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Protein C deficiency.

E S Rappaport, V O Speights, B Helbert

    Southern Medical Journal
    |February 1, 1987
    PubMed
    Summary
    This summary is machine-generated.

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    Severe homozygous protein C deficiency can cause purpura fulminans in newborns. Fresh frozen plasma improved a neonate’s thrombotic complications, unlike heparin.

    Area of Science:

    • Neonatal Medicine
    • Hematology
    • Genetics

    Background:

    • Severe homozygous protein C deficiency is a rare genetic disorder.
    • It presents in newborns with life-threatening purpura fulminans.
    • Early diagnosis and management are crucial for patient outcomes.

    Observation:

    • A 1,870 gm female neonate presented with purpura fulminans.
    • Clinical findings included disseminated intravascular coagulation (DIC) with extensive ecchymosis and gangrene.
    • Thrombotic complications began on the third day of life without a precipitating infection.

    Findings:

    • The patient's protein C antigen level was less than 3% (normal 70-130%).
    • Heparin therapy was ineffective against progressive gangrenous necrosis.

    Related Experiment Videos

  • Treatment with fresh frozen plasma led to clinical improvement.
  • Other coagulation factors and antithrombin III levels were normal.
  • Heterozygous protein C deficiency was identified in both parents.

    • Implications:

    • This case highlights the critical role of protein C in neonatal hemostasis.
    • Fresh frozen plasma can be an effective treatment for severe protein C deficiency.
    • Long-term management with anticoagulants like warfarin is necessary for clinical stability.
    • Genetic counseling and screening for family members are important.