Depression of functional and antigenic plasma antithrombin III (AT‐III) due to therapy with L‐asparaginase

• Published in: Cancer 1982-08, Vol.50 (3), p.451-456
• Main Authors: Liebman, Howard A., Wada, Jerry K., Patch, Mary Jane, McGehee, William
• Format: Article
• Language: English
• Subjects: Adult; Antithrombin III - immunology; Antithrombin III - physiology; Asparaginase - adverse effects; Asparaginase - therapeutic use; Burkitt Lymphoma - drug therapy; Escherichia coli - enzymology; Humans; Leukemia - blood; Leukemia - drug therapy; Leukemia, Lymphoid - drug therapy; Leukemia, Myeloid - drug therapy; Lymphoma - blood; Lymphoma - drug therapy; Lymphoma, Non-Hodgkin - drug therapy; Male; Middle Aged
• ISSN: 0008-543X; 1097-0142
• DOI: 10.1002/1097-0142(19820801)50:3<451::AID-CNCR2820500312>3.0.CO;2-4

Eleven patients with leukemia and lymphoma were treated with 14 courses of E. coli L‐asparaginase. Abnormalities of the coagulation screening tests and decreased fibrinogen levels were observed in all patients during treatment. Significant depressions of functional (mean 32%) and antigenic (mean 48%) antithrombin III were observed by day 14 of therapy. There was no laboratory evidence of intravascular coagulation during 11/14 courses of L‐asparaginase. Crossed immunoelectrophoresis of plasma obtained at the antithrombin nadir did not demonstrate an abnormal pattern which can be associated with an abnormal antithrombin III or an increase in antithrombin III‐coagulation factor complexes. The major underlying mechanism of this depression is believed to be decreased hepatic synthesis, and the low levels of antithrombin III may be associated with an increased risk of thrombosis.