血块(可能);由于TNF-α抑制的丧失。

J Broussard, M Berlinger, D Lauret
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引用次数: 0

摘要

炎症与静脉血栓形成有着密切的关系。我们提出了一个病人谁有多个dvt后停止抗TNF-α治疗。病例:一名34岁非裔美国女性,有多处深静脉血栓、流产史,报告克罗恩病表现为呼吸短促。在急诊室,CTA显示双侧肺栓塞。患者停用阿达木单抗一年,报告腹痛,每日6-7次无血性肠蠕动。她因无端深静脉血栓而被开了爱维诺,但在入院前报告少服了几剂。入院后,患者出现严重腹痛,进行了紧急CT血管造影,随后出现左下肢无脉痛。CT显示肾下腹主动脉、左髂总动脉近端及右肾动脉出现部分闭塞血栓,并发右肾梗死。在紧急血管手术恢复左下肢血流后,患者接受了四天的血浆交换和大剂量类固醇治疗潜在的灾难性抗磷脂综合征。APLA血清学阴性。患者终身抗凝治疗出院。讨论:内皮表面是一个复杂的器官,它与周围环境协同工作。炎症与血栓形成密切相关。TNF-α可增加内皮细胞表面粘附分子特别是组织因子的表达,促进血栓形成。在动物模型中,低分子肝素抑制TNF-α表达已被证明可以抑制炎症级联并减少血栓形成。临床数据不太清楚。中断TNF阻滞剂已被证明会增加类风湿关节炎患者接受骨科手术时发生DVT的风险。对于Bechet综合征患者,抗肿瘤坏死因子药物似乎有助于治疗肺动脉血栓患者。进一步回顾抗tnf -α治疗在我们的普通医学患者人群中可能会发现与停药相关的额外风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A Clot (Possibly); Due to Loss of TNF-α Supression.

Introduction: Inflammation and venous thrombosis enjoy a close Relationship. We present a patient who had multiple DVTs following the discontinuation of anti- TNF-α therapy.

Case: A 34 year old African American female with a history of multiple DVT's, miscarriages, and reported Crohn's disease presented with shortness of breath. In the Emergency Department, CTA showed bilateral pulmonary emboli. The patient had been off adalimumab for one year and reported abdominal pain with 6-7 non-bloody bowel movements daily. She had been prescribed lovenox for her unprovoked DVTs yet reported missing several doses prior to admission. Following admission, she developed severe abdominal pain prompting an emergent CT angiogram and she then developed a pulseless painful left lower extremity. CT revealed a partially occlusive thrombus in the infra-renal abdominal aorta, proximal left common iliac artery, and right renal artery with subsequent right renal infarction. Following emergent vascular surgery to restore blood flow to the left lower extremity, the patient received four days of plasma exchange and high dose steroids for potential catastrophic antiphospholipid syndrome. Serology for APLA was negative. The patient was discharged with lifelong anticoagulation.

Discussion: The endothelial surface is a complex organ that works in concert with the surrounding environment. Inflammation and thrombus formation is closely associated. TNF-α can increase the expression of adhesion molecules, specifically, tissue factor, on the surface endothelial cells and promote thrombosis. Suppression of TNF-α expression by low molecular weight heparin has been shown to inhibit the inflammatory cascade and reduce thrombus formation in animal models. Clinical data is less clear. Interruption of TNF blockers has been shown to increase the risk of DVT in patients with rheumatoid arthritis undergoing orthopedic surgery. For patients with Bechet's syndrome, anti-TNF agents appear help treat patients with pulmonary artery thrombosis. Further review of anti-TNF-α therapy in our general medicine patient population may disclose additional risks associated with discontinuation of these medications.

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