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PubMed1979

[Hemorrhagic diathesis in patients with malignant neoplasms (author's transl)].

Clotting analysis in 30 patients with bleeding complications in malignant hematological diseases revealed the following troubles: The global tests, Quick's index and partial thromboplastin time markedly differed from normal. Activity of clotting factors revealed hypo- or hyperfibrinogenemia, disturbances of the prothrombin complex (factors II, VII, IX and X), decrease of factors V, VIII, XII. Factor XI (= PTA) was not diminished in any case. Regarding the fibrin-stabilizing factor (factor XIII), its activity was significantly decreased in 30 patients with solid tumors and in 30 patients with hemoblastoses. Faulty clotting balance was characterized by hyperfibrinolysis or disseminated intravascular coagulation (DIC) accompanied by reactive hyperfibrinolysis. About one quarter of the patients with malignant disturbances of the hematopoetic system demonstrated (mostly amegacaryocyte) thrombocytopenia. Finally, treatment of bleeding complications in malignant neoplastic diseases is pointed out.

Blood Coagulation Tests↗
PubMed2002

[From gene to disease; from mutations in the Von Willebrand factor gene to hemorrhagic diathesis and thrombocytopenia].

The broad spectrum of both clinical presentation and severity of bleeding complications observed in Von Willebrand's disease is the result of a high number of mutations. Most are clustered in specific functional domains, leading to quantitative (types 1 and 3) or qualitative (types 2: A, B, M and N or Normandy) defects in the Von Willebrand factor (VWF) protein. Unlike all the other subtypes, type 2B is the result of a 'gain of function' phenotype characterised by an enhanced binding affinity of the VWF protein to the glycoprotein (Gp) Ib complex of platelets, which causes the platelets to disappear from the circulation, resulting in thrombocytopenia. The thrombocytopenia can be triggered by stress or desmopressin, among other causes, and therefore the latter is contraindicated. Type 2B is characterised in vitro by enhanced platelet agglutination with ristocetin. All 2B mutations are located in exon 28, in a small region encoding the Gp-Ib binding site within the A1 domain of VWF. These mutations inactivate a regulatory function of the A1 domain which facilitates Gp-Ib binding.

Hemorrhagic Disorders↗
PubMed1975

An electron microscopic study of the vascular factor in hemorrhagic diathesis.

Experimental diapedetic hemorrhage (oozing) was produced by streptokinase in rabbits and the fine structures of mesenterial microvessels were observed. Diapedesis of erythrocytes was seen in the venular side of microcirculation. On the contrary, no diapedesis was seen in true capillary on the arteriolar side. Sticking of erythrocytes to venular wall prior to diapedesis was proved, electron microscopically, to be the state in which red blood cells were trapped in the gaps on the endothelial junction. It was considered to be the morphological findings of the prediapedetic state. Erythrocytes passed through gaps on the endothelial junctions with high plasticities under any diapedetic conditions mentioned above. Furthermore, in author's experiments by ruthenium red staining, erythrocytes were observed just passing through the basement membrane under electron microscopy, in spite of its high speed process. It was found that the basement membrane is a very important barrier in erythrocyte diapedesis.

Animals↗