Biomedical subjects

U Knutson

Publications and source records attributed to U Knutson.

16 recordsLinked to original sources

PubMed1988

The effects of omeprazole and cimetidine on duodenal ulcer healing and the relief of symptoms.

In a Swedish double-blind multicentre study, omeprazole (30 mg o.m.) was compared with the H2-receptor antagonist cimetidine (400 mg b.d.) in 152 patients. Clinical assessments and laboratory investigations were carried out at 2 and 4 weeks, and again at 6 weeks in unhealed patients. Endoscopy was performed at 2 weeks, and again at 4 and 6 weeks in unhealed patients. The patients in the two groups were well-matched prior to treatment. Omeprazole was superior to cimetidine in ulcer-healing rate after 2, 4 and 6 weeks. After 2 weeks of treatment, 66% of the omeprazole- and 45% of the cimetidine-treated patients were healed (P = 0.02), after 4 weeks 97 and 84% (P = 0.01), and after 6 weeks 100 and 92% (P = 0.02), respectively. There was a more pronounced improvement in the patients' symptoms in the omeprazole group after 2 weeks (P = 0.05). Both drugs were well-tolerated, but there was a high prevalence of patients with adverse events in the cimetidine group (51%, compared to 30% of the omeprazole group; P = 0.02). A total of 125 patients were followed for 6 months after healing. The patients were investigated by endoscopy after 6 months, or whenever symptoms occurred. There was no significant difference in the rate of relapse within 6 months between the two treatment groups: 54% relapsed in the omeprazole group and 52% in the cimetidine group. In conclusion, 30 mg of omeprazole, given once daily, is superior to 400 mg of cimetidine twice daily in duodenal ulcer healing; but ulcer relapse in the two groups appears to be equivalent.

Adolescent↗

PubMed1978

Gastric acid responses to adequate and modified sham feeding and to insulin hypoglycemia in duodenal ulcer patients.

In duodenal ulcer patients the effect of vagal activation of gastric acid secretion by the intricate procedure of adequate sham feeding for 15 min has been compared with the effects of vagal stimulation induced by more easily accomplishable methods. The comparison involved modified sham feeding for 15 min by a 'chew-and-spit' technique and insulin hypoglycemia produced by i.v. injected insulin in the doses 0.1, 0.15, or 0.2 U/kg b.w. In 6 patients the peak and 2-hour acid responses to adequate sham feeding (10.7 mmol/30 min and 29.7 mmol) did not significantly differ from corresponding responses to modified sham feeding (9.1 mmol/30 min and 25.2 mmol). The peak and 2-hour acid responses to insulin in a dose of 0.1 U/kg (8 patients) were not significantly different from the sham-feeding responses. The 2-hour acid responses to insulin in the doses of 0.15 (6 patients) and 0.2 U/kg (17 patients) were significantly higher than the sham-feeding response. Furthermore, the peak acid response to insulin in a dose of 0.15 U/kg was significantly higher than the peak sham-feeding response. The gastric acid responses to modified sham feeding and insulin in a dose of 0.1 U/kg b.w. in duodenal ulcer patients seem to satisfactorily reflect physiological vagal activation of acid secretion.

Duodenal Ulcer↗

PubMed1978

The vagogastrone mechanism in man.

From experiments on the dog evidence has accumulated of vagal release of a candidate hormone inhibiting gastric acid secretion--vagogastrone. The nature and origin of vagogastrone are uncertain. The inhibitory effect of vagogastrone is characteristically exerted against gastrin-stimulated acid secretion from the vagally denervated parietal cell area. In the present study vagal activation by sham feeding significantly inhibited the submaximal acid response to continuous i.v. infusion of pentagastrin in seven duodenal ulcer patients previously subjected to proximal gastric vagotomy. The inhibitory effect was slight--16% reduction--and of short duration. Sham feeding had no effect on the pentagastrin-stimulated acid secretion in six subjects with an intact stomach. The results favour the existence of a vagogastrone mechanism in man, but the inhibitory effect seems to be of quantitatively minor importance, at least in the duodenal ulcer patient.

Adult↗

PubMed1977

The effect of intragastric pH-variations on the gastric acid response to insulin hypoglycaemia in healthy subjects and duodenal ulcer patients.

The gastric acid response to i.v. injection of 0.15 U of soluble insulin/kg b.w. was determined in healthy subjects and duodenal ulcer patients during intragastric perfusion with water, 0.1 M HC1, and alkaline buffer (pH 8.3). Perfusion with hydrochloric acid significantly reduced the peak gastric acid output following insulin in 6 healthy subjects (reduction 45%, p less than 0.05) but had no significant effect on the peak gastric acid response to insulin in 7 DU patients (reduction 16%, p greater than 0.05). The 2.5-hour gastric acid response to insulin was, however, significantly reduced in both groups (56% and 35%, respectively) by exogenous acidification of the stomach. The gastric acid response to insulin hypoglycaemia in 3 DU patients was the same with intragastric water and alkaline buffer perfusion. The reduction of the gastric acid response to insulin hypoglycaemia by intragastric acidification corresponded to a reduced volume secretion and could not be ascribed to increased back diffusion of hydrogen ions or duodenal inhibition. These findings suggest that the gastric acid response to insulin hypoglycaemia is inhibited by a low intragastric pH in man, and that DU patients are less sensitive to the inhibitory mechanism than healthy subjects.

Adult↗

PubMed1976

Gastric acid responses to graded i.v. infusion of pentagastrin and histalog in peptic ulcer patients before and after antrum-bulb resection.

Gastric acid responses to graded i.v. infusion of pentagastrin and Histalog were determined in peptic ulcer patients. Single-day multiple-dose tests were performed. The sensitivity to the humoral stimuli as determined by the calculated ED50's was not significantly different for duodenal ulcer patients with moderate (DUmod) or massive (DUmass) observed hypersecretion or for gastric ulcer (GU) patients: median ED50's of pentagastrin were 6.2, 6.6, and 13.1 mug/h in 18 DUmod, 22 DUmass and 7 GU patients respectively, and median ED50's of Histalog were 16.6, 25.3, and 17.1 mg/h in 14 DUmod, 10 DUmass and 6 GU patients respectively. Antrum-bulb resection significantly reduced basal acid secretion and maximal acid responses to the humoral stimuli (about 45% reduction) but did not significantly change the loss of gastric contents to the intestine or the sensitivity to the humoral stimuli (median ED50 of pentagastrin increased from 5.2 to 6.7 mug/h in 14 patients, and median ED50 of Histalog increased from 16.0 to 20.8 mg/h in 12 patients), suggesting that the intact antrum-bulb region of the ulcer patient is controlling the capacity to secrete acid, and indicating that antrum-bulb gastrin is an important trophic factor for the parietal cells in man.

Betazole↗

PubMed1975

The effect of intragastric neutralization on the gastric acid response to antral distension in man.

The gastric acid secretion in response to graded antral distension was determined in healthy subjects and in peptic ulcer patients with water perfusion or alkaline buffer perfusion of the stomach, giving an intragastric pH of 1.8-3.0 and 6.2-8.3 respectively. Intragastric neutralization increased the basal acid secretion in healthy subjects and gastric ulcer patients but did not change the basal acid secretion in duodenal ulcer patients. Distension of the antrum produced the same secretory effect with and without intragastric neutralization: no increased acid response in healthy subjects, a slight acid response in patients with a quiescent duodenal ulcer or a gastric ulcer, and a more pronounced acid response in patients with an active ulcer, amounting to about 30% of the peak acid response to pentagastrin. The results show that: a) the peptic ulcer patients - and particularly patients with an active duodenal ulcer - are more sensitive to the acid secretory effect of antral distension than healthy subjects; b) increasing the intragastric pH above 20 does not enhance the acid response to antral distension; c) the acid secretory effect of antral distension is markedly less in man than the effect observed in the dog.

Adult↗

PubMed1974