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Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
08:43

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Calcium homeostasis and skeletal integrity in individuals with familial hypercholesterolemia and aortic calcification

Zuhier Awan1, Khalid Alwaili, Ali Alshahrani

  • 1Cardiovascular Research Laboratories, McGill University Health Centre and McGill University, Montreal, Quebec, Canada.

Clinical Chemistry
|August 13, 2010
PubMed

Insights

Familial hypercholesterolemia (FH) patients with low-density lipoprotein receptor (LDLR) gene mutations show no bone loss but reduced bone formation and calcium excretion. This may contribute to vascular calcification in FH.

Area of Science:

  • Cardiovascular Medicine
  • Endocrinology
  • Nephrology

Background:

  • Familial hypercholesterolemia (FH) is linked to premature aortic calcification.
  • Mutations in the low-density lipoprotein receptor (LDLR) gene cause FH.
  • The relationship between FH, aortic calcification, and mineral/skeletal indices is not fully understood.

Purpose of the Study:

  • To investigate associations between LDLR-deficient FH, aortic calcification, and mineral/skeletal homeostasis.
  • To explore the impact of FH on bone mineral density, bone turnover markers, and calcium metabolism.

Main Methods:

  • Computed tomography (CT) scans were used to measure aortic calcium scores (AoCS) in 19 FH patients.
  • Bone mineral density (BMD) at the femoral neck was assessed.
  • Serum osteocalcin, urinary calcium, and estimated glomerular filtration rate (eGFR) were measured.

Main Results:

  • No significant difference in femoral neck BMD was observed compared to controls.
  • Aortic calcium scores (AoCS) showed no association with bone resorption markers.
  • Negative correlations were found between AoCS and osteocalcin, urinary calcium, and eGFR.

Conclusions:

  • LDLR-deficient FH is not associated with significant bone loss or major calcium disturbances.
  • Reduced bone formation and urinary calcium excretion in FH patients may contribute to vascular calcification.
  • LDLR deficiency might alter osteoblast function and calcium distribution.
Abstract

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