Anticoagulant Activity in Cell Homogenate of Adult T Cell Leukemia

H Wada; M Tomeoku; A Deguchi; H Suzuki; Y Mori; M Ito; K Deguchi; S Shirakawa

doi:10.1055/s-0038-1642753

Thrombosis and Haemostasis, Inhaltsverzeichnis

Thromb Haemost 1988; 59(02): 197-201
DOI: 10.1055/s-0038-1642753

Original Articles

Schattauer GmbH Stuttgart

Anticoagulant Activity in Cell Homogenate of Adult T Cell Leukemia

Authors

H Wada

The 2nd Division, Department of Internal Medicine, Faculty of Medicine, Mie University, Mie, Japan
M Tomeoku

The 2nd Division, Department of Internal Medicine, Faculty of Medicine, Mie University, Mie, Japan
A Deguchi

The 2nd Division, Department of Internal Medicine, Faculty of Medicine, Mie University, Mie, Japan
H Suzuki

The 2nd Division, Department of Internal Medicine, Faculty of Medicine, Mie University, Mie, Japan
Y Mori

The 2nd Division, Department of Internal Medicine, Faculty of Medicine, Mie University, Mie, Japan
M Ito

^*The Department of Obstetrics and Gynecology, Faculty of Medicine, Mie University, Mie, Japan
K Deguchi

The 2nd Division, Department of Internal Medicine, Faculty of Medicine, Mie University, Mie, Japan
S Shirakawa

The 2nd Division, Department of Internal Medicine, Faculty of Medicine, Mie University, Mie, Japan

Abstract

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Summary

The hemostatic abnormality in 18 patients with adult T cell leukemia (ATL) was studied. Activated partial thromboplastin time (APTT) was slightly prolonged and prekallikrein activity was markedly low in these patients. The leukemic cell homogenate from these patients prolonged the recalcification time (RCT) of normal plasma; homogenates containing more than 3 ×10³ cells/μi prolonged it, although a lower cell concentration shortened it. The crude anticoagulant fraction from the gel filtration, with a molecular weight of about 34,000, prolonged RCT. The crude anticoagulant did not affect prothrombin time (PT), thrombin activity or activated X activity at any concentration, but prolonged the contact activation test, inhibited the activation of prekallikrein and prolonged RCT of Fletcher trait, Fitzgerald trait and F XII deficient plasma. These effects of ATL cell homo-genate were stronger on platelet poor plasma than on platelet rich plasma. Although ATL cells had low procoagulant activity, increase of leukemic cells made anticoagulant activity predominant, might be the cause of hemostatic abnormality or amplify the bleeding tendency in patients with ATL.

Keywords

Anticoagulant activity - Adult T cell leukemia (ATL) - Leukemic cell homogenate - Prekallikrein - Contact phase of coagulation system

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Referenzen

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