Editorials

Nutritional hyperhomocysteinaemia

BMJ 1999; 318 doi: https://doi.org/10.1136/bmj.318.7198.1569 (Published 12 June 1999) Cite this as: BMJ 1999;318:1569

This article has a correction. Please see:

Evidence mounts for its role in vascular disease

  1. I V Mohan, Research fellow,
  2. G Stansby, Senior lecturer in vascular surgery (g.stansby@ic.ac.uk)
  1. Academic Surgical and Regional Vascular Units, Imperial College of Science, Technology and Medicine, St Mary's Hospital, London W2 1NY

    A raised concentration of serum homocysteine is increasingly being implicated as a risk factor for clinical vascular disease. It is known to be injurious to the vascular endothelium in animals,1 and many reports have now confirmed the presence of raised homocysteine concentrations in patients with peripheral vascular disease, myocardial infarction, stroke, and venous thromboembolism. Indeed, moderate and intermediate increases in homocysteine concentration have been found in up to 40% of patients with vascular disease2 and in up to 35% of patients with venous thromboembolism.3 The obvious question is: is this cause or effect? And, if it is causal, should we be screening for and treating hyperhomocysteinaemia?

    All circulating homocysteine is derived from methionine in the diet, and it is removed by either remethylation to methionine or conversion to cysteine via a transsulphuration pathway. Classic homocystinuria, a rare autosomal recessive condition, of which premature vascular disease and thrombosis are major features, is the result of a deficiency of …

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