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一名36岁患有因子V莱顿突变的男性患者的右心室血栓形成

Right Ventricular Thrombus in a 36-Year-Old Man with Factor V Leiden.

作者信息

Hajsadeghi Shokoufeh, Naghshin Roozbeh, Hejrati Maral, Kerman Scott Reza Jafarian

机构信息

Rasoul-e-Akram Hospital, Iran University of Medical Sciences, Tehran, Iran.

Students' Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran.

出版信息

J Tehran Heart Cent. 2015;10(1):46-9. Epub 2015 Jan 8.

PMID:26157463
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4494519/
Abstract

Factor V Leiden deficiency is the most common hereditary hypercoagulable disease in the United States and involves 5% of the Caucasian population. Up to 30% of patients who present with deep vein thrombosis (DVT) or pulmonary thromboembolism present with this condition. This is a case report of a 36-year-old man who experienced one episode of DVT within the previous year and was admitted to our hospital due to productive coughs and hemoptysis. Paraclinical studies demonstrated a right ventricular thrombus. Additional investigation was done to find the underlying cause. Laboratory tests were positive for Factor V Leiden mutation. Other factors for hypercoagulability states were normal. Given that Factor V Leiden mutation is a life-threatening condition with a relatively high prevalence and considering its thrombogenesis, screening tests are necessary in young patients without obvious reasons for recurrent thrombus formation. It seems that medical noninvasive treatments can be an alternative therapy to surgery when a ventricular thrombus is suspected in these patients.

摘要

因子V莱顿缺乏症是美国最常见的遗传性易栓症,在白种人群中的发病率为5%。在出现深静脉血栓形成(DVT)或肺血栓栓塞的患者中,高达30%患有此病。本文报告一例36岁男性,该患者在过去一年内发生过一次DVT,并因咳痰和咯血入院。辅助检查显示右心室有血栓。为寻找潜在病因进行了进一步检查。实验室检查显示因子V莱顿突变呈阳性。其他易栓状态的因素均正常。鉴于因子V莱顿突变是一种患病率相对较高的危及生命的疾病,并考虑到其血栓形成机制,对于无明显复发性血栓形成原因的年轻患者,进行筛查测试是必要的。当怀疑这些患者有心室血栓时,医学无创治疗似乎可以作为手术的替代疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c51f/4494519/6a2ea4929b2f/JTHC-10-46f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c51f/4494519/b57bd44a9f81/JTHC-10-46f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c51f/4494519/4f9614d84a16/JTHC-10-46f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c51f/4494519/a619cbccb2f4/JTHC-10-46f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c51f/4494519/c0a801c48b37/JTHC-10-46f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c51f/4494519/6a2ea4929b2f/JTHC-10-46f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c51f/4494519/b57bd44a9f81/JTHC-10-46f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c51f/4494519/4f9614d84a16/JTHC-10-46f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c51f/4494519/a619cbccb2f4/JTHC-10-46f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c51f/4494519/c0a801c48b37/JTHC-10-46f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c51f/4494519/6a2ea4929b2f/JTHC-10-46f5.jpg

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Thrombosis. 2012;2012:380681. doi: 10.1155/2012/380681. Epub 2012 Jun 12.
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Mechanism and pathophysiology of activated protein C-related factor V leiden in venous thrombosis.活化蛋白C相关的因子V莱顿突变在静脉血栓形成中的机制及病理生理学
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一例巨大的右心移行血栓:因子V莱顿突变型易栓症抗凝治疗的挑战
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