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Lee, Park, Ko, An, Kwon, and Kim: Two Cases of Pulmonary Thromboembolism in Young Patients with Hyperhomocysteinemia
Case Report
Tuberculosis and Respiratory Diseases

Tuberculosis and Respiratory Diseases 2008; 64(6): 460-465.

Published online: 30 June 2008

DOI: https://doi.org/10.4046/trd.2008.64.6.460

Two Cases of Pulmonary Thromboembolism in Young Patients with Hyperhomocysteinemia

Wook-hyun Lee, M.D., Cheol-hong Park, M.D., Hoon-yung Ko, M.D., Ho-jung An, M.D., Soon Seog Kwon, M.D., Yong Hyun Kim, M.D.

Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea.

Address for correspondence: Yong-hyun Kim, M.D. Department of Internal Medicine, Holy Family Hospital, The Catholic University of Korea College of Medicine, 2, Sosadong, Wonmi-gu, Bucheon 420-717, Korea. Phone: 82-32-340-2114, Fax: 82-32-340-2255, kyh30med@catholic.ac.kr

Received 25 May 2008       Accepted 13 June 2008

Copyright © 2008 The Korean Academy of Tuberculosis and Respiratory Diseases

Abstract

Incidences of pulmonary thromboembolism markedly increase with age. Risk factors of pulmonary thromboembolism are surgery, trauma, acute medical illness, immobilization, pregnancy, usage of hormone, and advanced age. In the cases of thrombomembolism occurred in young age, the possibility of thrombophilc state is needed to be investigated. Among many diseases or state associated thrombophilic state, homocyteinemia should be considered a cause of thromboembolism before fifth decade. Homocyteinemia is caused by deficiency of N-5-methyltetrahydrofolate, cystathionie β-synthase and vitamin B12. The presence of the mutation of 5,10-methyleneterahydrofolate lead to homocyteinemia by deficiency of N-5-methyltetrahydrofolate. Homocysteine is acknowledged the risk factor of cardiovascular event, and storke. Homocysteinemia can be the cause of thromboemboism via damaging endotheial cell. We present two cases of pulmonary thromboembolism in young age which seem to be associated with homocysteinemia precipitated by mutation of 5,10-methyleneterahydrofolate.

Keywords: Pulmonary thromboembolism, Homocysteine, 5,10-methyleneterahydrofolate reductase, Young age

Figures and Tables

Figure 1
Chest CT scan shows a low density in left lower lobe of lung (A), and a perfusion defect in left pulmonary artery (B).
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Figure 2
Doppler sonography shows echogenic lesions in left popliteal vein (A, B) and left femoral vein (C, D).
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Figure 3
Abdomen CT scan shows a focal defect in right common iliac artery.
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Figure 4
Chest CT scan shows low density thromboemboli seen in the lateral aspect of the right lower lobar artery (A), left lower lobar superior and posterolateral basal segmental arteries (B).
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Figure 5
Metabolism of homocysteine.
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