Defective Platelet Aggregation and Increased Platelet Turnover in Patients with Myelofibrosis and Other Myeloproliferative Diseases

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Abstract
In 9 patients with myeloproliferative diseases (MPD) (6 with myelofibrosis, MF, 1 with Ph1 positive chronic granulocytic leukemia, CGL, 1 with primary eosinophilia, PE, 1 with pre-leukemia syndrome, preL) collagen, epinephrine and ADP-induced aggregation, N-ethylmaleimide-induced malondialdehyde (MDA) production, .beta.-thromboglobulin (.beta.-TG) plasma levels and platelet [PLT] turnover were studied. Collagen-induced aggregation was normal in 7 patients, absent in 1 and reduced in 1. In all but 3 patients, aggregation with ADP was markedly reduced. Epinephrine-induced aggregation was decreased in 7 patients. No difference was found between mean MDA production in MPD (3.21 .+-. 0.50 nmol/109 PLT) and in a control group of 21 normal subjects (3.04 .+-. 0.26 nmol/109 PLT). Mean .beta.-TG levels were significantly higher (P < 0.01) in MPD patients (165.00 .+-. 28.29 ng/ml) than in healthy controls (81.76 .+-. 14.63 ng/ml). Mean platelet production half-time was significantly shorter in MPD (2.48 .+-. 0.24 d [days]) than in the control group (3.43 .+-. 0.17 d), after adjustment for age by covariance analysis (P < 0.005). An abnormal prostaglandin synthesis was not indicated; this is consistent with the hypothesis that a disseminated intravascular platelet aggregation might take place in MPD patients.