1978 Volume 9 Issue 2 Pages 179-183
Tissue thromboplastin (TP) have been detected in various types of leukocytes as well as many other organs and it is suggested to play important roles in blood coagulation. In this report, we studied on TP in the leukocytes from various types of leukemia in order to estimate its responsibility for the development of DIC, which accompained by these patients. We also compared it to brain (B) and placenta (P) TP by means of immunological techniques.
Washed leukocyte suspensions were prepared by centrifugation and hypotonic lysis technique from 9 acute myelocytic leukemias (AML), 5 acute promyelocytic leukemias (APL), 4 chronic myelocytic leukemias and 20 healthy subjects. The TP activity was estimated by Nemerson's two stage method and effects on clotting times of various deficient plasmas were studied by Quick's one stage method. The distribution of the activity in the homogenate of APL leukocytes was studied by defferential centrifugation. Anti-P-TP was produced and used for immunological studies employing Ouchterlony method and clotting activity neutralization technique.
Homogenates of APL leukocytes showed significant TP activity as much as 152 units per 10 million cells on the average, while homogenates of other blood cells, except a case of AML which had an activity of 3.8 units per 10 million cells, showed little activity. APL homogenates demonstrated striking shortening of the clotting times of Factor VIII and IX deficient plasmas but did not show this effect on Factor VII and X deficient plasmas. This activity was week, when cell suspensions were used without homogenization. It sedimented mainly at 700G in the centrifugation study and was neutralized time dependently by anti-P-TP in the same manner as when B- and P-TP were examined. By Ouchterlony method, desoxycholate extract of APL leukocytes showed single precipitin line against anti-P-TP, which fused into the lines formed by purified B- and P-TP.
In conclusion, APL leukocytes have strong TP, which has similar antigenicity to B- and P-TP. It is conceivable that this TP causes or enhances DIC, especially when leukemic cells were destroyed by anti-leukemic therapy.
