August 1989

Plasma a2-Antiplasmin ActivityRole in the Evaluation and Management of Fibrinolytic States and Other Bleeding Disorders

Author Affiliations

From the Departments of Medicine and Pathology and Laboratory Medicine, University of Wisconsin, Madison.

Arch Intern Med. 1989;149(8):1769-1772. doi:10.1001/archinte.1989.00390080049012

• To determine the clinical significance of acquired α2-antiplasmin deficiency in patients with bleeding disorders, I reviewed the results of assays performed on 184 patients over a 4-year period. Thirty-two evaluable patients had α2-antiplasmin activity levels of less than 50% of normal (defined as severe deficiency), and 35 patients had levels between 50% and 75% of normal (mild deficiency). Records of these patients and of 32 patients who had normal levels were reviewed. Most patients with severe α2-antiplasmin deficiency had either liver disease or disseminated intravascular coagulation and/or fibrinolysis, or both. There was a high incidence of severe α2-antiplasmin deficiency among patients with acute promyelocytic leukemia. Five patients with pathologic bleeding had no identifiable coagulation abnormalities other than α2-antiplasmin deficiency. The group with severe α2-antiplasmin deficiency had a significantly higher incidence of life-threatening or fatal bleeding and the most striking laboratory evidence of hyperfibrinolysis. Using the presence of severe α2-antiplasmin deficiency as an indication for therapy, ε-aminocaproic acid treatment was associated with cessation of life-threatening bleeding in 8 of 11 patients.

(Arch Intern Med. 1989;149:1769-1772)