[A case of congenital protein C deficiency with pulmonary thromboembolism].

Abstract

A 47-year-old woman, with a history of recurrent venous thrombosis in her lower limbs (1988 and June, 1992), was admitted because of pulmonary thromboembolism in the right middle lung lobe. She was given anti-coagulant therapy with warfarin. The consolidation in the right middle lobe disappeared within two months. Hematological examinations concerning the coagulation and fibrinolytic system showed a significant decrease in both the serum concentration and the activity of protein C, a vitamin K-dependent hepatic protein which acts as an anticoagulant by shutting off fibrin formation and stimulating fibrinolysis. Since a sister of the patient also has a history of venous thrombosis, several members of her family were tested for protein C deficiency. The familial study revealed that her sister and mother had both a decreased concentration and depressed activity of protein C, indicating that this is a case of congenital protein C deficiency. Warfarin therapy has been continued to reduce the prothrombin time to 70% of the normal control level, resulting in no further episodes of thrombosis.

• Authors: K Takeda, H Kumagai, S Hayashi, Y Tanio, I Kawase, T Kishimoto, M Fujiwara
• Journal: Nihon Kyobu Shikkan Gakkai zasshi (Nihon Kyobu Shikkan Gakkai Zasshi) Vol. 32 Issue 5 Pg. 497-501 (May 1994) ISSN: 0301-1542 [Print] Japan
• PMID: 8084108 (Publication Type: Case Reports, English Abstract, Journal Article)

Chemical References

• Protein C
• Warfarin

Topics

• Female
• Humans
• Middle Aged
• Protein C (genetics)
• Protein C Deficiency
• Prothrombin Time
• Pulmonary Embolism (drug therapy, etiology)
• Recurrence
• Thrombophlebitis (drug therapy, etiology)
• Warfarin (administration & dosage, therapeutic use)