Elsevier

Metabolism

Volume 37, Issue 2, February 1988, Pages 175-178
Metabolism

Higher total plasma homocysteine in vitamin B12 deficiency than in heterozygosity for homocystinuria due to cystathionine β-synthase deficiency

https://doi.org/10.1016/S0026-0495(98)90014-2Get rights and content

Abstract

Homocysteine is an amino acid considered to cause vascular injury, arteriosclerosis, and thromboembolism. Total plasma homocysteine (free and protein-bound) was found to be twice as high in asymptomatic vitamin B12-deficient subjects (23.8 ± 3.8 μmol/L, means ± SEM, n = 20) as in controls (11.5 ± 0.9 μmol/L, P < .0001, n = 21), and higher than in heterozygotes for homocystinuria due to cystathionine β-synthase deficiency (13.8 ± 1.6 μmol/L, P < .01, n = 14), who were recently shown to be much more common among patients with premature vascular disease than expected. Eight (40%) vitamin B12-deficient and two (14%) heterozygote subjects had significant homocysteinemia (>mean +2 SD for controls). After administration of hydroxycobalamin to vitamin B12-deficient subjects, homocysteine levels decreased to normal (−49%, 12.2 ± 1.5 μmol/L, P < .0001, n = 20). Thus, if homocysteine does cause vascular injury, theoretically vitamin B12-deficiency might be associated with an increased frequency of vascular disease.

References (27)

  • GHJ Boers et al.

    Heterozygosity for homocystinuria in premature peripheral and cerebral occlusive arterial disease

    N Engl J Med

    (1985)
  • DEL Wilcken et al.

    The pathogenesis of coronary artery disease: A possible role for methionine metabolism

    J Clin Invest

    (1976)
  • LE Brattström et al.

    Moderate homocysteinemia—a possible risk factor for arteriosclerotic cerebrovascular disease

    Stroke

    (1984)
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    Supported by the Ernhold Lundström Foundation and the Swedish National Association Against Heart And Chest Diseases.

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