再発性虚血性脳卒中における第VIII因子高値
Nika Bakshi1, Maya S Kardouh1, Claire Wang1
1Internal Medicine, Oakland University William Beaumont School of Medicine, Royal Oak, USA.
Cureus
|December 24, 2025
まとめ
患者はラクナ梗塞や脳底動脈狭窄を含む複数の脳卒中を経験し、テネクテプラーゼおよびステント留置術で治療を受けた。ステント留置後も脳底動脈が開存していたにもかかわらず、橋梗塞が再発し、高凝固状態を示す第VIII因子高値が発見された。
科学分野:
- 神経学; 血管医学; 血液学
背景:
- 再発性虚血性脳卒中は、動脈狭窄や高凝固状態を含む様々な要因によって起こりうる。 脳底動脈狭窄のような後部循環における血栓性イベントは、臨床的に重大な課題をもたらす。 再発性脳血管イベントの管理には、潜在的な高凝固性障害の特定が不可欠である。
研究 の 目的:
- 脳底動脈狭窄を有する患者における再発性虚血性脳卒中、およびその後の橋梗塞の症例を提示する。 血管内治療が成功した後も再発性梗塞の原因を調査する。 原因不明の脳卒中の再発管理における高凝固能検査の診断的価値を強調する。
主な方法:
- 複数の虚血性脳卒中を呈した52歳女性の臨床経過、診断的検査、および治療の詳細を記載した症例報告。 急性梗塞のMRI、血管評価のためのMRA/CTAを含む神経画像所見のレビュー。 高凝固能検査を含む臨床検査。
主要な成果:
- 患者は初期のラクナ梗塞に続き、脳底動脈中部の狭窄による脳卒中を発症し、テネクテプラーゼおよびステント留置術で治療を受けた。 脳底動脈ステント留置後も開存していたにもかかわらず、橋梗塞が再発した。 高凝固能検査により、第VIII因子高値が明らかになった。
結論:
- 第VIII因子高値は、動脈狭窄の管理が成功した後でも、再発性虚血性脳卒中に寄与する可能性がある。 従来の危険因子や治療法では十分に説明できない再発性脳卒中の場合、包括的な高凝固能検査が不可欠である。 本症例は、原因不明および再発性の脳血管イベントの病因において血栓性素因を考慮することの重要性を強調する。
関連する概念動画
Venous Thrombosis III: Interprofessional Care
257
Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...
257
Anticoagulant Drugs: Low-Molecular-Weight Heparins
1.6K
Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
1.6K
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants
2.0K
Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K antagonists, exemplified by warfarin, and direct thrombin inhibitors (DTIs), such as dabigatran, as well as factor Xa inhibitors, including rivaroxaban.
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
2.0K
Venous Thrombosis II: Clinical Manifestations and Diagnostic Studies
266
The key difference between Superficial Vein Thrombosis (SVT) and Deep Vein Thrombosis (DVT) lies in their location and severity.Clinical ManifestationsSVT typically presents with localized pain, tenderness, and redness along the course of a superficial vein, often accompanied by a palpable, cord-like structure under the skin. This condition is usually less dangerous than DVT but can be uncomfortable and may lead to complications such as cellulitis or, rarely, a clot extension into the deep...
266
Disorders of Hemostasis
1.9K
Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
1.9K
Extrinsic and Intrinsic Pathways of Hemostasis
11.8K
Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
11.8K


