Cerebral infarction associated with protein C deficiency.
OBJECTIVE
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.


METHODS
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.
Matsushita
K
K
Department of Medicine, National Cardiovascular Center, Osaka, Japan.
Kuriyama
Y
Y
Sawada
T
T
Uchida
K
K
D000328:Adult; D015901:Angiography, Digital Subtraction; D001921:Brain / Q000000981:diagnostic imaging; D002544:Cerebral Infarction / Q000150:complications* / Q000000981:diagnostic imaging / Q000378:metabolism; D005260:Female; D006801:Humans; D020151:Protein C Deficiency