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Sixtus Thorsen

Publications and source records attributed to Sixtus Thorsen.

8 recordsLinked to original sources
PubMed2006

[Serious bleeding in systemic lupus erythematosus complicated by lupus anticoagulant-hypoprothrombinaemia syndrome].

Severe hemorrhagic diathesis due to lupus anticoagulant complicated by hypoprothrombinaemia resulting from prothrombin autoantibodies is a rare disorder and is often associated with systemic lupus erythematosus (SLE). We report a case in which a 15-year-old girl with SLE developed marked haemorrhagic manifestations due to menorrhagia and nosebleeds. The acute bleeding episode was treated with SAGM, tranexamic acid and recombinant factor VIIa. Lupus anticoagulant, cardiolipin antibodies and antiprothrombin antibodies were successfully depressed within weeks after corticosteroid therapy was begun.

Adolescent↗
PubMed2002

[Pregnancy-related thrombocytosis].

Pregnancy-related thrombocythaemia comprises myeloproliferative and inflammatory reactive subsets. In pregnant women treated for myeloproliferative disorders, especially polycythaemia vera and primary thrombocytosis, only 50-70 per cent are delivered successfully of a normal healthy baby. The maternal complications are cerebral, cardiac, and abdominal arterial thrombosis, and with deep venous thrombosis of the legs, whereas bleedings are mainly seen in the case of extreme thrombocythaemia, owing to absorption of factors by the platelets. The foetal complication are dominated by abruptio placentae, pre-eclampsia, placental insufficiency, and death. Reactive thrombocythaemia includes the physiological rise in platelets postpartum, believed to be part of the normal maternal haemostasis, which almost never causes thromboembolic complications, as far as is known today. In contrast, the inflammatory reactive thrombocythaemia, related to severe foetal and/or maternal necrosis, is generally related only to a moderate rise in the platelet count. As the blood-platelet count does not appear to be routine at general pregnancy check-ups, it is necessary to be aware of risk groups, consisting of women with otherwise unexplained abortions or stillbirths, unexplained foetal and placental malformations, and pre-eclampsia, even if the woman has never had any thromboembolic complications.

Anticoagulants↗
PubMed2002

Frequent occurrence of anticardiolipin antibodies, Factor V Leiden mutation, and perturbed endothelial function in chronic myeloproliferative disorders.

Chronic myeloproliferative disorders (MPD) are characterized by a high incidence of thrombohaemorrhagic complications, possibly related to platelet abnormalities and disturbances of the coagulation system. In an attempt to define abnormalities in coagulation and fibrinolysis, we investigated risk markers for venous thromboembolism, fibrinolytic, and haemostatic system activation markers and antiphospholipid antibodies in blood samples from 50 MPD patients and 30 controls. Compared with controls median levels of protein S free and protein C were significantly decreased in the patients (0.27 vs. 0.38 arbitrary units; P < 0.001 and 0.86 vs. 0.99 arbitrary units; P < 0.001, respectively), and activated partial thromboplastin time was significantly prolonged in patients (33 vs. 27 sec; P < 0.001). No differences were observed in levels of antithrombin, thrombin-antithrombin complex, and fibrin D-dimer. In patients the median value of thrombomodulin was significantly increased indicating perturbed endothelial function. Anticardiolipin antibodies of IgM subtype (median 38 U/mL, 33-99) were detected in 11 patients (22%) and only in one control (3%) (P < 0.021; patients vs. controls). Seven patients were heterozygous for the Factor V Leiden, one patient was heterozygous for the prothrombin G20210A mutation, and one patient was homozygous for the Factor V Leiden mutation. Among controls, two were heterozygous for the Factor V Leiden mutation. Comparing the allele frequency of the Factor V Leiden mutation in patients with MPD and the background population disclosed a significantly increased allele prevalence of the Factor V Leiden mutation in the patients (9% vs. 3.4%; P = 0.003). Alterations in the level of anticoagulant proteins, disturbances of endothelial cell function, and the presence of cardiolipin antibodies and Factor V Leiden mutation may increase the cumulative thrombotic risk in MPD besides the risk imposed by platelet activation.

Adult↗