[The treatment of thrombosis in pregnancy (author's transl)]. / Zur thrombolytischen Behandlung der Schwangerschaftsthrombose

The treatment of thrombophlebitis in pregnancy with streptokinase is reviewed. Four personal cases are reported. In 3 cases the streptokinase treatment of thrombosis was carried out in the first trimester of pregnancy. Two pregnancies ended in spontaneous term deliveries of well infants without malformations. In one case the pregnancy ended by a spontaneous abortion two weeks following the treatment of the thrombosis. It is suggested that the abortion was much more likely due to a severe state of shock with pulmonary embolism following laparotomy in early pregnancy. The authors are of the opinion that the thrombolytic therapy with streptokinase should also be carried out in the first trimester of pregnancy to prevent embolization of thrombotic material and to prevent a post-thrombotic syndrome. In each case, streptokinase treatment should be followed up with subcutaneous prophylactic treatment with Heparin until term to prevent recurrent thrombophlebitis in pregnancy. With the onset of labour Heparin medication should be interrupted and the thrombin time should be normal with the beginning of the second stage of labour or the Heparin effect should be neutralized by protamine chloride. At the earliest six hours postpartum, the subcutaneous Heparin prophylaxis can be resumed in order to prevent recurrent thrombo-embolism during the postpartum stay.

Mutations in the human factor XII gene.

The factor XII gene from 31 unrelated factor XII-deficient patients from Germany, Switzerland, and Austria was screened for mutations at the genomic level. Several novel mutations were detected and their absence in a control group of 74 healthy unrelated individuals was checked. Most changes are in the serine protease domain affecting the catalytic triad His-393-Asp-442-Ser-544; two missense mutations, R398Q (arginine 398 to glutamine; gene bank accession no. U71276) and L395M (leucine 395 to methionine; gene bank accession no. U71277), are close to the active site histidine at position 393. Another mutation detected in a cross-reacting material (CRM)-positive female with a history of three abortions affects the active site aspartic acid by changing it to asparagine (D442N; gene bank accession no. U71275). The novel mutation G570R (glycine 570 to arginine; gene bank accession no. U71274) giving rise to a CRM-positive phenotype is located next to Cys571, which forms a vital disulfide bridge. Two mutations are causing reading frame shifts: one single basepair deletion in exon 12 [exon 12: 10590(DelC); gene bank accession no. U71278] and one acceptor splice site mutation [exon 14: 11397(G --> A); gene bank accession no. L43615]. The putative regulatory mutation exon 1:-8 (g --> c) in the upstream region of the gene is associated with an aberrant Taq I restriction site allele in intron B of the gene (gene bank accession no. X80393).