Association of metabolic syndrome with development of new-onset diabetes after transplantation.

Association of metabolic syndrome with development of new-onset diabetes after transplantation.
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DOI:
10.1097/tp.0b013e3181f1543c
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发表时间:
2010-10-27
期刊:
影响因子:
6.2
通讯作者:
Rosas SE
Rosas SE
中科院分区:
医学2区
文献类型:
--
作者:
Bayer ND;Cochetti PT;Anil Kumar MS;Teal V;Huan Y;Doria C;Bloom RD;Rosas SE

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移植后新发糖尿病(NODAT)是移植后的主要并发症,与移植物和受体存活率降低有关。我们的目标是确定移植前代谢综合征是否与NODAT的发展独立相关。我们在1999-2004年间从3个学术中心连续招募了640名非糖尿病肾移植受者。NODAT被定义为在移植后30天后使用降糖药物、随机血糖200 mg/dL或2个空腹血糖水平≥126 mg/dL。代谢综合征在移植前较为常见(57.2%)。31.4%的受者在移植后一年发生NODAT。与没有代谢综合征的受试者相比,有代谢综合征的受试者更有可能发生非代谢综合征(34.4%比27.4%,p=0.057)。代谢综合征阳性成分增多的受者发生非代谢综合征的可能性更大(代谢综合征评分-1年患病率:0.001~0.0%,1~24.2,2~29.3%,3~31.0%,4~34.8%,5~73.7%,p=0.05)。调整人口学因素后,年龄(HR-1.34(1.20-1.5),p<0.0001)、非裔美国人(HR-1.35(1.01-1.82,p=0.043)、累积泼尼松用量(HR-1.18(1.07-1.30,p=0.001)和代谢综合征(HR-1.34(1.00-1.79),p=0.047)是移植后1年发生NODAT的独立预测因素。在将个体代谢综合征成分本身作为协变量的多变量分析中,移植前代谢综合征成分仍然是NODAT的独立预测因子的唯一因素是低高密度脂蛋白(HR-1.371.01-1.85,p=0.042)。代谢综合征是NODAT的独立预测因子,也可能是预防NODAT的干预目标。未来需要进行研究,以评估移植前对代谢综合征因子的修改是否会减少NODAT的发生。
New-onset diabetes after transplantation (NODAT) is a major post-transplant complication associated with lower allograft and recipient survival. Our objective was to determine if metabolic syndrome pre-transplant is independently associated with NODAT development. We recruited 640 consecutive incident non-diabetic renal transplant recipients from 3 academic centers between 1999 and 2004. NODAT was defined as use of hypoglycemic medication, a random plasma glucose >200 mg/dL, or 2 fasting glucose levels ≥126 mg/dL beyond 30 days post-transplant. Metabolic syndrome was common pre-transplant (57.2 %). NODAT developed in 31.4% of recipients one year post-transplant. Participants with metabolic syndrome were more likely to develop NODAT compared to recipients without metabolic syndrome (34.4% v. 27.4%, p=0.057). Recipients with increasing number of positive metabolic syndrome components were more likely to develop NODAT (metabolic syndrome score-prevalence at 1 year: 0-0.0%, 1-24.2, 2-29.3%, 3-31.0%, 4-34.8%, and 5-73.7%, p=0.001). After adjustment for demographics, age by decade (HR-1.34 (1.20-1.50), p<0.0001), African American race (HR-1.35 (1.01-1.82), p=0.043), cumulative prednisone dosage (HR-1.18 (1.07-1.30), p=0.001), and metabolic syndrome (HR-1.34 (1.00-1.79), p=0.047) were independent predictors of development of NODAT at 1 year post-transplant. In a multivariable analysis incorporating the individual metabolic syndrome components themselves as covariates, the only pre-transplant metabolic syndrome component to remain an independent predictor of NODAT was low HDL (HR-1.37 (1.01-1.85), p=0.042). Metabolic syndrome is an independent predictor for NODAT and is a possible target for intervention to prevent NODAT. Future studies to evaluate if modification of metabolic syndrome factors pre-transplant reduces NODAT development are needed.