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

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
› Author Affiliations
Further Information

Publication History

Received 12 August 1986

Accepted after revision 16 November 1987

Publication Date:
21 May 2018 (online)

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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.