背景:关于2型糖尿病(T2D)患者血清25-羟基维生素D[25(OH)D]与感染之间关系的证据,一个易受维生素D缺乏和感染的群体,是有限的。
目的:我们旨在研究T2D患者的这种关联,并评估维生素D受体(VDR)的遗传变异是否会改变这种关联。
方法:本研究包括来自英国生物银行的19,851名患有T2D的参与者。通过与医院住院和死亡登记册的联系来识别感染。负二项回归模型用于估计发病率比率(IRRs)和95%置信区间(CIs)。调整潜在的混杂因素。
结果:在T2D患者中,感染率为29.3/1000人年。与25(OH)D为50.0-74.9nmol/L相比,总感染的多变量调整IRR和95%CI,肺炎,胃肠道感染和败血症分别为1.44(1.31,1.59),1.49(1.27,1.75),1.47(1.22,1.78),和1.41(1.14,1.73),分别,25(OH)D<25.0nmol/L的患者观察到25(OH)D浓度与总感染风险(P-总体<0.001;P-非线性=0.002)和胃肠道感染(P-总体<0.001;P-非线性=0.040)之间的非线性负相关,阈值效应在~50.0nmol/L。维生素D感染相关性未被VDR中的遗传变异改变(所有P相互作用>0.050)。
结论:在T2D患者中,较低的血清25(OH)D浓度(<50nmol/L)与较高的感染风险相关,无论VDR中的遗传变异。值得注意的是,发现25(OH)D浓度与感染风险之间的非线性逆关联,阈值效应在~50.0nmol/L。这些发现强调了维持充足的维生素D对降低T2D患者感染风险的重要性。
BACKGROUND: Evidence on the association between serum 25-hydroxyvitamin D [25(OH)D] and infections among patients with type 2 diabetes (T2D), a group susceptible to vitamin D deficiency and infections, is limited.
OBJECTIVE: We aimed to examine this association in individuals with T2D, and to evaluate whether genetic variants in vitamin D receptor (VDR) would modify this association.
METHODS: This
study included 19,851 participants with T2D from United Kingdom Biobank. Infections were identified by linkage to hospital inpatient and death registers. Negative binomial regression models were used to estimate incidence rate ratios (IRRs) and 95% confidence intervals (CIs), with adjustment of potential confounders.
RESULTS: In patients with T2D, the incidence rate of infections was 29.3/1000 person-y. Compared with those with 25(OH)D of 50.0-74.9 nmol/L, the multivariable-adjusted IRRs and 95% CIs of total infections, pneumonia, gastrointestinal infections, and sepsis were 1.44 (1.31, 1.59), 1.49 (1.27, 1.75), 1.47 (1.22, 1.78), and 1.41 (1.14, 1.73), respectively, in patients with 25(OH)D <25.0 nmol/L. Nonlinear inverse associations between 25(OH)D concentrations and the risks of total infections (P-overall < 0.001; P-nonlinear = 0.002) and gastrointestinal infections (P-overall < 0.001; P-nonlinear = 0.040) were observed, with a threshold effect at ∼50.0 nmol/L. The vitamin D-infection association was not modified by genetic variants in VDR (all P-interaction > 0.050).
CONCLUSIONS: In patients with T2D, lower serum 25(OH)D concentration (<50 nmol/L) was associated with higher risks of infections, regardless of genetic variants in VDR. Notably, nonlinear inverse associations between 25(OH)D concentrations and the risks of infections were found, with a threshold effect at ∼50.0 nmol/L. These findings highlighted the importance of maintaining adequate vitamin D in reducing the risk of infections in patients with T2D.