Marginal folate deficiency as a possible cause of hyperhomocystinaemia in stroke patients.
It has been reported that patients with vascular disease seem to increase their concentration of plasma homocysteine after the acute episode, whereas reexamined control subjects do not change their concentration of plasma homocysteine over time. Since the main determinants of plasma homocysteine are serum cobalamin, blood folate and serum creatinine we measured these quantities in 20 control subjects and 49 stroke patients in the acute phase and at reexamination 1.5-2 years after acute stroke onset. There were no significant differences between the levels of blood folate, serum cobalamin and serum creatinine in the acute and convalescent phase of all 49 stroke patients. However, we noted a significant decrease of blood folate concentrations in a subgroup of patients (n = 25) who had increased plasma homocysteine concentrations. Thus the increase in plasma homocysteine concentrations in this group of patients may partly be caused by a marginal folate deficiency.
Hultberg
B
B
Department of Clinical Chemistry, University Hospital, Lund, Sweden.
Andersson
A
A
Lindgren
A
A
D000368:Aged; D016022:Case-Control Studies; D002561:Cerebrovascular Disorders / Q000097:blood* / Q000150:complications*; D003404:Creatinine / Q000097:blood; D005260:Female; D005492:Folic Acid / Q000097:blood; D005494:Folic Acid Deficiency / Q000097:blood* / Q000150:complications*; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D008297:Male; D008875:Middle Aged; D013997:Time Factors; D014805:Vitamin B 12 / Q000097:blood
D006710:Homocysteine; D005492:Folic Acid; D003404:Creatinine; D014805:Vitamin B 12