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Protein C levels in patients with Legg-Calve-Perthes disease: is it a true deficiency?

J S Mehta1, M E Conybeare, B L Hinves

  • 1Department of Orthopaedic Surgery, Kent and Canterbury Hospital, Canterbury, Kent, UK. Jwalant_mehta@hotmail.com

Journal of Pediatric Orthopedics
|March 25, 2006
PubMed

Insights

Protein C deficiency may contribute to Legg-Calve-Perthes disease (LCPD). Lower protein C levels were observed in LCPD patients, suggesting a potential link to thrombosis and avascular necrosis.

Area of Science:

  • Pediatric Orthopedics
  • Hematology
  • Vascular Biology

Background:

  • Legg-Calve-Perthes disease (LCPD) is characterized by avascular necrosis of the femoral head.
  • A hyper-coagulable state secondary to protein C deficiency has been hypothesized as a cause of LCPD.

Purpose of the Study:

  • To investigate the association between protein C levels and Legg-Calve-Perthes disease.
  • To test the hypothesis that protein C deficiency contributes to LCPD pathogenesis.

Main Methods:

  • Plasma protein C levels were measured in 51 unselected patients with LCPD.
  • Protein C levels were compared to a control group matched for age.

Main Results:

  • A significant proportion (74.5%) of LCPD patients exhibited protein C levels below the age-matched mean.
  • While below average, protein C levels in LCPD patients remained within the normal physiological range.

Conclusions:

  • Reduced protein C levels in LCPD patients suggest a potential predisposition to a hyper-coagulable state.
  • Prothrombotic factors, such as passive smoking, may trigger clinical thrombosis in susceptible individuals, leading to LCPD.

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