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<p>Severe thrombocytopenia accompanied by acute pulmonary embolism (PE) represents a rare and challenging clinical scenario, particularly in elderly patients, where both thrombotic and hemorrhagic risks coexist.</p><p>We report the case of a 78-year-old man who presented with acute dizziness and was found to have severe thrombocytopenia (platelet count 32 × 10⁹/L) and objectively confirmed pulmonary embolism. Given the high bleeding risk, prophylactic-dose low-molecular-weight heparin was initiated. Shortly thereafter, the patient developed intracerebral hemorrhage, prompting immediate discontinuation of anticoagulation.</p><p>Extensive evaluation excluded heparin-induced thrombocytopenia, thrombotic microangiopathy, malignancy, and infection. Autoimmune testing revealed persistent isolated positivity for anti–β2-glycoprotein I IgM antibodies, suggesting an APS-like autoimmune thrombophilic state, although high-specificity classification criteria for antiphospholipid syndrome were not fully met.</p><p>Notably, both thrombocytopenia and pulmonary embolism gradually improved without further anticoagulation. At follow-up, no recurrent thrombosis occurred.</p><p>This case highlights the diagnostic uncertainty and therapeutic complexity of managing venous thromboembolism in the setting of severe thrombocytopenia and APS-spectrum autoimmunity.</p>

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Concomitant pulmonary embolism and severe thrombocytopenia associated with an APS-like autoimmune thrombophilic condition: a case report

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月14日

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  • Zhongshan Yang,
  • Hanbin Lin,
  • Yuxiong Hu,
  • Ying Zhang,
  • Qingyu Lin,
  • Maohe Chen

摘要

Severe thrombocytopenia accompanied by acute pulmonary embolism (PE) represents a rare and challenging clinical scenario, particularly in elderly patients, where both thrombotic and hemorrhagic risks coexist.

We report the case of a 78-year-old man who presented with acute dizziness and was found to have severe thrombocytopenia (platelet count 32 × 10⁹/L) and objectively confirmed pulmonary embolism. Given the high bleeding risk, prophylactic-dose low-molecular-weight heparin was initiated. Shortly thereafter, the patient developed intracerebral hemorrhage, prompting immediate discontinuation of anticoagulation.

Extensive evaluation excluded heparin-induced thrombocytopenia, thrombotic microangiopathy, malignancy, and infection. Autoimmune testing revealed persistent isolated positivity for anti–β2-glycoprotein I IgM antibodies, suggesting an APS-like autoimmune thrombophilic state, although high-specificity classification criteria for antiphospholipid syndrome were not fully met.

Notably, both thrombocytopenia and pulmonary embolism gradually improved without further anticoagulation. At follow-up, no recurrent thrombosis occurred.

This case highlights the diagnostic uncertainty and therapeutic complexity of managing venous thromboembolism in the setting of severe thrombocytopenia and APS-spectrum autoimmunity.