[Influence of antiplatelet drugs (AD) on the efectiveness of combined therapy in patients with small cell lung cancer. Part I. Influence of AD on the haemostatic system].
In the last years, a sharp rise in the morbidity due to lung cancer is observed, especially in the male population. Despite the intensive, multidirectional development of oncology, early detection and effective treatment of lung cancer is still limited. Its detection is delayed because of the lack of characteristic early signs. Especially poor in prognosis are patients with small cell lung cancer (SCLC), who usually die in consequence of distant metastases. This may result due to coating of the surface of circulating neoplastic cells with thrombocytes and clots. Platelets aggregates on the surface of neoplastic cells may have a protective action in relation to cytostatic drugs. This is why neoplastic cells that persist through this phase, implant themselves into various organs giving rise to metastases. The aim of the 1st part of the paper was to evaluate the influence of antiplatelet drugs (AD) on the haemostatic system of patients with SCLC. There is data in literature indicating a ameliorating influence of AD on time of survival of patients with certain neoplasms. The study was performed in 87 male patients aged 35-73 years with SCLC, limited to half of the chest (limited disease). After 2 i.v. chemotherapy series in 3 week intervals (VAC scheme according Greco): --Adriamycin (ADR) 40 mg on 1sq.m of body surface; --Vincristin (VCR) 1 mg; on 1sq.m of body surface; --Cyclophosfamid (CTX) 1000 mg on 1sq.m of body surface; radiation was also applied--40 Gy during 20 days on the tumor and mediastinum. The described treatment was performed in 22 patients from controls (Group I). Patients from Group II (n = 22) received additionally Defibrotide, Group III (n = 22) Ticlide and Group IV (n = 21) Aspirin. To evaluate of the influence of AD on the haemostatic system--every 3 months during the consecutive 27 weeks, the following tests were performed: bleeding time, clotting time, platelet aggregation, platelets aggregation ratio, euglobulin clot lysis time (ECLT), fibrinogen and fibrinogen degradation products (FDP). It was shown that AD prolonged bleeding and clotting time, increased the threshold ADP and collagen concentration causing platelets aggregation as well as increased platelet aggregation ratio. The used AD (Defibrotide, Ticlide) resulted in activation of the plasma fibrynolytic system as expressed by a shortening of the ECLT, lowering of fibrinogen level and increasing FDP. The influence of observed changes in the haemostatic system, as a result of AD on the remission and survival time of patients with SCLC will be presented in the 2nd part of this paper.
Ochmański
Władysław
W
Katedra Chorób Wewnetrznych i Gerontologii, Uniwersytet Jagielloński, Collegium Medicum, 31-531 Kraków, ul. Sniadeckich 10.
D000328:Adult; D000368:Aged; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use*; D001241:Aspirin / Q000008:administration & dosage; D001777:Blood Coagulation / Q000187:drug effects*; D018288:Carcinoma, Small Cell / Q000188:drug therapy* / Q000401:mortality / Q000556:secondary*; D003520:Cyclophosphamide / Q000627:therapeutic use; D003609:Dactinomycin / Q000627:therapeutic use; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000401:mortality; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage*; D011089:Polydeoxyribonucleotides / Q000008:administration & dosage; D018714:Radiotherapy, Adjuvant; D015996:Survival Rate; D013988:Ticlopidine / Q000008:administration & dosage; D014750:Vincristine / Q000627:therapeutic use
D010975:Platelet Aggregation Inhibitors; D011089:Polydeoxyribonucleotides; D003609:Dactinomycin; C036901:defibrotide; D014750:Vincristine; D003520:Cyclophosphamide; D013988:Ticlopidine; D001241:Aspirin
Wpływ leków przeciwpłytkowych (LPP) na efektywność skojarzonego leczenia chorych na drobnokomórkowego raka płuca. Cześć I. Wpływ LPP na układ hemostatyczny.