Background <p>Superior sagittal sinus thrombosis (SSST) is a rare but life-threatening form of cerebral venous thrombosis. Although several prothrombotic and autoimmune conditions are recognized risk factors, SSST occurring in patients with rheumatoid arthritis (RA) receiving tumor necrosis factor-alpha (TNF-α) inhibitor therapy remains exceptionally rare and poorly described in the literature.</p> Case presentation <p>We present a 59-year-old Caucasian female with RA treated with infliximab who developed extensive superior sagittal sinus thrombosis with concurrent intracranial and subarachnoid hemorrhage. The patient was managed with anticoagulation, blood pressure control, and seizure prophylaxis, with subsequent clinical and radiologic improvement at one-month follow-up. Hypercoagulability evaluation was overall unrevealing, and no other clear provoking etiology was identified.</p> Conclusions <p>Given the rarity of this presentation, we report this case to raise awareness of a possible association between cerebral venous thrombosis and TNF-α inhibitor therapy in patients with rheumatoid arthritis. This is especially important given the increasing and widespread use of biologic agents in the treatment of autoimmune diseases.</p>

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Superior sagittal sinus thrombosis with intracranial hemorrhage in a patient on infliximab: a case report

  • Mohammad Rizwan Alam,
  • Juan Corona-Ruiz,
  • Joseph Cahill,
  • William Goldsmith,
  • Michael Sabra,
  • Maro Issac,
  • Peter Fahim

摘要

Background

Superior sagittal sinus thrombosis (SSST) is a rare but life-threatening form of cerebral venous thrombosis. Although several prothrombotic and autoimmune conditions are recognized risk factors, SSST occurring in patients with rheumatoid arthritis (RA) receiving tumor necrosis factor-alpha (TNF-α) inhibitor therapy remains exceptionally rare and poorly described in the literature.

Case presentation

We present a 59-year-old Caucasian female with RA treated with infliximab who developed extensive superior sagittal sinus thrombosis with concurrent intracranial and subarachnoid hemorrhage. The patient was managed with anticoagulation, blood pressure control, and seizure prophylaxis, with subsequent clinical and radiologic improvement at one-month follow-up. Hypercoagulability evaluation was overall unrevealing, and no other clear provoking etiology was identified.

Conclusions

Given the rarity of this presentation, we report this case to raise awareness of a possible association between cerebral venous thrombosis and TNF-α inhibitor therapy in patients with rheumatoid arthritis. This is especially important given the increasing and widespread use of biologic agents in the treatment of autoimmune diseases.