Independent Effect of Methylcobalamin on Hyperhomocysteinemia in Hemodialysis Patients

甲基維生素B12對血液透析病人高同胱胺酸血症之獨立療效

郭弘典(Hong-Tien Kuo) ； 蔡哲嘉(Jer-Chia Tsai) ； 陳玲娜(Ling-Na Chen) ； 陳鴻鈞(Hung-Chun Chen) ； 顧進裕(Jinn-Yuh Guh) ； 黃尚志(Shang-Jyh Hwang) ； 張哲銘(Jer-Ming Chang) ； 賴永勳(Yung-Hsiung Lai)

《Acta Nephrologica》 14卷4期 (2000/10) Pp. 261-261

並列摘要

Hyperhomocysteinemia is frequently observed in uremic patients and it is an independent risk factor for cardiovascular diseases. Several lines of evidence suggests that hyperhomocysteinemia in renal failure is due to impaired remethylation metabolism caused by folate deficiency or methylenetetrahydrofolate reductase (MTHFR) mutation. Folic acid-based regimens were effective in treating hyperhomcysteinemia in uremic patients. The independent effect of vitamin B12 supplementation on homcysteine metabolism in hemodialysis (HD) patients was seldom reported. The purposes of this study are to evaluate the efficacy of methylcobalamin (methl form of vitamin B12) on hyperhomocysteinema in HD patients and the impact of MTHFR mutation on its efficacy.
We enrolled 57 HD patients with elevate plasma total homocysteine (Hcy) levels more than 15 μmol/L. Folic acid acid was discontinued for at least for 3 months and there was no evidence of deficiencies of folic acid or vitamin B12 at baseline. The prevalence of MTHFR mutation was 58%(667CC, n=33), 42%(667CT, n=24), and 0% (667TT, n=0), respectively, We randomly divided these patients into methylcobalamin treatment group and control group. Twenty-eight patients (M/F: 15/13, mean age:56.2±11.7 years) received methylcobalamin 500 μg intravenously thrice a thrice a week after each HD for 2 months. Their plasma Hcy levels decreased significantly (23.9±5.2 vs. 18.2±4.1 μmol/L, p ＜0.0001), %decrement: 22.8±14.1%). Plasma Hcy in 7 of them (25%) could be reduced to normal (＜15 μmol/L). The control group included 29 patients (M/F: 11/18, mean age: 57±10.8 years). Their plasma Hcy levels did not change significantly (23.5±6.0 vs. 22.7±8.0 μmol/L , p=NS) after 2 months. The efficacy of methylcobalamin is similar between patients with wild type of with MTHFR mutation at C667T(25.4±31.8% vs. 19.9±26.8%).
This study shows that methylcobalamin supplementation further improves hyperhomocysteinemaia in HD patients without absolute vitamin B12 deficiency. This homocysteine-lowering effect by the remethylation pathway is independent of folic acid status or MTHFR genotypes.