RESUMO
Effect of different antitumor drugs on the hemostasis system in oncological patients is shown to have many features in common. The differences mainly consist in the degree and duration of disorders, a shift of the balance toward hyper- or hypocoagulation, which was due to drugs toxicity with relation to the chains of the hemostasis system, individual susceptibility, the state of essential thrombocytopoiesis, etc.
Assuntos
Antibióticos Antineoplásicos/efeitos adversos , Hemostasia/efeitos dos fármacos , Melfalan/efeitos adversos , Neoplasias/tratamento farmacológico , Testes de Coagulação Sanguínea , Feminino , Humanos , Contagem de Plaquetas , Fatores de TempoAssuntos
Transtornos da Coagulação Sanguínea/induzido quimicamente , Hemorragia/induzido quimicamente , Neoplasias/tratamento farmacológico , Compostos de Mostarda Nitrogenada/efeitos adversos , Adolescente , Neoplasias Femorais/tratamento farmacológico , Humanos , Masculino , Osteossarcoma/tratamento farmacológico , Trombocitopenia/induzido quimicamenteAssuntos
Plaquetas/efeitos dos fármacos , Vasos Sanguíneos/efeitos dos fármacos , Hemostasia/efeitos dos fármacos , Heparina/farmacologia , Relação Dose-Resposta a Droga , Endocitose/efeitos dos fármacos , Exocitose/efeitos dos fármacos , Humanos , Neoplasias/sangue , Agregação Plaquetária/efeitos dos fármacosAssuntos
Transtornos Hemorrágicos/etiologia , Linfoma/complicações , Animais , Feminino , Masculino , PapioRESUMO
It has been demonstrated in experiments in vitro that addition of heparin to platelet enriched plasma potentiates the ADP-induced platelet aggregation and that heparin itself can provoke aggregation of platelets. Heparin exerts an inhibitory action on the thrombin-induced aggregation, which seems likely to be associated with its inhibitory effect on thrombin, an inducer of aggregation. It has been discovered that heparin action on the hemostasis is determined by its concentration. The doses under 0.05 U/ml enhance the ADP-induced platelet aggregation and accelerate the time of blood coagulation, whereas the doses from 0.3 to 2 U/ml exert a more powerful effect on aggregation, inhibiting blood coagulation.
Assuntos
Heparina/farmacologia , Agregação Plaquetária/efeitos dos fármacos , Difosfato de Adenosina/farmacologia , Relação Dose-Resposta a Droga , Humanos , Técnicas In Vitro , Masculino , Neoplasias/fisiopatologia , Tromboelastografia , Trombina/farmacologiaRESUMO
Systems of blood coagulation in patients treated with antibiotics of the anthracycline group were studied. Rubomycin was used in the treatment of patients with acute leukemia Adriamycin and carminomycin were used in the treatment of patients with solid tumors. The antibiotics affected the process of blood coagulation mainly through their cytostatic effect on thrombocytopoesis. Thrombocytopenia induced deficit of thrombocytal factors participating in the process of blood coagulation which resulted in hypocoagulation and hemorrhagic complications. The plasmic factors did not significantly change during the antibiotic therapy. A tendency to decrease in the levels of prothrombine, fibrinase and fibrinogen was noted which was possible due to an inhibitory effect of the antibiotics on the function of the reticuloendothelial tissue cells or indirectly to suppression of the tumor process. More pronounced changes in the system of blood coagulation of patients treated with rubomycin were probably associated with inferiority of the thrombocytal apparatus of the patients with acute leukemia treated with the antibiotic.