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[Post-varicella cerebral thrombophlebitis with anti-protein S: report of a pediatric case]

Brice Samyn1, Lélia Grunebaum, Jean Amiral

  • 1Pôle de pédiatrie, Hôpital de Hautepierre, Strasbourg.

Annales De Biologie Clinique
|February 2, 2012
PubMed

Insights

Chickenpox can rarely cause purpura fulminans and cerebral venous thrombosis. Antibodies against protein S after varicella (chickenpox) can lead to a temporary hypercoagulable state.

Area of Science:

  • Neurology
  • Pediatrics
  • Hematology

Background:

  • Purpura fulminans and venous thrombosis are rare but serious complications of varicella (chickenpox).
  • Cerebral thrombophlebitis, a type of venous thrombosis affecting the brain, is an uncommon manifestation.

Observation:

  • A 6-year-old child developed cerebral thrombophlebitis and a frontal parenchymal hematoma three weeks after varicella.
  • Magnetic Resonance Imaging (MRI) confirmed longitudinal sinus thrombosis and the hematoma.
  • Recent varicella seroconversion was identified in the patient.

Findings:

  • Thrombophilia assessment revealed significantly decreased free protein S levels and activity.
  • Acquired protein S deficiency was confirmed by the presence of anti-protein S antibodies (IgG and IgM).
  • Anticoagulation therapy was initiated, leading to favorable clinical and biological outcomes, including normalization of protein S levels.

Implications:

  • The presence of anti-protein S antibodies following varicella can induce a transient hypercoagulable state in children.
  • This acquired protein S deficiency may predispose individuals to various thrombotic events, including cerebral venous thrombosis.
  • Understanding this mechanism is crucial for managing rare but severe post-varicella thrombotic complications.

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