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NEUROLOGY 2003;61:1595-1599
© 2003 American Academy of Neurology

Hyperhomocysteinemia as an independent risk factor for silent brain infarction

N. K. Kim, PhD, B. O. Choi, MD PhD, W. S. Jung, MD PhD, Y. J. Choi, MD and K. G. Choi, MD PhD

From the Department of Neurology and Ewha Medical Research Center (Drs. B.O. Choi, Y.J. Choi, and K.G. Choi), College of Medicine, Ewha Womans University, Seoul; Institute for Clinical Research (Dr. Kim), College of Medicine, Pochon CHA University, Sungnam; and Stroke Center (Dr. Jung), College of Oriental Medicine, Kyung Hee University, Seoul, South Korea.

Address correspondence and reprint requests to Dr. Byung-Ok Choi, Department of Neurology, Ewha Womans University, Dongdaemun Hospital, 70, Jongro 6-ga, Jongro-gu, Seoul, 110-783, South Korea; e-mail: bochoi{at}ewha.ac.kr

Objective: To evaluate whether hyperhomocysteinemia is an independent risk factor for silent brain infarction (SBI), and to determine the relationship between homocysteine and folate in each type of methylenetetrahydrofolate reductase (MTHFR) polymorphism, in order to identify a way of reducing the risk for SBI.

Methods: The authors enrolled 161 patients with SBI and 126 healthy people, checked their fasting homocysteine and folate levels, and analyzed for the MTHFR C677T polymorphism.

Results: The mean plasma homocysteine level in patients with SBI (12.17 ± 5.35 µmol/L) was significantly higher than in normal healthy people (9.37 ± 4.11 µmol/L; p < 0.05). By subgroup analysis, based on the classification of plasma homocysteine levels as high (>=11.77 µmol/L), moderate (8.71 to 11.76 µmol/L), and low (<=8.70 µmol/L), the adjusted OR (AOR) of the high group for SBI was significantly greater than that of the low group (AOR, 4.78; 95% CI, 2.45 to 9.33). The homocysteine level showed a significant inverse correlation with folate level only in patients with SBI with the MTHFR 677TT genotype (p < 0.05).

Conclusions: This study demonstrates that hyperhomocysteinemia is an independent risk factor for SBI, and provides the possibility of reducing the risk for SBI in the MTHFR 677TT genotype by folate supplementation.

Received May 2, 2003. Accepted in final form August 13, 2003.




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