[Abstract] [Full Text PDF] (in Japanese / 7289KB) [Members Only And Two Factor Auth.]

J.Jpn. Surg. Soc.. 87(2): 220-230, 1986


Original article

THE PLASMA LEVEL OF PROTEIN C IN PATIENTS WITH PERIPHERAL ARTERIAL OR VENOUS OCCLUSIVE DISEASES AND MYOCARDIAL INFARCTION WAS INVESTIGATED, SO HOMOZYGOUS PROTEIN C DEFICIENCY ASSOCIATED WITH HETEROZYGOUS DYSPLASMINOGENEMIA WAS FOUND AMONG PATIENTS WITH DEEP VEIN THROMBOSIS

First Department of Surgery, Tokyo University School of Medicine, Tokyo, Japan

Shun-ichiro Manabe

Protein C (PC) is the zymogen of a serine protease which regurates blood coagulation by inactivating activated blood coagulation factors V and VIII.
We investigated the plasma level of PC in patients with deep vein thrombosis (DVT, n=50), Buerger’ s disease (n=34), arteriosclerosis obliterans (n=37) and myocardial infarction (n=17). PC in plasma was determined by rocket immunoelectrophoresis using a monospecific anti-PC antiserum raised in rabbits. Our study indicated that only in DVT the level of PC was decreased in comparison with the normal control (p<0.05). This decrease may be accounted for by increased utilization of PC for the reguration of continuously activated blood coagulation mechanism possibly ongoing in patients with DVT.
On the other hand, among the patients with the DVT, we found a homozygous PC deficiency combined with a heterozygous dysplasminogenemia in a 22-year old male who had been suffering from recurrent venous thrombosis since the age of 14. Although the homozygous form of PC deficiency has been reported to be closely associated with fatal thrombotic disorders including purpura furminans during the neonatal period, the patient reported here had surprisingly survived the neonatal period and the childhood without any clinical manifestation relevant to thrombosis.


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