[Reduced plasminogen activator activity in patients with inactive ulcerative colitis].
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Biomedical subjects
Publications and source records attributed to J Z Mortensen.
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A family with inherited AT-III deficiency is presented. This variant is unlike those formerly described, as the plasma concentration is high, the thrombin inhibition with heparin is slow, and factor Xa inhibition is decreased.
Diverging results from studies of marine oil supplementation to western diets initiated the undertaking of a double-blind crossover study, with administration to healthy volunteers for 4 weeks of either 10 g of fish oil or 10 g of vegetable oil. Each oil containing approx. 40% of n-3 and n-6 polyunsaturated fatty acids (PUFA) respectively. During the n-3 PUFA period, systolic blood pressure, plasma total lipids, triglycerides and VLDL concentrations fell significantly whereas plasma antithrombin-III (AT-III) rose. Cutaneous bleeding time increased significantly. In contrast only AT-III rose during the n-6 PUFA feeding, however, more marked than during the n-3 oil period. It is concluded that a n-3 PUFA oil supplement to the western diet exerts an effect that generally is considered as beneficial in terms of the risk of developing cardiovascular diseases. It is in this respect superior to that of n-6 PUFA, stressing the necessity of a more differentiated approach to advice on dietary PUFA enrichment than presently is exerted.
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The excretion of methylmalonic acid was measured and deoxyuridine suppression test (dU-test) was performed in 5 patients before and after 24 h of ventilation with nitrous oxide. The mean urinary 2-methylmalonic acid was increased from 90 to 320 mumol/24 h and the dU-tests became abnormal. These findings indicate that the 2 vitamin B-12 dependent enzymes, methylmalonyl-CoA-mutase and methione synthetase, are depressed by nitrous oxide.
A description is given of acute fatty liver of pregnancy in a 26-year-old primigravida who survived. Complicating disseminated intravascular coagulation was diagnosed at parturition, and the importance of early diagnosis of this is emphasized. A suggestion for treatment is given as a possible means of improving the prognosis in this mostly fatal disease.
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6 members of a family with a tendency to thrombosis and defective fibrinolysis were examined. After stimulation of plasminogen activator release from the vessel wall by local venous occlusion or by submaximal physical exercise, they had a lower plasminogen activator activity in blood than a healthy control group (P less than 0.01). 5 of the examined members suffered from recurrent venous thrombosis. The defect appeared to be autosomal dominant.
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