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Biomedical subjects

H Gudjónsson

Publications and source records attributed to H Gudjónsson.

17 recordsLinked to original sources
PubMed1999

Omeprazole and ranitidine in the prevention of relapse in patients with duodenal ulcer disease.

BACKGROUND: Although the eradication of Helicobacter pylori is of primary importance when initiating treatment, it is also important to have a strategy for patients who are H pylori-negative, fail to demonstrate eradication or have a tendency to become re-infected or relapse. PATIENTS AND METHODS: In a double-blind, parallel-group clinical trial of 928 patients (from 70 centres in 16 countries) with duodenal ulcers who after a short term study had relief of symptoms and healed ulcers proved endoscopically, 308 were randomly assigned to receive omeprazole 10 mg in the morning, 308 to receive omeprazole 20 mg in the morning and 312 to receive ranitidine 150 mg at bedtime for up to 12 months. Symptoms were assessed every three months and endoscopy repeated at three, six and 12 months, or more often if indicated by recurrence of symptoms. The safety screening included basal serum gastrin concentrations and gastric mucosal histopathology. RESULTS: The remission rates up to 12 months were 87% for the omeprazole 20 mg group, 71% for the omeprazole 10 mg group and 63% for the ranitidine group. Omeprazole 20 mg differed significantly from both omeprazole 10 mg (P=0.0001, 95% CI 9 to 23) and ranitidine (P=0.0001, 95% CI 17 to 31). There was no statistically significant difference between omeprazole 10 mg and ranitidine over the 12-month period, but the 95% confidence interval allowed differences between 0% and 16% in favour of omeprazole at 12 months. A Cox regression analysis revealed that longer treatment courses to heal, smoking, a long ulcer history and young age negatively contributed to the odds of staying in remission. The treatments were well tolerated. There was a slight increase in basal serum gastrin concentrations, reflecting the different degrees of acid inhibition induced by the three treatments. No dysplastic or neoplastic lesions were found in any biopsies. CONCLUSIONS: More duodenal ulcer patients are maintained in remission with omeprazole 20 mg daily than with omeprazole 10 mg daily or with ranitidine 150 mg at bedtime.

Adolescent↗
PubMed1994

The association between coeliac disease, dermatitis herpetiformis and certain HLA-antigens in Icelanders.

Twenty-eight cases of coeliac disease (CD) and seven of dermatitis herpetiformis (DH) have been verified in Iceland. Standard serological techniques were used for HLA typing. Twenty-five individuals with CD were typed, 21 (84%) of whom carried DR3,DQ2. Twelve of these 25 (48%) had DR3,DR7, DQ2, which makes them possibly homozygous for DQ2, and suggests that homozygosity of DQ2 increases the risk for CD. The four DH patients that were typed all had HLA-B8,DR3,DQ2. It is concluded that CD and DH are associated with DR3, DQZ in Icelanders.

Adult↗
PubMed1994

Does sucralfate prevent short-term NSAID induced damage to the gastroduodenal mucosa?

The objective of the study was to assess whether sucralfate can prevent or diminish short-term nonsteroidal anti-inflammatory drug (NSAID)-induced damage in the stomach and duodenum. Sixteen healthy subjects were randomly treated for 7 days with sucralfate 2 g b.d. or placebo in a double-blind cross-over manner. Naproxen 500 mg b.d. was given on days 3-7. Gastrointestinal endoscopy was performed before and after each treatment period. Mucosal damage was measured by counting erosions, submucosal hemorrhages or ulcers on a fixed point scale of 0-4 for stomach and duodenum separately. The mean posttreatment injury score in the stomach was 2.13 +/- 1.51 and 2.0 +/- 0.97 for the placebo and sucralfate periods, respectively (p = 0.72). The possibility of type II error was 7%. In the duodenum, the injury score was 1.69 +/- 1.08 and 1.06 +/- 0.93 for the placebo and sucralfate periods, respectively (p = 0.08). The possibility of type II error was 37%. Sucralfate has no efficacy as a prophylactic agent against short-term NSAID-induced gastroduodenal injury.

Adult↗
PubMed1993

Leiomyomatous colonic polyp.

Leiomyomatous colonic polyps are rare. We report a patient with an asymptomatic 15-mm submucosal polyp in the sigmoid colon. The tumor was successfully removed by endoscopy. Histopathological examination revealed a leiomyoma originating in the muscularis mucosa.

Colon, Sigmoid↗
PubMed1993

Efficacy of sucralfate in treatment of non-ulcer dyspepsia. A double-blind placebo-controlled study.

The object of this study was to assess the efficacy of sucralfate in the treatment of non-ulcer dyspepsia (NUD). The diagnosis of NUD was made by exclusion. All patients underwent an upper gastrointestinal endoscopy and abdominal ultrasound, and blood tests were done as clinically indicated. Patients with a history of peptic ulcer disease were not included. Symptomatic assessment was made at the beginning and at the end of the study. The patients registered their most prominent dyspeptic symptoms and whether they improved, were unchanged, or worsened. The study was double-blind. Placebo or 1 g sucralfate four times daily was given for 3 weeks. Over a 2-year period 104 patients were included in the study; 56 received sucralfate and 48 placebo. Nine patients were excluded because of poor compliance or side effects, six from the sucralfate group and three from the placebo group. The sucralfate and placebo groups were comparable with regard to symptom and clinical variables. Global assessment of symptoms showed that in the sucralfate group 34 improved (68%), 11 were unchanged, and 5 were worse. In the placebo group 31 improved (69%), 11 were unchanged, and 3 were worse. There was no statistically significant difference between the groups. The 3-week course of sucralfate in patients with NUD did not show symptomatic improvement over placebo.

Adolescent↗
PubMed1992

Do adults with high gliadin antibody concentrations have subclinical gluten intolerance?

Gliadin antibodies of the IgG and IgA isotypes and IgG subclasses were measured in 200 adults who were randomly selected from the Icelandic National Register. Those with the highest gliadin antibody concentrations were invited with negative controls to participate in a clinical evaluation. Neither the study subjects nor the physicians who recorded and evaluated the clinical findings were aware of the antibody levels. Significantly higher proportion of the gliadin antibody positive individuals reported unexplained attacks of diarrhoea (p = 0.03), and IgA gliadin antibodies were associated with increased prevalence of chronic fatigue (p = 0.0037). The gliadin antibody positive group also showed significantly decreased transferrin saturation, mean corpuscular volume and mean corpuscular haemoglobin compared with the gliadin antibody negative controls. Serum folic acid concentrations were significantly lower in the IgA gliadin antibody positive individuals. On blind global assessment 15 of the 48 participants were thought to have clinical and laboratory features that are compatible with gluten sensitive enteropathy, and 14 of these were in the gliadin antibody positive group (p = 0.013). Complaints that have not been associated with gluten intolerance had similar prevalence in both groups with the exception of persistent or recurrent headaches that were more common in the gliadin antibody positive group. These findings raise the possibility that a subclinical form of gluten intolerance may be relatively common.

Adult↗
PubMed1992

Comparison between ranitidine and omeprazole for protection against gastroduodenal damage caused by naproxen.

Acute gastroduodenal injury is commonly associated with the use of nonsteroidal anti-inflammatory drugs. The mechanism of injury is not well understood. The objectives of this study were to evaluate the protective effect of two drugs that give different degrees of acid inhibition against naproxen-induced gastroduodenal injury. Fifteen volunteers aged 22-28 years underwent pre- and post-treatment gastroduodenoscopies during three treatment periods (that is, six examinations), and mucosal injury was graded on a Lanza scale ranging from 0 to 4. The subjects received placebo, 150 mg rantidine twice daily, or 40 mg omeprazole in a double-blind, random-order design for 7 days. Plain naproxen, 500 mg twice daily, was given on days 3-7. The mean injury score for the stomach during placebo treatment was 1.53, and ranitidine gave 44% and omeprazole 40% reduction compared with placebo, which did not reach statistical significance. About 70% of the stomach injury was located in the antrum. The mean injury score during placebo for the duodenum was 1.93, and ranitidine gave 80% and omeprazole 90% reduction (p = 0.004). In conclusion, a correlation between different degrees of acid suppression and a protective effect on the gastroduodenal mucosa could not be shown. The study suggests that acid plays a major role in acute naproxen-induced injury to the duodenal mucosa, and a moderate acid reduction is adequate for protection. In the stomach acid seems to play a minor role in the mucosal injury, but physiochemical contact with naproxen in the antrum and a cyclooxygenase inhibition are of greater importance.

Acute Disease↗