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Asymmetric dimethylarginine in adults with cystathionine β-synthase deficiency

Monica S Rocha1, Tom Teerlink, Mirian C H Janssen

  • 1Department of Clinical Chemistry, Metabolic Unit, Institute for Cardiovascular Research (ICAR-VU), VU University Medical Center, Amsterdam, The Netherlands.

Atherosclerosis
|April 10, 2012
PubMed

Insights

Hyperhomocysteinemia (HHcy) is linked to cardiovascular issues. This study found that elevated homocysteine levels in cystathionine β-synthase deficiency do not increase ADMA, suggesting HHcy

Area of Science:

  • Biochemistry and Molecular Biology
  • Cardiovascular Research
  • Metabolic Disorders

Background:

  • Hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular diseases.
  • Endothelial dysfunction, characterized by reduced nitric oxide bioavailability, is a common finding in HHcy.
  • Asymmetric dimethylarginine (ADMA), a nitric oxide synthase inhibitor, is implicated in HHcy-related endothelial dysfunction, but its link to cystathionine β-synthase (CBS) deficiency is unclear.

Purpose of the Study:

  • To investigate the association between CBS deficiency, elevated total homocysteine (tHcy), and ADMA levels.
  • To determine if ADMA contributes to endothelial dysfunction in HHcy caused by CBS deficiency.

Main Methods:

  • Plasma samples from 22 adult patients with CBS deficiency were analyzed.
  • High-performance liquid chromatography (HPLC) was used to measure total homocysteine (tHcy), ADMA, and symmetric dimethylarginine (SDMA).
  • Statistical analysis was performed to assess correlations between tHcy, ADMA, and SDMA.

Main Results:

  • CBS-deficient patients exhibited elevated tHcy levels.
  • Plasma ADMA and SDMA levels were found to be normal in these patients.
  • No significant correlation was observed between tHcy and ADMA concentrations (r(s)=0.017, p=0.94).

Conclusions:

  • Elevated tHcy in CBS deficiency is not associated with increased ADMA levels.
  • The findings suggest that the vascular complications of HHcy in CBS deficiency may stem from mechanisms independent of ADMA.
  • This study provides evidence for an ADMA-independent etiology of homocysteine-induced endothelial dysfunction.

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