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Biomedical subjects

I M Nilsson

Publications and source records attributed to I M Nilsson.

At least 19 recordsLinked to original sources
PubMed1979

In vivo recovery of factor VIII: a comparison of one-stage and two-stage assay methods.

The recovery and half-life of VIII:C in the plasma of severely haemophilic patients was measured by one-stage and two-stage assays after injection of two Factor VIII concentrates (Hemofil, Hyland and Fraction I-O, Kabi). Plasma volumes were measured with an Evans' Blue technique, and both concentrates and post-infusion samples were measured against the same plasma standard. There was a highly significant difference in recoveries estimated by the two assay methods. The one-stage assays gave the most consistent results, in that the average recovery was 100%, whereas the two-stage assays gave only about 80% of the value expected from in vitro assays. There was no differences in recoveries between the two concentrates. The two-stage assays gave a slightly shorter half-life than the one-stage assays, and the half-life of Hemofil was also shorter than that of Fraction I-O.

Biological Assay↗
PubMed1979

VIIIR; Ag in platelets from patients with various forms of von Willebrand's disease.

Thirty patients with various forms of von Willebrand's disease were investigated for VIIIR:Ag in their platelets. VIIIR:Ag was extracted from washed platelets and measured both with electroimmunoassay and a sensitive immunoradiometric assay. Six patients had severe von Willebrand's disease, type I, with very low or no VIIIR:Ag in their plasma. None of these patients had any VIIIR:Ag detectable in their platelets. All 19 patients with mild von Willebrand's disease had VIIIR:Ag in their platelets but the values often fell below those of normal controls. Five patients with genetic variants of von Willebrand's disease also had values in their platelets corresponding to those in plasma.

Adolescent↗
PubMed1979

[Haemophilia].

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Adolescent↗
PubMed1979

Surgery in von Willebrand's disease.

Fifty-eight major surgical procedures were performed in 38 patients with von Willebrand's disease (VWD), one of the most common of the inheritable hemorrhagic disorders. Specific treatment with fraction I-0, (AHF-Kabi) in addition to a fibrinolytic inhibitor, was given to all patients. The effect of the treatment was checked by measuring the Duke bleeding time and factor VIII:C level. A marked difference between hemophilia and VWD from a surgical point of view is demonstrated. While most of the surgery in hemophiliacs is performed for severe joint deformities, contractures and blood cysts, surgery in VWD is mostly general surgery, often necessitated by massive hemorrhages from mucous membranes.

Adolescent↗
PubMed1979

Factor VIII concentrate prepared from DDAVP stimulated blood donor plasma.

Human fraction I-0 (AHF-Kabi) was prepared from plasma from blood donors who had received an i.v. injection of DDAVP (0.2 microgram per kg b.w.) and tranexamic acid (0.01 g per kg b.w.) 15 min before collection of the blood. The factor VIII preparation from such plasma contained twice as much VIII:C,VIIIR:Ag, and VIIIR:RFC as normal fraction I-0. Normal fraction I-0 and DDAVP fraction I-0 were given to 2 patients with severe haemophilia A. The in vivo response of the DDAVP fraction I-0 corresponded to the in vitro values. No differences in survival time were seen. Hence, it is possible to produce factor VIII concentrates with at least double the yield by increasing the factor VIII level in blood donors by i.v. injection of DDAVP.

Adult↗
PubMed1979

Fatal iron intoxication with multiple coagulation defects and degradation of factor VIII and factor XIII.

A severe iron intoxication in a 15-year-old girl resulted in profound damage to vital organs and multiple clotting defects, but no haemorrhagic diathesis. Investigation revealed not only impaired synthesis of coagulation factors but also abnormal proteolysis by plasmin as well as by other proteolytic enzymes liberated from leucocytes and damaged tissue cells affecting especially factor VIII and factor XIII.

Adolescent↗
PubMed1979

Measurement of antihaemophilic factor A antigen (VII:CAg) with a solid phase immunoradiometric method based on homologous non-haemophilic antibodies.

Antihaemophilic-factor-A-antibodies, which had spontaneously arisen in 2 patients, were used to develop an immunoradiometric method for measurement of antihaemophilic factor A antigen (VIII:CAg). 13 patients with severe haemophilia A had VII:CAg below the limit of detection (0.01 U/ml). Patients with moderate and mild haemophilia A either had VII:CAg roughly equal to factor VIII clotting activity (VIII:C) or a not detectable VII:CAg, suggesting 2 different molecular mechanisms in moderate and mild haemophilia A. VIII:CAg could be detected in serum but in lower amounts than in plasma. In 2 patients with von Willebrand's disease VIII:CAg equalled VII:C. The post-transfusional retarded increase of VII:C in 1 patient with von Willebrand's disease was accompanied by a slight increase in VIII:CAg. Fetal plasma contained measurable amounts of VII:CAg.

Antibodies↗
PubMed1979

Hereditary alpha 2-macroglobulin deficiency.

On screening of a normal material 1 man was found (age 37) who on repeated determinations had a low alpha 2M, namely 25 % with electroimmuno assay according to Laurell. Investigation of the family revealed that the mother (age 69) and one daughter (age 5) had low values too. All other coagulation and fibrinolytic components were normal. They had no signs of increased fibrinolysis and normal levels of alpha 2-antiplasmin, alpha 1-antitrypsin and antithrombin III. Liver function tests were normal. It seems to be an inherited deficiency. The transmission is apparently autosomal dominant and the affected members heterozygotes. The defect has not caused any clinical symptoms. This family appears to be the first reported with an alpha 2M deficiency.

Adult↗
PubMed1978

Fibrinolytic activity in the vein wall after surgery.

The fibrinolytic system, including the fibrinolytic activator activity of vein wall and fibrinolytic activity in blood after venous occlusion, was analysed in 43 patients before and on the third day after operation. Twenty-two of the patients underwent abdominoperineal amputation of the rectum and 21 had a cholecystectomy. The incidence of postoperative thrombosis was asssessed by means of the isotope method and phlebography. The results indicate that a decrease in fibrinolytic activity of the vein wall and/or in the release of fibrinolytic activator from the vein wall is a regular postoperative phenomenon, especially after major surgery. Malignant tumour of the rectum did not have any depressing effect on the fibrinolytic activator. All the patients with thrombosis after operation had a postoperative fibrinolytic defect of the vein wall compared with about 60 per cent of the other patients. It is concluded that postoperative changes in the parameters studied might be of significance for the development of thrombosis after operation.

Aged↗