Namazi Mohammad Hasan, AlipourParsa Saeed, Roohigilani Kobra, Safi Morteza, Vakili Hossein, Khaheshi Isa, Abdi Fatemeh, Zare Adel, Esmaeeli Shooka
Cardiovascular Research Center, Modarres hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran..
Labbafinegad hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran..
Acta Biomed. 2018 Jun 7;89(2):227-232. doi: 10.23750/abm.v89i2.5446.
Although metformin is not directly nephrotoxic, it has been postulated that it can impair gluconeogenesis from lactate, which may lead lactate to be accumulated under circumstances such as contrast-induced nephropathy. The present study aims to assess the role of metformin in lactate production in a group of diabetic patients with GFR > 60 ml/min per 1.73 m2undergoing coronary angiography.
In the present randomized clinical trial, 162 metformin-treated diabetic patients were enrolled. The enlisted patients were scheduled to undergo coronary angiography at Modarres Hospital from Feb 2012 to Nov 2012. Patients were randomly allocated to continue metformin during peri-angiography period (M (+) group) or to stop the medication 24 hours prior the procedure (M (-) group). All the patients had glomerular filtration rate of >60 mL/min per 1.73 m2. Iodixanol was the only contrast media which in all patients. Metformin-associated lactic acidosis (MALA) was defined as an arterial pH <7.35 and plasma lactate concentration >5 mmol⁄L.
162 patients, including79 (48.7%) male and 83 (51.3%) female patients were enrolled in the study. The average of GFR was comparable in both groups (76 ml/min per 1.73 m2 in the M (+) group versus 79 ml/min per 1.73 m2 in the M (-) group, p=0.53). No significant difference was observed in the mean dose of metformin before the study between the 2 groups (2.18 tablets per day in M (+) group vs. 2.21 tablets per day in M(-) group, p=0.62).No lactic acidosis was observed in the studied groups.
In conclusion, the results of the present study indicate that metformin continuation in diabetic patients with a GFR of more than 60 ml/min per 1.73 m2 undergoing coronary angiography does not enhance the risk of MALA development.
尽管二甲双胍并非直接具有肾毒性,但据推测它可能会损害乳酸的糖异生作用,这可能导致在诸如造影剂诱导的肾病等情况下乳酸积累。本研究旨在评估二甲双胍在一组估算肾小球滤过率(GFR)>60ml/(min·1.73m²)的糖尿病患者进行冠状动脉造影时对乳酸生成的作用。
在本项随机临床试验中,纳入了162例接受二甲双胍治疗的糖尿病患者。入选患者计划于2012年2月至2012年11月在莫达雷斯医院接受冠状动脉造影。患者被随机分配在血管造影术期间继续服用二甲双胍(M(+)组)或在手术前24小时停药(M(-)组)。所有患者的肾小球滤过率均>60ml/(min·1.73m²)。所有患者均使用碘克沙醇作为唯一的造影剂。二甲双胍相关乳酸酸中毒(MALA)定义为动脉血pH<7.35且血浆乳酸浓度>5mmol/L。
162例患者纳入研究,其中男性79例(48.7%),女性83例(51.3%)。两组的平均肾小球滤过率相当(M(+)组为76ml/(min·1.73m²),M(-)组为79ml/(min·1.73m²),p=0.53)。两组在研究前二甲双胍的平均剂量无显著差异(M(+)组为每日2.18片,M(-)组为每日2.21片,p=0.62)。研究组中未观察到乳酸酸中毒。
总之,本研究结果表明,在估算肾小球滤过率>60ml/(min·1.73m²)的糖尿病患者进行冠状动脉造影时继续使用二甲双胍不会增加发生二甲双胍相关乳酸酸中毒的风险。