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首页> 外文期刊>Endocrine journal >Relationship between metformin use, vitamin B12 deficiency, hyperhomocysteinemia and vascular complications in patients with type 2 diabetes
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Relationship between metformin use, vitamin B12 deficiency, hyperhomocysteinemia and vascular complications in patients with type 2 diabetes

机译：2型糖尿病患者使用二甲双胍，维生素B12缺乏症，高同型半胱氨酸血症与血管并发症之间的关系

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References(25) Cited-By(10) Aim of the study was to clarify the relationship between metformin-induced vitamin B12 (B12) deficiency, hyperhomocysteinemia and vascular complications in patients with type 2 diabetes. Serum B12 concentrations, homocysteine plasma levels, the presence of retinopathy and history of macroangiopathy (stroke or coronary heart disease) were analyzed in patients without renal dysfunction (serum creatinine115 μmol/L). Firstly, B12 status was analyzed in 62 consecutive metformin-treated patients. Secondly, the relationship between B12, homocysteine and vascular complications was analyzed in 46 metformin-treated and 38 age- and sex-matched non-metformin-treated patients. Among the 62 consecutive metformin-treated patients, B12 was deficient (150 pmol/L) in 8 (13%) and borderline-deficient (150-220 pmol/L) in 18 (29%): the larger the metformin dosage, the lower the B12 (P=0.02, Spearman’s ρ=-0.30). There were independent correlations between metformin use and B12 lowering (P=0.02, r = -0.25), and B12 lowering and elevation of homocysteine (Pr=-0.34). Elevation of homocysteine was a risk for retinopathy (P=0.02, OR 1.26, 95%CI 1.04-1.52). There was no significant relation between homocysteine and macroangiopathy. Correlation between B12 and homocysteine was stronger in metformin-treated (Pr=-0.48) than non-metformin-treated (P=0.04, r=-0.38) patients. In ten B12 deficient patients, B12 supplementation (1,500 μg/day) for 2.2±1.0 months with continued use of metformin raised B12 levels: 152±42 and 299±97 pmol/L before and after treatment, respectively (P<0.01). Metformin-induced B12 lowering in diabetes was associated with elevation of homocysteine, and hyperhomocysteinemia was independently related to retinopathy. Metformin-induced B12 deficiency was correctable with B12 supplementation.
机译：参考文献（25）Cited-By（10）该研究的目的是阐明2型糖尿病患者二甲双胍引起的维生素B12（B12）缺乏症，高同型半胱氨酸血症和血管并发症之间的关系。在没有肾功能不全（血清肌酐<115μmol/ L）的患者中分析血清B12浓度，高半胱氨酸血浆水平，视网膜病变的存在和大血管病变的历史（中风或冠心病）。首先，对连续接受二甲双胍治疗的62例患者的B12状况进行了分析。其次，分析了46名二甲双胍治疗的患者和38名年龄和性别匹配的非二甲双胍治疗的患者中B12，高半胱氨酸与血管并发症之间的关系。在连续接受二甲双胍治疗的62例患者中，B12缺乏（<150 pmol / L）占8（13％），临界边界缺乏（150-220 pmol / L）占18（29％）：二甲双胍的剂量越大， B12越低（P = 0.02，斯皮尔曼的ρ= -0.30）。二甲双胍的使用与B12降低（P = 0.02，r = -0.25）和B12降低与同型半胱氨酸升高（Pr = -0.34）之间存在独立的相关性。高半胱氨酸升高是视网膜病变的风险（P = 0.02，或1.26，95％CI 1.04-1.52）。同型半胱氨酸与大血管病变之间没有显着关系。二甲双胍治疗组（Pr = -0.48）的B12与高半胱氨酸之间的相关性强于非二甲双胍治疗组（P = 0.04，r = -0.38）。在十名缺乏B12的患者中，在继续使用二甲双胍的情况下补充B12（1,500μg/天）2.2±1.0个月，可使治疗前和治疗后B12的水平分别升高：152±42和299±97 pmol / L（P <0.01）。二甲双胍诱导的糖尿病B12降低与同型半胱氨酸升高有关，高同型半胱氨酸血症与视网膜病变独立相关。二甲双胍诱导的B12缺乏症可以通过补充B12来纠正。

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