Biomedical subjects

A Berstad

Publications and source records attributed to A Berstad.

At least 145 records · Page 8Linked to original sources

PubMed1990

[Helicobacter pylori infection among employees at the gastroenterologic section, Haukeland Hospital].

Using the C-14 urea breath test we estimated the gastric urease activity among 46 healthy Norwegians, all employed at the section of gastroenterology, Haukeland Hospital, Norway. The overall prevalence of Helicobacter pylori-infection (30.4%) is similar to that reported previously among healthy subjects outside hospitals. The tendency towards higher prevalence among the gastroenterologists (41.7%) may be accounted for partly by the preponderance of males in this profession. The results do not support the notion that gastroenterologists are more liable to attract gastric H pylori-infection than other hospital personnel.

Adult↗

PubMed1990

[Endoscopic hemostasis in hemorrhagic peptic ulcer. A review and pilot study of local thrombin injection combined with systemic fibrinolysis inhibition (with tranexamic acid)].

Today, most upper GI-haemorrhages can be handled without surgery. We discuss the available endoscopic haemostatic methods. Injection therapy seems to be as effective as laser-, heater probe- and bipolar electrocoagulation, and is often preferred because the equipment is inexpensive. In a pilot study of 37 patients with haemorrhage from peptic ulcer (13 with active bleeding and 24 with stigmata of recent hemorrhage) we injected thrombin in the ulcer base and treated the patients systemically with an antifibrinolytic drug (tranexamic acid) for five days. Endoscopic follow-up revealed stigmata of recent haemorrhage in 23 patients on day 1 and in eight patients on day 5. "Blood in stomach" was seen in eight patients on day 1 and in two patients on day 5. Four patients had clinical signs of rebleeding, but only one of them needed operation (definite hemostasis 97%). There were no obvious side effects of the treatment. Contrary to other endoscopic methods, local injection of thrombin does not damage the normal mucosa. However, the method has not been sufficiently explored as yet, and cannot be recommended without strict control and follow-up measures. Early control endoscopy seems to be a sensitive way of monitoring haemostasis.

Cyclohexanecarboxylic Acids↗

PubMed1990

Acute effects of antacids on gastric juice components in duodenal ulcer patients.

In 10 duodenal ulcer patients gastric juice was aspirated every 10 min for 20 min before and 200 min after sham feeding. One antacid tablet or placebo was given 80 min after the sham feeding. Analyses of the aspirates showed that antacids reduced mean hydrogen ion activity and pepsin concentration significantly for 40 and 60 min, respectively, and increased phospholipid concentration for 30 min, compared with placebo. Highest mean pH was 2.52. The percentage of pH readings at or above pH levels of 2, 3, and 4 during the 2 h period following antacid administration was 29, 10, and 2%, respectively. No significant differences between antacid and placebo were found regarding intragastric concentrations of bile acids and prostaglandin E2. When one antacid tablet was administered 80 min after a real meal, the effect on intragastric pH was similarly weak, but lasted slightly longer. Acid neutralization' alone can hardly explain the ulcer-healing effect of low-dose antacids. Antacid-induced increase in intragastric concentration of phospholipids is a new and potentially important observation.

Adult↗

PubMed1990

Misoprostol treatment exacerbates abdominal discomfort in patients with non-ulcer dyspepsia and erosive prepyloric changes. A double-blind, placebo-controlled, multicentre study.

One hundred and thirty-seven consecutive outpatients with non-ulcer dyspepsia (NUD) and erosive prepyloric changes (EPC) were randomly allocated to double-blind treatment with 400-micrograms misoprostol tablets twice daily or placebo for 4 weeks. Misoprostol had a significant worsening effect on epigastric pain, nausea, meteorism, lower abdominal pain, and diarrhoea, as compared with placebo. The fact that symptoms in patients with NUD and EPC were exacerbated by an antisecretory dose of misoprostol indicates that the symptoms are largely unrelated to gastric acid.

Adolescent↗

PubMed1990

Gastric mucosal bleeding after unfractionated and low molecular weight heparin in rats.

The bleeding from an induced gastric mucosal lesion was monitored after intravenous administration of unfractionated heparin and enoxaparin, a low molecular weight heparin. The gastric mucosa was exposed in a chamber, which was superfused with saline and emptied at 1-min intervals for quantitation of bleeding. Both heparins prolonged the bleeding time and increased the blood loss dose-dependently. Five to ten times higher doses of enoxaparin (in terms of anti-Xa units) were required to achieve similar prolongation of the bleeding times as with unfractionated heparin. The results indicate a more favourable antihaemostatic effect of enoxaparin than of unfractionated heparin.

Animals↗

PubMed1990

Suppression of gastric urease activity by antacids.

Campylobacter pylori (CP) infection among healthy employees at the section of gastroenterology was studied by means of the carbon-14 urea breath test. Fourteen of 46 individuals (30.4%) were infected with Campylobacter pylori (CP+). Eleven CP+ individuals were treated with a low-dose regimen of antacids (four tablets a day) for 2 weeks. The 14C recovery dropped from 8.36 +/- 1.26% before treatment to 5.70 +/- 1.24% (p = 0.023) approximately 12 h after the last intake of antacids, a 31.8% reduction, indicating suppression but no eradication of the C. pylori infection. A new breath test 2 weeks after cessation of treatment indicated that the suppressive effect of antacid on C. pylori infection was short-lived.

Adult↗

PubMed1990

A new model to assess the haemorrhagic potential of various heparin preparations.

In the gastric mucosa, haemostasis is hampered by the acidity and peptic activity of the gastric juice and by the fibrinolytic activity of plasmin. The hostile intragastric environment may be responsible for the unsecure haemostasis, with episodes of rebleeds often seen in gastroduodenal haemorrhage. Secondly, the haemostatic mechanisms of the gastric mucosa are largely independent of platelet aggregation and thus rely mainly on the coagulation system, making the gastric mucosa a unique model to test haemorrhagic effects of anticoagulants. Using a rat gastric chamber technique, we studied bleeding times from induced gastric mucosal lesions after intravenous administration of unfractionated and low molecular weight heparins. The bleeding times were dose-dependently prolonged by all heparins. With unfractionated heparin, significant prolongation of the bleeding times was seen already at a dose of 75 anti-Factor Xa U/kg, proving that the present model is more sensitive than previous models. The bleeding time per unit dose of both Kabi 2165 (p less than 0.05) and enoxaparin (p less than 0.001) was significantly less than that of unfractionated heparin.

Animals↗

PubMed1990

Low-dose antacids versus 400 mg cimetidine twice daily for reflux oesophagitis. A comparative, placebo-controlled, multicentre study.

Ninety-one patients with reflux oesophagitis were randomly allocated to treatment with one chewable antacid tablet (acid-neutralizing capacity, 30 mmol) four times daily, 400 mg cimetidine twice daily, or placebo. The study was double-blind, with a double-dummy technique. Endoscopy was performed before inclusion and after 8 weeks' treatment. Symptoms were recorded on diary cards and on visual analogue scales. Statistically significant healing of oesophagitis was achieved in all three treatment groups, but none of the active regimens were significantly superior to placebo. Symptoms were significantly reduced with both cimetidine and antacids compared with placebo. Patients taking antacids consumed significantly less extra antacids for pain relief and had significantly better global assessment score than patients taking cimetidine during the first and second half of the study, respectively. In conclusion, neither cimetidine nor antacids were significantly superior to placebo in healing of reflux oesophagitis. Both the active regimens were superior to placebo for symptomatic relief.

Administration, Oral↗

PubMed1989

Acute damage of gastroduodenal mucosa by acetylsalicylic acid: no prolonged protection by antacids.

Twenty healthy volunteers participated in a double-blind, crossover study to evaluate endoscopically whether low-dose antacids have any prolonged and pH-independent protective capacity against gastroduodenal mucosal damage induced by acetylsalicylic acid. Antacid or placebo one tablet q.d.s. was given for 1.5 days. Acetylsalicylic acid (1.5 g) was administered 3 h after the last dose of antacid/placebo, and gastroscopy was performed 1 h thereafter. Thirteen of 20 subjects showed a decrease in total damage with antacids as compared with placebo, but the difference did not reach statistical significance. Thus, protection by antacids against acetylsalicylic acid-induced gastric mucosal lesions could not be documented at a time when intragastric pH presumably had returned to normal.

Adult↗

PubMed1989

Symptomatic effect of a low-dose antacid regimen in reflux oesophagitis.

The symptomatic effect of a 2-week low-dose antacid tablet regimen was assessed in a prospective, double-blind, randomized, placebo-controlled, crossover trial in 47 patients with endoscopically verified reflux oesophagitis. During treatment with antacid there were lower global symptomatic scores (p less than 0.05), less acid regurgitation (p less than 0.05), and fewer days (p less than 0.01) and nights (p less than 0.05) with heartburn than during placebo therapy. Also, significantly more patients preferred antacid than placebo treatment (p less than 0.05). Thus, a low-dose antacid tablet regimen relieves symptoms significantly better than placebo in patients with reflux oesophagitis.

Adult↗

PubMed1989

Follow-up study of erosive prepyloric changes.

A follow-up study of erosive prepyloric changes (EPC) was undertaken in 60 patients who originally presented with non-ulcer dyspepsia and EPC grade 2 or 3. After 45 (range, 24-60) months EPC grade 2 or 3 was still present in 80% of the patients, and 82% had unchanged dyspeptic symptoms. Most of the patients (77%) experienced a 'stressful' life situation. None of the patients had developed peptic ulceration during the follow-up period, and there were no indications of active or healed ulcerations or cancer at the follow-up study. The results indicate that EPC are chronic changes in the gastric mucosa closely associated with long-lasting dyspeptic symptoms.

Adult↗

PubMed1989

Erosive prepyloric changes--a manifestation of stress?

To study the relationship between stress and the endoscopic diagnosis of erosive prepyloric changes (EPC), upper gastrointestinal endoscopy was performed twice in 19 cadets from the Military Academy, once in a 'non-stressed' situation and once after exposure to a standardized stress model. Five biopsy specimens per examination were obtained from the prepyloric mucosa, and the features of acute and chronic inflammation, erosion, and campylobacter-like structures (CLS) were evaluated. The endoscopy showed a significant (p less than 0.001) aggravation of EPC after stress. The histologic examination showed an increase of acute inflammation (p less than 0.05) and a higher density of CLS (p less than 0.01) after stress, as compared with the findings under non-stressed conditions. No association was observed between CLS and EPC. The study sheds new light on the pathogenesis of EPC, as it shows that EPC is aggravated during stress.

Adult↗

PubMed1988

Antacids reduce Campylobacter pylori colonization without healing the gastritis in patients with nonulcer dyspepsia and erosive prepyloric changes.

Antral biopsy specimens from 89 consecutive patients with nonulcer dyspepsia and erosive prepyloric changes included in a prospective, randomized, double-blind 4-wk study of the effect of an aluminum-magnesium antacid (120 mmol/day) or pirenzepine (50 mg b.i.d.) vs. placebo were examined histologically. Campylobacter pylori (CP) was found by light microscopy of silver-stained sections in 25 patients (28%). Campylobacter pylori-positive patients were on average older than CP-negative patients (p = 0.02). There was a strong association between CP colonization and acute inflammation (p less than 0.001), both being rare in the absence of chronic inflammation. During treatment with antacids, the density of CP decreased (p less than 0.001) without any improvement of the inflammatory reaction. On the contrary, the number of patients with gastritis tended to increase after antacids as compared with placebo (p less than 0.10). A separate analysis showed no symptomatic effect of the drugs. Thus, neither nonulcer dyspepsia nor erosive prepyloric changes are strongly associated with antral CP colonization or acute inflammation. Aluminum-magnesium antacids may suppress antral CP infection without healing the gastritis or relieving symptoms.

Adult↗

PubMed1988

Effect of enprostil on basal and meal-stimulated gastric acid and pepsin secretion, serum gastrin and gastric emptying in healthy persons.

Ten healthy volunteers took part in a double-blind, randomized, cross-over study of the effect of single doses of enprostil (70 micrograms) and placebo on basal and meal-stimulated gastric acid, pepsin secretion and serum gastrin. Meal-stimulation was induced by modified sham feeding combined with repeated gastric instillation and withdrawal of meat soup. When studied between 1 and 2.5 hours after oral administration of the drug, enprostil decreased basal acid output by 92% (P less than 0.001) and stimulated acid output by 70% (P less than 0.001). Basal and stimulated volumes of gastric juice were decreased by 50% (P less than 0.02) and 35% (P less than 0.002), respectively. Enprostil decreased stimulated pepsin output by 34% (P less than 0.05), but had no effect on the concentration of pepsin. Neither basal nor stimulated serum gastrin concentrations were affected by enprostil. Percent recovery of the meal was measured by an unabsorbable marker, polyethylene glycol, instilled into the stomach mixed with the soup. Polyethylene glycol recovery decreased from 89% with placebo to 67% with enprostil (P less than 0.01), indicating an enhanced gastric emptying rate with enprostil.

Adult↗

PubMed1988

The influence of prolonged physical stress on gastric juice components in healthy man.

Eight healthy men were exposed to 5 days of continuous heavy exercise combined with caloric deficiency and sleep deprivation. Immediately after the stress period the fasting and postprandial intragastric bile acid concentration, pepsin concentration, and gastric juice acidity were measured. Compared with a control experiment performed 8 weeks later, the results from the stress period showed a sevenfold increase in the fasting concentration of intragastic bile acids (from 35 mumol/l to 256 mumol/l; p less than 0.02), there was a tendency towards an increase in the fasting intragastric pepsin concentration, and there was an increase (p less than 0.05) in the intragastric pH level throughout the 3rd postprandial hour. It appears that physical stress induces changes in the intragastric milieu that might dispose for mucosal lesions.

Adult↗

PubMed1988

Effect of tranexamic acid on gastric bleeding in rats.

Bleeding from an induced gastric mucosal wound was monitored for 2 h in a rat model, in which normal hemostasis was disturbed mechanically by perfusing the lesion with saline. The hemorrhage was characterized by continuous bleeding and/or episodes of spontaneous rebleeding, as often seen in patients with gastric hemorrhage. The antifibrinolytic agent, tranexamic acid, significantly reduced total bleeding volume and number of rebleeding episodes, suggesting that plasmin-induced fibrinolysis might aggravate gastric mucosal hemorrhage.

Animals↗

PubMed1988

Relationship of overweight to hiatus hernia and reflux oesophagitis.

In a prospective study in 1224 patients referred for upper alimentary endoscopy, reflux oesophagitis was found in 195 (16%) of the patients and hiatus hernia in 249 (20%). In patients with reflux oesophagitis a coexisting hiatus hernia was found in 68%. The weight-for-height index (W/H1.8), which expresses the degree of overweight, was significantly higher both in patients with hiatus hernia and in the patients with reflux oesophagitis, indicating an overweight of approximately 5% in both groups. The overweight was most pronounced in oesophagitis grades 1 and 2, whereas in patients with severe oesophagitis (grade 3) body weight was normal, possibly owing to weight loss caused by dysphagia and excessive regurgitation. The results support the view that adiposity is associated with both sliding hiatus hernia and reflux oesophagitis and that hiatus hernia plays a role in the development of reflux oesophagitis.

Adult↗

PubMed1988

Effect of platelet-activating factor and its receptor antagonist, SRI 63-675, on gastric bleeding in rats.

Gastric bleeding from an induced mucosal wound was monitored for 2 h in a rat model in which the normal haemostasis was disturbed mechanically by perfusing the lesion with saline. The bleeding pattern was characterized by continuous and/or rebleeding episodes. Intravenous infusion of platelet-activating factor (PAF) in a dose of 25 ng/kg/min reduced the blood loss by 92% without affecting the bleeding pattern or the macroscopic appearance of the mucosa significantly. Concomitant administration of the PAF receptor antagonist SRI 63-675 in a dose of 50 micrograms/kg/min completely reversed the effects of PAF. The bleeding was unchanged after PAF receptor antagonist alone, suggesting that endogenous PAF might not participate in the in vivo haemostasis after an acute gastric mucosal lesion.

Animals↗