Stroke, Vol 23, 108-111, Copyright © 1992 by American Heart Association
K Matsushita, Y Kuriyama, T Sawada and K Uchida
BACKGROUND AND PURPOSE: A deficiency of plasma protein C, both the
hereditary and acquired types, is one cause of thromboembolic disease.
Several antineoplastic agents have been reported to decrease the production
of protein C in the liver by impairing either the absorption or metabolism
of vitamin K, leading to acquired protein C deficiency. CASE DESCRIPTION:
We treated a young woman with protein C deficiency, who had developed a
cerebral infarction of the right parietal cortex of sudden onset. On
admission, the antigenic level of plasma protein C was 38%. Serial cerebral
angiography revealed occlusion of the right middle cerebral artery, which
subsequently recanalized completely. This patient had taken fluorouracil
derivatives orally for as long as 3 years following a left mastectomy for
stage II breast cancer. Tests revealed that the patient's mother had only
one-half the normal activity of plasma protein C despite a normal antigenic
level. CONCLUSIONS: We speculate that the etiology of the cerebral
infarction in this patient might involve an embolic mechanism associated
with protein C deficiency induced by an interaction between inherited and
acquired factors.
ARTICLES
Cerebral infarction associated with protein C deficiency
Department of Medicine, National Cardiovascular Center, Osaka, Japan.
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