Korean J Hematol.  2006 Jun;41(2):110-114. 10.5045/kjh.2006.41.2.110.

A Case of Hyperhomocysteinemia Manifested by Deep Vein Thrombosis and Pulmonary Embolism

• Lee SH
• Choi SH
• Lee JH
• Seon KY
• Joo SB

• KMID: 2083485
• DOI: http://doi.org/10.5045/kjh.2006.41.2.110

Abstract

Homocysteine has been reported as an independent risk factor of intravascular thrombosis and atherosclerosis by its participation in vascular endothelial cell dysfunction, platelet activation and thrombus formation. The serum homocysteine concentration is influenced by not only heredity, but also by environmental factors, and it interacts with the former reported risk factors of atherosclerosis. We report here on a case of a young patient with hyperhomocysteinemia that manifested by deep vein thrombosis and pulmonary embolism.

Keyword

Pulmonary embolism; Deep vein thrombosis; Hyperhomocysteinemia

MeSH Terms

Atherosclerosis
Endothelial Cells
Heredity
Homocysteine
Humans
Hyperhomocysteinemia*
Platelet Activation
Pulmonary Embolism*
Risk Factors
Thrombosis
Venous Thrombosis*
Homocysteine

Figure

• 

  Fig. 1 Pulmonary angiogram shows filling defect in right pulmonary artery.

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  Fig. 2 Dynamic enhanced computed tomography (CT) scan of the chest on admission shows near total filling defect in right pulmonary artery and partial filling defect in left pulmonary artery (A) and decreased amount of filling defect in right pulmonary artery and disappeared filling defect in left pulmonary artery after management by recombinant tissue plasminogen activator and urokinase (B). Dynamic enhanced CT scan with lung window on admission shows collateral circulations of both lungs (C) and slightly improved collateral circulations of both lungs after management by recombinant tissue plasminogen activator and urokinase (D).

• 

  Fig. 3 Right lower extremity venography on sixth day of hospitalization shows long segmental filling defects in popliteal vein and proximal portion of superficial femoral vein (A) and decreased amount of filling defects in popliteal vein and proximal portion of superficial femoral vein after management by recombinant tissue plasminogen activator and urokinase (B).

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