(Stroke. 1995;26:795-800.)
© 1995 American Heart Association, Inc.
Articles |
Presented at the Third European Stroke Conference, Stockholm, Sweden, May 26-28, 1994.
From the Departments of Neurology (A.L., B.N., B.B.J.) and Clinical Chemistry (B.H., A.A.), University Hospital, Lund; and the Department of Internal Medicine (L.B.), County Hospital, Kalmar, Sweden.
Correspondence to Arne Lindgren, MD, Department of Neurology, University Hospital, S-221 85 Lund, Sweden.
Background and Purpose Stroke patients frequently manifest moderate hyperhomocysteinemia. In most published studies, plasma homocysteine was measured at least 1 month after stroke (or the interval was not reported). To determine whether plasma homocysteine concentrations change in the acute phase, we compared acute-phase values with both convalescent-phase and control values.
Methods Plasma homocysteine concentrations were measured in the acute phase (mean, 2 days after stroke onset) in 162 first-ever stroke patients aged 50 years or more (median, 75 years) and again at a median interval of 583 days (range, 460 to 645 days) after stroke onset in a subgroup of 17 patients, with values for 60 age-matched subjects serving as controls. Twenty of the control subjects were reexamined 2 to 3 years after their initial examination.
Results The median plasma homocysteine concentration was 13.4 µmol/L in the patient group compared with 13.8 µmol/L for control subjects (NS, Mann-Whitney U test) and increased from 11.4 µmol/L in the acute phase to 14.5 µmol/L in the convalescent phase in the subgroup of patients examined twice (P<.01, Wilcoxon signed rank test). In the 20 reexamined control subjects, no significant change over time in plasma homocysteine concentration was found.
Conclusions The postacute-phase increase in plasma homocysteine may explain why higher values were obtained for stroke patients than for control subjects in previous studies. Possible reasons for the variation in plasma homocysteine concentrations over time are (1) an acute-phase reduction secondary to a decrease in plasma albumin and (2) an increase in plasma homocysteine during the convalescent phase due to modified vitamin intake and/or lifestyle. The timing of plasma homocysteine measurements relative to stroke onset is a factor to be considered in the interpretation of results.
Key Words: cerebral infarction homocysteine risk factors stroke onset
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