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Stroke, Vol 20, 815-818, Copyright © 1989 by American Heart Association

ARTICLES

Progressing ischemic stroke in a homozygote with variant antithrombin III

H Ueyama, Y Hashimoto, M Uchino, Y Sasaki, E Uyama, K Okajima and S Araki
First Department of Internal Medicine, Kumamoto University Medical School, Japan.

A 31-year-old woman developed disturbance of consciousness and left hemiparesis. Cerebral computed tomograms showed a low-density area in the right temporal lobe that extended to the right parietal and left frontal lobes as her clinical symptoms worsened. The diagnosis of familial variant of antithrombin III (AT-III) was based on decreased biologic activity and a normal immunologic level of AT-III in this patient and in her family members. Transfusion of normal AT-III concentrate led to a striking clinical recovery. Blood coagulation studies revealed that nine of 13 family members had decreased biologic AT-III activity and that the patient herself was the only homozygote with variant AT-III. We conclude that variant AT-III, especially in a homozygote, seems to be one cause of ischemic stroke in young adults and that simultaneous measurement of both the biologic and immunologic activities of AT-III is necessary to detect it.