Abnormality of blood coagulation in thrombocytopenia and thrombocythemia

Blood coagulation was studied in patients with idiopathic thrombocytopenic purpura (ITP), essential thrombocythemia (ET), polycythemia (PC), myelodysplastic syndrome (MDS), and aplastic anemia (AA), and prolongation of APTT was observed in ITP, ET, MDS and PC with thrombocythemia, but shortening of...

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Published inBlood & Vessel Vol. 18; no. 3; pp. 246 - 249
Main Authors WADA, Hideo, SUZUKI, Hikoji, MORI, Yoshitaka, DEGUCHI, Akira, OHKUBO, Itsuko, TSUDA, Masayuki, NISHIKAWA, Masakatu, MIMAMI, Nobuyuki, DEGUCHI, Katsumi, SHIRAKAWA, Shigeru
Format Journal Article
LanguageEnglish
Published The Japanese Society on Thrombosis and Hemostasis 1987
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Summary:Blood coagulation was studied in patients with idiopathic thrombocytopenic purpura (ITP), essential thrombocythemia (ET), polycythemia (PC), myelodysplastic syndrome (MDS), and aplastic anemia (AA), and prolongation of APTT was observed in ITP, ET, MDS and PC with thrombocythemia, but shortening of APTT was seen in AA. Circulating anticoagulant was detected in only 4 ITP patients by cross mixing experiment and the effect of high-dose platelin on kaolin clotting time. The prolongation of APTT was statistically improved after treatment of ITP with steroid and high-dose gammaglobulin therapy (HDGT). In ITP patients with prolonged APTT, megakaryocytes were increased, serological tests were more positive and weight of spleen was increased compared with patients with normal APTT. In terms of effectiveness on therapy, steroid therapy and HDGT were more effective in patients with prolonged APTT than in patients with normal APTT. Homogenate of more than 4×105/μl platelets prolonged APTT, PTT and recalcification time but shortened kaolin clotting time. Phospholipids (phosphatidylcholine, phosphatidylserine, phosphatidylinositol, phosphatidylethanolamine, sphingomyelin, phosphatidic acid) also prolonged APTT at high concentration. In ITP and MDS, phospholipids from destroyed platelets might be increased and prolong APTT, and it was suspected that increased platelets also prolonged APTT in ET and PC. In these diseases, APTT might reflect the function of reticuloendothelium system and the number of destroyed platelets.
ISSN:0386-9717
1884-2372
DOI:10.2491/jjsth1970.18.246