Abstract
The aim of this study is to evaluate whether any relationship between stroke and vitamin B12, folic acid concentration. We examined 50 patients with stroke (male: 26 and female: 24) aged between (mean +/- SD, year) 59 +/- 14 and 16 control subjects (male: 6 and female: 10) aged between (mean +/- SD, year) 53 +/- 11. Patients were classified into two groups as infarct and hemorrhagic by using Computerised Brain Tomography and Cranial Nuclear Magnetic Resonance Imaging techniques. The percentage of patients with infract was 47.5% in female and 52.5% in male while it was 40% in female and 60% in male with hemorrhagic. The vitamin B12 levels of patients with infarct, hemorrhagic and control group were found as mean +/- SEM, 355 +/- 47 pg/ml, 313 +/- 58 pg/ml, 1569 +/- 258 pg/ml and folic acid levels 13.4 +/- 2.6 ng/ml, 7.7 +/- 1.0 ng/ml, 14.8 +/- 4.0 ng/ml, respectively. The significant difference was found between subgroups of patients with stroke and control group in both folic acid and B12 vitamin levels (p < 0.001 and p < 0.0001, respectively). But, there was no significant difference between vitamin B12 and folic acid levels of patients with hemorrhagic and infarct. In order to well understand the effects of these vitamin in patients with stroke, more detailed follow up studies with long period are needed.
Highlights
Homocyst(e)ine refers to the sulfur-containing amino acids homocysteine, homocystine and homocysteine-cystine mixed disulfide, which is normally exist in plasma in the both free and protein bound forms [3]
A number of investigations support the theory that the decreased vitamin B12 and folic acid levels are associated with stroke
Vitamin B12, folic acid and some biochemical parameter levels are given in Tab. 2
Summary
Homocyst(e)ine refers to the sulfur-containing amino acids homocysteine, homocystine and homocysteine-cystine mixed disulfide, which is normally exist in plasma in the both free and protein bound forms [3]. Homocysteine can be metabolised by two pathway, either catabolised by the transulfuration pathway to cysteine or remetyllated to methionine mainly by the folate and vitamin B12 dependent enzyme methionine synthase [7]. Both these vitamins occupy a key position in the remethylation and synthesis of S-adenosylmethionine (SAMe). While hyperhomocysteinemia increase the risk of stroke, it is unlikely to be a primary initiating factor [4,13] It has been found an inverse relationship between the status of the relevant B vitamins and homocysteine blood concentration. This study was done to examine whether decreased vitamin B12 and folic acid concentrations in patient with stroke
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