetylsalicylic acid, non-steroidal anti-inflammatory drugs or oral anticoagulants. Diagnostic endoscopy was performed in 85% within 24 hours. The most frequent diagnosis was ulcerative disease (48%). Medication was given to 86% of the patients, 20% underwent endoscopic (injection) therapy and only 17% were operated on. Recurrent haemorrhage was seen in 24%, overall mortality was 6%. CONCLUSION: Ulcerative disease is still the most common cause of upper gastrointestinal haemorrhage. Medication is still more or less routinely administered, despite lacking proof of efficacy.

Adolescent↗
PubMed1994

Long-term treatment with omeprazole for refractory reflux esophagitis: efficacy and safety.

OBJECTIVE: To evaluate the long-term efficacy and safety of omeprazole in patients with gastroesophageal reflux disease resistant to treatment with histamine-2 (H2)-receptor antagonists. DESIGN: Cohort analytic study with a mean follow-up of 48 months (range, 36 to 64 months). SETTING: Patients receiving ambulatory care from referral centers. PATIENTS: 91 patients with gastroesophageal reflux disease resistant to treatment with an H2-receptor antagonist but subsequently responsive to 40 mg of omeprazole daily. INTERVENTION: Open maintenance therapy consisting of 20 mg of omeprazole daily in 86 patients and 40 mg daily in 5 patients. OUTCOME MEASURES: Endoscopy to assess healing; side effects, laboratory values, fasting serum gastrin level, and gastric corpus biopsies to assess safety. RESULTS: Esophagitis recurred in 47% of the patients receiving 20 mg of omeprazole daily, but all rehealed after the dose was doubled. Seven of 40 patients (18%) had a second relapse after a mean follow-up time of 24 months (range, 9 to 36 months) that was successfully treated with a further 20-mg dose increment for a mean period of 36 months (range, 6 to 39 months). Median gastrin levels increased initially from 60 ng/L before study entry to 162 ng/L (P < 0.01) with treatment and reached a plateau during maintenance treatment. Very high gastrin levels (> 500 ng/L) were observed in a subgroup (11%) of patients. The incidence of micronodular hyperplasia increased from 2.5% of the patients at first biopsy to 20% at the last biopsy (P = 0.001), with a corresponding progression of gastritis to subatrophic or atrophic gastritis from less than 1% to 25% (P < 0.001), which was more pronounced in patients with very high serum gastrin levels. CONCLUSIONS: Maintenance therapy with omeprazole was effective for at least 5 years in patients with gastroesophageal reflux disease resistant to treatment with H2-receptor antagonists. Treatment was accompanied by a persistent increase in serum gastrin levels and an increase of micronodular argyrophil cell hyperplasia and subatrophic or atrophic gastritis.

Barrett Esophagus↗
PubMed1993

Long-term omeprazole therapy does not affect Helicobacter pylori status in most patients.

Fifty-one patients were treated with 20-60 mg omeprazole for reflux oesophagitis resistant to H2-blocker therapy during a mean of 49 months of follow-up. With use of a standardized enzyme-linked immunosorbent assay technique specific IgG and IgG Helicobacter pylori antibodies were determined in serum obtained at the start of therapy and at the most recent visit. At the start of therapy 26 patients (51%) had evidence of H. pylori infection, as demonstrated by increased IgG and IgA antibody levels. During follow-up, 4 of these 26 patients (15%) became H. pylori seronegative. It is concluded that long-term treatment with omeprazole has no effect on H. pylori status in most patients.

Aged↗
PubMed1993

Persistent diarrhoea in cholecystocolic and gastrocolic fistula after gastric surgery.

In patients presenting with diarrhoea and vitamin deficiency even years after gastro-intestinal surgery, the possibility of fistulas should be considered. Four patients with persistent diarrhoea years after gastric surgery are described. Diagnosis of cholecystocolic and gastrocolic fistulas were made by barium enema and resection of the fistulas was performed.

Aged↗
PubMed1990

Effect of long-term treatment with omeprazole on serum gastrin and serum group A and C pepsinogens in patients with reflux esophagitis.

Twenty-nine nongastrectomized and three partially gastrectomized patients with chronic reflux esophagitis resistant to 12 weeks' treatment with histamine H2-receptor antagonists were treated with a daily oral dose of 20-40 mg of omeprazole for 12-30 months. Basal serum gastrin, serum pepsinogen A, and serum pepsinogen C concentrations were monitored at regular intervals. Serum gastrin levels significantly (P less than 0.01) increased threefold to fourfold during the first 1-2 months of the study when all patients ingested 40 mg of omeprazole daily. Dose reduction to 20 mg did not significantly decrease gastrin levels. Serum gastrin levels showed a trend to further increase after the first 3 months of treatment, reaching statistically significant differences for values from the 3-12-month period (P less than 0.05) and from the 3-24-month period (P less than 0.005). Women and patients with high basal serum gastrin levels before omeprazole treatment were more likely to achieve higher serum gastrin levels during omeprazole treatment. Serum pepsinogen A and C levels were significantly (P less than 0.01) increased at all time intervals during long-term treatment with omeprazole. No significant tendency toward higher serum pepsinogen C levels in time was observed. However, serum pepsinogen A levels and the ratio of pepsinogen A to pepsinogen C further increased significantly (P less than or equal to 0.05) during the initial 3-12-month period. However, this trend was not observed anymore afterward. Antrectomized patients did not show increases in serum gastrin and serum pepsinogen A and C levels, suggesting that hypergastrinemia may be involved in the observed hyperpepsinogenemia.

Aged↗
PubMed1989

Efficacy of the H+/K+-adenosine triphosphatase inhibitor omeprazole in peptic ulcer.

In duodenal ulcer studies comprising more than 2,000 patients the efficacy of omeprazole in doses of 20-40 mg once daily has been compared with the recommended doses of the H2-receptor antagonists cimetidine and ranitidine. At 2 weeks the differences in healing rates in favour of omeprazole were 12-33%; while they were somewhat lower at 4 weeks, ranging from 4 to 20%. In most studies the difference in healing rate was statistically significant. In some studies pain relief at 2 weeks was more pronounced on omeprazole. In three gastric ulcer studies omeprazole in doses of 20 or 40 mg once daily has been compared with ranitidine 150 mg twice daily. Healing rates on omeprazole were significantly greater in 2 of the 3 studies. Pain relief was faster on the higher dose of omeprazole. In prepyloric gastric ulcer the healing rate at 2 weeks was not significantly greater on 20 or 40 mg omeprazole than on ranitidine, while in another study the healing rate was significantly greater on 30 mg omeprazole as compared with cimetidine. In the first week of treatment more patients on omeprazole became free of pain in the latter study. The relapse rate after stopping therapy was similar for omeprazole and the H2-receptor antagonists independent of the type of ulcer. In conclusion, omeprazole heals ulcers faster than the recommended doses of H2-receptor antagonist. The difference in healing rate is more pronounced halfway than at the end of the treatment course.

Cimetidine↗
PubMed1989

Use of omeprazole in the management of reflux oesophagitis resistant to H2-receptor antagonists.

Severe reflux oesophagitis, which is resistant to treatment with high doses of H2-receptor antagonists, can be treated successfully with the H+,K+-ATPase inhibitor omeprazole. Experience from more than 3 years of continuous treatment with omeprazole, in doses adjusted to prevent recurrences, has demonstrated its high efficacy in the long-term management of the patients. The use of this drug emphasizes the importance of long-standing, effective, 24-hour acid inhibition for reflux oesophagitis. Fasting gastrin levels increase 2-fold during the initial treatment period but continued treatment does not induce any further elevation. Omeprazole does not induce pathological changes in the endocrine cell population of the gastric oxyntic mucosa, though in some patients an increase in the argyrophilic cell volume density during omeprazole treatment has been reported. Careful surveillance of the safety profile of this drug is continuing.

Esophagitis, Peptic↗