Search PubMed⌕ Search

Biomedical subjects

D G Hansen

Publications and source records attributed to D G Hansen.

7 recordsLinked to original sources
PubMed1999

[General practitioners want continuing education. Audit registrations among 369 physicians in Copenhagen].

The purpose of the study was to evaluate general practitioners' (GPs') interest in CME. A medical audit comprising 369 GPs in three counties was conducted in 1996. During 28,550 consultations the participating GPs recorded clinical subject, handling of the consultation, problems in the consultation and perceived need for training in relation to the consultation. The interest in CME varied from GP to GP and from one clinical subject to another. Desire for CME was expressed in relation to 16% of the consultations, most frequently in relation to psychiatry, community medicine and musculoskeletal diseases. Theoretical courses were the learning style most often preferred, especially for subjects requiring biomedical knowledge. Newer educational methods were also listed. Organisers of CME for general practitioners should be aware of the wide range of needs and wishes for CME among general practitioners.

Clinical Competence↗
PubMed1983

Aspirin can inhibit gastric mucosal cyclo-oxygenase without causing lesions in rat.

Dose-response relationships between aspirin-induced cyclo-oxygenase inhibition and gastric mucosal injury were studied in rats. Oral or parenteral aspirin, 25 mg/kg, inhibited prostaglandin generation by 87%-95% at 1, 3, and 6 h with no lesion formation. Aspirin, 100 mg/kg, inhibited prostaglandin generation by 95%-98% at 1, 3, and 6 h, but lesions were observed only when aspirin was given orally. Three-hour pretreatment with intraperitoneal aspirin, 12.5 mg/kg, did not enhance the mucosal injury caused by 10 mM acidified taurocholate, although prostaglandin generation was inhibited by 80%. Pretreatment with 25 mg/kg aspirin inhibited prostaglandin generation by 89% and was associated with significant mucosal injury by acidified taurocholate. We conclude that aspirin-induced 95% inhibition of gastric mucosal cyclo-oxygenase is not, by itself, sufficient to produce lesions and inhibition by greater than 80% is required to predispose the gastric mucosa to injury by otherwise mild irritants.

Administration, Oral↗
PubMed1982

Salicylic acid blocks indomethacin- and aspirin-induced cyclo-oxygenase inhibition in rat gastric mucosa.

Salicylic acid reduces gastric mucosal lesions induced by aspirin and indomethacin. Aspirin and indomethacin reduce gastric mucosal cyclo-oxygenase activity. These studies were designed to determine whether or not salicylic acid interacts with gastric mucosal cyclo-oxygenase, decreasing the inhibitory effect of aspirin and indomethacin as has been observed in platelets and vascular tissue. The interaction between salicylic acid and two cyclo-oxygenase inhibitors, indomethacin and aspirin, was assessed on ex vivo prostaglandin generation in the rat gastric mucosa. Salicylic acid (100 mg/kg) was administered orally 30 min before the subcutaneous injection of either indomethacin (0.5-10 mg/kg) or aspirin (5.0-20 mg/kg). Pretreatment produced a shift of the mean 50% inhibitory dose for PGF2 alpha formation from 0.92 to 7.6 mg/kg for indomethacin and from 7.8 to 20 mg/kg for aspirin. Similar results were achieved with ex vivo prostacyclin synthesis as measured by the level of 6-keto-PGF 1 alpha. These data are consistent with competitive enzyme kinetics, and may, in part, explain the protective effect of salicylic acid against the ulcerogenicity of aspirin and indomethacin on the gastric mucosa.

Animals↗
PubMed1980

Comparison of human urine gastric inhibitor (HUGI) and bacterial endotoxin as inhibitors of acid secretion.

In conscious cats with gastric fistulas, 10 micrograms . kg-1 of human urinary gastric inhibitor (HUGI) given as an intravenous bolus injection increased mean rectal temperature 1.4 degree C and inhibited mean gastrin-stimulated acid secretion by 64%. The sample of HUGI contained an amount of beta-hydroxymyristic acid corresponding to a 5% contamination of the HUGI with bacterial endotoxin. Injection of bacterial endotoxin in an amount corresponding to the beta-hydroxymyritic acid content of HUGI mimicked, both in magnitude and time course, the increase in body temperature and the inhibition of acid secretion produced by HUGI. We conclude that inhibition of acid secretion by HUGI may be due to the presence of an endotoxin-like contaminant.

Animals↗
PubMed1978

Histamine augments gastric ulceration produced by intravenous aspirin in cats.

In unanesthetized cats, continuous intravenous infusion of aspirin for 36 hr did not produce gastric ulcers when given alone but did when combined with 160 microgram kg-1 hr-1 of histamine-2HCl intravenously. The ulcers were mainly antral in location. The incidence and severity of ulcers increased with duration of the infusion up to 36 hr and with dose of aspirin up to 4 mg kg-1 hr-1. With the highest doses and longest durations some of the antral ulcers perforated. Antral ulcers occurred in more than half of the cats getting 0.25 mg kg-1 hr-1 or more of aspirin for 36 hr or getting 4 mg kg-1 hr-1 of aspirin for 6 or more hr. Intravenous aspirin plus intragastric infusion of 40 ml hr-1 of 150 mM HCl for 16 hr also produced gastric ulcers. Plasma salicylate concentrations were less than 350 microgram ml-1 with all doses and durations of aspirin used (400 microgram ml-1 is regarded as the upper limit of the therapeutic range in man). These studies show that when the stomach is acidified by giving histamine intravenously or HCl intragastrically, intravenous aspirin produces large deep gastric ulcers. The mechanism of the ulcerogenic action of intravenous aspirin is not known.

Animals↗
PubMedDate not supplied

Dapsone intoxication: two case reports.

Two patients with dapsone intoxication, an adult and a 16-month-old child, are reported. Both developed symptomatic methemoglobin concentrations, of 35% and 37%, respectively, and improved with intravenous methylene blue. Methemoglobin levels subsequently rose in both cases to 25% at 24 and 37 hours, respectively. The recurrence of elevated methemoglobin levels resulted from either continued absorption of dapsone or its toxic metabolite from the gastrointestinal tract. Both patients were begun on serial oral activated charcoal and the child received a second methylene blue treatment. During the intoxication, serum hemoglobin concentrations dropped 2 gm with an increase in the reticulocyte count. Review of 20 cases of dapsone overdose from the literature showed that the major toxic manifestations are methemoglobinemia and hemolysis. Delayed sulfhemoglobinemia, reported in only one case, resolved spontaneously. The treatment of dapsone intoxication is intravenous methylene blue for symptomatic methemoglobinemia, gastric decontamination, and early administration of serial oral activated charcoal. Hemolysis is mild but transfusions may be required for patients with a glucose-6-phosphate dehydrogenase deficiency.

Adolescent↗