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Biomedical subjects

S Stenbjerg

Publications and source records attributed to S Stenbjerg.

42 records · Page 3Linked to original sources

Resistance to activated F IX concentrate (FEIBA).

A 10-year-old haemophiliac with an inhibitor to Factor VIII was treated by repeated infusion of an activated Factor IX concentrate (FEIBA). During therapy the patient was monitored with extensive coagulation studies, and the initial effect of FEIBA on the whole blood coagulation time was seen to disappear in spite of increased doses of concentrate. A fall in Factor IX activity and a rise of antithrombin III and anti-Factor Xa was recorded, while the titer of anti-F VIII remained unchanged. The exact nature of this FEIBA-resistant state was not revealed, however, it was speculated that a rise of natural inhibitors of the coagulation system could explain the findings.

Antithrombins↗

The impact of HLA-A, B or HLA-D identity on the MIF production in MLC.

The relative influence on MIF release in MLC of different parts of the HLA region was studied in 1) MLCs between cells from HLA-A and B identical (probably HLA-D unidentical) unrelated persons and 2) MLCs between cells from HLA-D identical, HLA-A and B unidentical unrelated persons. It was found that the HLA-D part of the region has the major effect on the MIF production. Studies of MIF activity in supernatants from mitomycin treated cultures lent some evidence to the hypothesis that there is an extreme linkage disequilibrium between the HLA-D alleles and hypothetical separate MIF alleles. Examination of families with crossover between the HLA-A, B and HLA-D part of the region is required for confirmation of these findings.

Epitopes↗

A circulating factor V inhibitor: possible side effect of treatment with streptomycin.

A potent inhibitor of factor V was discovered in a middle aged woman shortly after streptomycin therapy. The patient suffered from severe bleeding over a period of 10 days and the inhibitor was demonstrable for 6 weeks. By use of specific antisera the anticoagulant was found to be of an IgG nature. In agar electrophoresis the inhibitor mowed with the immunoglobulin fraction and was separable from factor V activity in the pathological plasma although no factor V activity was demonstrable in untreated patient plasma. It is suggested that this method should be used to distinguish between cases of inhibitors in patients with congenital factor V deficiency and cases of transient inhibitors in patients with normal factor V production.

Anticoagulants↗

Coagulation studies in patients with trisomy 8 syndrome.

Coagulation studies were performed in three patients with trisomy for chromosome No. 8. In contrast to the findings reported by others, all patients were found to have a normal coagulation status without sign of factor VII deficiency.

Adolescent↗

Diabetes-like alterations in hemostatic parameters after growth hormone administration for one week in normal man.

Excess production of growth hormone (GH) in poorly controlled diabetes is believed to be a causal factor in the development of diabetic angiopathy, the mechanism(s) of which is unknown. The present study was undertaken to determine whether exogenous growth hormone would specifically change some quantities and functional parameters known to often be abnormal in long-standing diabetes and thought to result from the development of vascular lesions in general. The authors studied capillary resistance, factor VIII coagulant antigen (F VIII:Ag), von Willebrand factor (vWf:Ag), fibronectin, fibrinogen, and tissue-type plasminogen activator (t-PA) before, during, and after 1 week's subcutaneous GH administration (6 IU per day divided into two doses). Capillary resistance decreased insignificantly, but returned to higher levels (p less than 0.05) 1 week after withdrawal. F VIII:Ag, vWf:Ag, fibronectin, and fibrinogen all increased significantly during GH treatment. Except for F VIII:Ag, these quantities returned to pre-medication levels 7 days after termination of GH administration. The present results may contribute to the clarification of the role of GH hypersecretion in diabetic microangiopathy and macroangiopathy.

Adult↗