Plasma homocysteine concentrations in the acute and convalescent periods of atherothrombotic stroke

Citation
Dj. Meiklejohn et al., Plasma homocysteine concentrations in the acute and convalescent periods of atherothrombotic stroke, STROKE, 32(1), 2001, pp. 57-62
Citations number
38
Categorie Soggetti
Neurology,"Cardiovascular & Hematology Research
Journal title
STROKE
ISSN journal
00392499 → ACNP
Volume
32
Issue
1
Year of publication
2001
Pages
57 - 62
Database
ISI
SICI code
0039-2499(200101)32:1<57:PHCITA>2.0.ZU;2-B
Abstract
Background and Purpose-Homocysteine is a proposed causal risk factor for at herosclerosis, but this remains controversial. We measured fasting plasma h omocysteine concentrations immediately after atherothrombotic stroke and in the convalescent period to investigate this controversy. Methods-One hundred six patients (59 men and 47 women, mean age 57.2 [25 to 70] and 56.5 [26 to 69] years, respectively) were recruited within 24 hour s of admission, and 82 patients were resampled at least 3 months later. Fas ting total plasma homocysteine (tHcy) concentrations were measured by high- performance liquid chromatography. Results-Median tHcy in the acute phase of stroke was not significantly high er than in matched control subjects (men 9.2 [range 4.4 to 22.8] versus 8.7 [4.9 to 20] mu mol/L, P=0.09, Mann-Whitney U test; women 8.1 [4.8 to 32.3] versus 7.6 [3.3 to 14.4] mu mol/L, P=0.58). Median plasma concentrations i ncreased significantly in the convalescent period (from 8.5 [4.8 to 19.2] t o 10.1 [4.3 to 31.5] mu mol/L, P<0.001, Wilcoxon signed rank test) and were then significantly higher than in control subjects in both men and women ( P=0.03 and 0.05, respectively, Mann-Whitney U test). This did not appear to be explained by alteration in the known covariates red-cell folate, serum B-12, or creatinine concentrations. Conclusions-Homocysteine concentrations are not elevated after recent ather othrombotic stroke but rise in the convalescent period. These data do not s upport the hypothesis that raised plasma homocysteine concentrations predat e atherothrombotic stroke. Instead, they offer an explanation for the discr epancies between prospective and retrospective studies and suggest that ele vated tHcy levels may be caused by the disease process itself.