Homocysteine as a risk factor for ischemic stroke: an epidemiological story in evolution.

Abstract:

:Homocysteine is a metabolite of methionine that may be remethylated by enzymes requiring folate and cobalamin (vitamin B12) to again form methionine or catabolized by the pyridoxine (vitamin B6) dependent enzyme, cystathionine beta synthase (CBS) to form cysteine (fig. 1) [1]. Homocysteine exists as a combination of various free and protein bound forms, but the total amount is what is usually measured and may be reported as homocyst(e)ine [2]. The biological plausibility that elevated homocysteine might lead to vascular disease noted in 1969 by McCully [3]. He reported that a child with abnormal cobalamin metabolism and hyperhomocysteinemia had arterial lesions similar to those seen in children with severe hyperhomocysteinemia from CBS deficiency. These findings led to the idea that moderate elevations in homocysteine, even those still within the so-called normal range, might also lead to vascular pathology through a variety of mechanisms including atherosclerosis and thrombosis [4].

journal_name

Neuroepidemiology

journal_title

Neuroepidemiology

authors

Sacco RL,Roberts JK,Jacobs BS

doi

10.1159/000026169

subject

Has Abstract

pub_date

1998-01-01 00:00:00

pages

167-73

issue

4

eissn

0251-5350

issn

1423-0208

pii

ned17167

journal_volume

17

pub_type

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