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At least 919 records · Page 51Linked to original sources
PubMed1977

Ditazole and platelets. I. Effect of ditazole on human platelet function in vitro.

Ditazole (4,5-diphenyl-2-bis-(2-hydroxyethyl)-aminoxazol) has been shown to be a strong in vitro inhibitor of human platelet aggregation brought about by release reaction inducers; in contrast, it did not significantly affect primary ADP-induced aggregation. Ditazole strongly inhibited the release of platelet-bound 14C-serotonin under the influence of Thrombofax, whereas it did not interfere with the transport and storage of serotonin in nonstimulated platelets. The effect of ditazole was not potentiated by acetylsalicylic acid. Ditazole also inhibited ADP-reptilase clot retraction and modified thrombin-induced clot formation. The inhibition of platelet aggregation exerted by ditazole in plasma could be removed following gel filtration of platelets on Sepharose 2-B gel. This would indicate that ditazole does not act on platelets by a 'hit and run' mechanism.

Adenosine Diphosphate↗
PubMed1982

[Coagulation disorders in tumors and hemoblastoses].

Thromboembolic and haemorrhagic complications are not rarely seen in the course of malignant diseases. The underlying coagulation disorders were investigated by means of coagulation analysis in 61 patients with solid tumors and 60 control persons as well as 51 patients with leukemia and 50 control persons. As a cause for the thrombotic diathesis in patients with solid tumors and leukemias can be demonstrated a hypercoagulability (shortened PTT and raised factor VIII activity). In addition we found a raised level of fibrinogen, a hypofibrinolysis (prolonged euglobulin lysis time) and in increased platelet aggregation in patients with solid tumors. Predominantly bleeding complications in leukemias are caused by thrombopenia. Another reason, however, may be an activated fibrinolysis or a clot instability because of the reduction of factor XIII. Pathogenetic mechanisms, underlying the tumor induced coagulation disorders, as for example the release of tumor cell thromboplastins from malignant cells are discussed.

Adult↗
PubMed1996

Thrombelastgram as a hemostatic monitor during recombinant factor VIIa treatment in hemophilia A patients with inhibitor to factor VIII.

Thrombelastgram (TEG) is an old but automated instrument that demonstrates changes occurring during blood coagulation and fibrinolysis. TEG was evaluated to be better than activated partial thromboplastin time (APTT) as a monitor of hemostatic effects when using recombinant factor VIIa (65-80 mu g/kg) in 3 hemophilia A patients with a high titer of factor VIII inhibitors. TEG was more suitable than APTT, because r, r + k and ma values of TEG were normalized at least for 4 h after the infusion, whereas APTT was variably shortened and was not always maintained at a normal level for 4 h.

Adult↗