RESUMO
Pentoxifylline is an orally active agent for the treatment of peripherial and cerebral vascular diseases. Pentoxifylline increases the deformability of red blood cells in vitro, reduces blood viscosity and decreases platelet aggregation and thrombus formation. Depogen has shown antiaggregatory effect both in vitro and in ex vivo. The inhibitory effect of Pentoxifylline was about 3-5 times weaker than that of Depogen. IC50 = 900/micrograms/ml for Depogén and 3600/micrograms/ml for Pentoxifylline on human platelet rich plasma. Depogen has shown ex vivo antiaggregatory effect on anesthetised rabbits, ID50 = 7 mg/kg in case of iv. administration, and ID50 = 300 mg/kg in case of orally administration. Both compound inhibit the release of platelet precoagulation factor, but the effect of Pentoxifylline was slighter.
Assuntos
Eritrócitos/efeitos dos fármacos , Leucócitos/efeitos dos fármacos , Papaverina/análogos & derivados , Pentoxifilina/farmacologia , Inibidores da Agregação Plaquetária/farmacologia , Agregação Plaquetária/efeitos dos fármacos , Teofilina/análogos & derivados , Animais , Agregação Celular/efeitos dos fármacos , Combinação de Medicamentos , Avaliação Pré-Clínica de Medicamentos , Humanos , Papaverina/farmacologia , Fator Plaquetário 3/antagonistas & inibidores , Coelhos , Teofilina/farmacologiaRESUMO
Factor V inhibitors are uncommon, bleeding manifestations variable and recommendations for management are unclear. We present a patient with non-Hodgkins lymphoma who developed gastrointestinal bleeding and was found to have a Factor V inhibitor. The inhibitor was active against both plasma Factor V and platelet associated Factor V, and was associated with a five-fold increase in platelet associated IgG. Fresh frozen plasma was ineffective in preventing bleeding. Resolution of bleeding was associated with a fall in the levels of the inhibitor and of platelet associated IgG. The patient had no further bleeding episodes nor evidence of progression of his lymphoma, but six months later died as a result of metastatic adenocarcinoma.
Assuntos
Transtornos da Coagulação Sanguínea/complicações , Fatores de Coagulação Sanguínea/antagonistas & inibidores , Plaquetas/metabolismo , Deficiência do Fator V/complicações , Hemorragia Gastrointestinal/etiologia , Adenocarcinoma/secundário , Idoso , Transtornos da Coagulação Sanguínea/sangue , Deficiência do Fator V/sangue , Hemorragia Gastrointestinal/sangue , Humanos , Imunoglobulina G/metabolismo , Leucemia Linfocítica Crônica de Células B/complicações , Masculino , Tempo de Tromboplastina Parcial , Fator Plaquetário 3/antagonistas & inibidores , Tempo de ProtrombinaAssuntos
Fatores de Coagulação Sanguínea/antagonistas & inibidores , Efedrina/análogos & derivados , Epoprostenol/análogos & derivados , Epoprostenol/farmacologia , Fator Plaquetário 3/antagonistas & inibidores , Adulto , Testes de Coagulação Sanguínea , Colágeno/farmacologia , Efedrina/farmacologia , Humanos , Agregação Plaquetária/efeitos dos fármacos , Fator Plaquetário 3/fisiologiaRESUMO
The effect of lomustin on platelet functions was investigated in vitro using a wide battery of tests. Lomustin was found to act as a specific inhibitor of platelet aggregation, release reaction and clot retraction and to induce acquired thrombocytopathy. Thus, impairment of platelet functions might play a role in hemorrhagic complications accompanying lomustin therapy in some cases.
Assuntos
Plaquetas/efeitos dos fármacos , Lomustina/farmacologia , Testes de Função Plaquetária , Difosfato de Adenosina/farmacologia , Retração do Coágulo , Colágeno/farmacologia , Epinefrina/farmacologia , Humanos , Agregação Plaquetária/efeitos dos fármacos , Fator Plaquetário 3/antagonistas & inibidores , Fator Plaquetário 4/antagonistas & inibidores , Antagonistas da Serotonina/farmacologiaRESUMO
Lysine salt of acetylsalicylic acid (ASA) was given to ten patients by intravenous infusion. Blood samples taken at intervals during the infusion permitted the examination of the influence of the dose of ASA on platelet functions. Aggregation was significantly reduced when 50 mg ASA had entered circulation, while a diminution of PF3 and PF4 availability could only be demonstrated when the dose had reached 500 and 200 mg, respectively. In order to exclude a longer latency time for the diminution of PF3 and pf4 availability, a second series of ten patients received intravenous injections of 100 and 300 mg ASA, respectively. From these patients, blood was taken 1 h after the injection. The decrease of PF3 and PF4 availability in these cases was comparable to the results of the first group. In a third series of patients, a daily intravenous dose of 2,000 mg ASA was given. In these cases, a moderate decrease of factors II, VII, IX and X was observed. Since the appearance of a PIVKA effect could also be demonstrated, vitamin K antagonism was assumed when a high dose of AS
