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Article
August 1989

The Importance of a2-Antiplasmin in the Defibrination Syndrome

Author Affiliations

Department of Pathology and Laboratory Medicine University of California at San Diego Medical Center 225 Dickinson St San Diego, CA 92103

Arch Intern Med. 1989;149(8):1724-1725. doi:10.1001/archinte.1989.00390080010002
Abstract

Two coagulation abnormalities may result in a marked decrease in plasma fibrinogen caused by prominent defibrination. The two conditions that cause defibrination with a bleeding diathesis are disseminated intravascular coagulation (DIC) and primary fibrinogenolysis (PF).1

Various conditions may be associated with DIC. These include serious infections; complications of pregnancy, such as abruptio placentae or toxemia (PIH); malignancy, such as carcinomas or acute promyelocytic leukemia; marked tissue injury, such as brain injury and incompatible hemolytic transfusion reaction; and venomous snakebite.

The cause of PF differs from DIC. Primary fibrinogenolysis is associated with cirrhosis, since the liver normally removes plasminogen activator from the circulation. Other conditions associated with PF are extensive cardiovascular or pulmonary surgery and metastatic carcinoma of the prostate, releasing plasminogen activator into the circulation. The recent utilization of tissue plasminogen activator to cause thrombolysis of coronary artery and cerebral artery thrombi causes local fibrinogenolysis.

The laboratory parameters used

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