Aims/hypothesis

A better understanding of the mechanisms underlying an elevated infection risk in individuals with type 2 diabetes is needed to guide risk stratification and prevention. We investigated the risk of infection in subgroups of individuals with type 2 diabetes according to indices of insulin sensitivity and beta cell function.

Methods

We classified 7265 individuals with recently diagnosed type 2 diabetes (median duration 1.4 years, IQR 0.5–2.9 years) into hyperinsulinaemic (high beta cell function [HOMA 2-beta-cell function, HOMA2-B], low insulin sensitivity [HOMA 2-insulin sensitivity, HOMA2-S]), classical (low HOMA2-B, low HOMA2-S) and insulinopenic (low HOMA2-B, high HOMA2-S) type 2 diabetes. Individuals were followed until first hospital-treated infection or first prescription for an anti-infective agent (community-treated infection). We used Cox regression analysis to estimate HRs adjusted for age, sex, index year, diabetes duration and treatment, lifestyle behaviours and comorbidities.

Results

Among study participants, 28% had hyperinsulinaemic, 63% had classical and 9% had insulinopenic type 2 diabetes. The 10 year risks of hospital-treated infections were 42.3%, 36.8% and 31.0% in the three subgroups, respectively. Compared with the insulinopenic subgroup, adjusted HRs for hospital-treated infections were elevated for hyperinsulinaemic (1.38 [95% CI 1.16, 1.65]) and classical type 2 diabetes (1.20 [95% CI 1.02, 1.42]). The 10 year risks of community-treated infections were high in all three subgroups at 91.6%, 90.1% and 88.3%, respectively, corresponding to adjusted HRs of 1.20 (95% CI 1.08, 1.33) for the hyperinsulinaemic and 1.10 (95% CI 1.00, 1.21) for the classical subgroup. Infection risk in the hyperinsulinaemic subgroup decreased substantially when further adjusted for abdominal obesity, metabolic derangements and low-grade inflammation.

Conclusions/interpretation

The risk of severe infections is clearly elevated in individuals with type 2 diabetes characterised by a higher degree of insulin resistance/hyperinsulinaemia.

Graphical Abstract

中文翻译：

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高胰岛素血症型 2 型糖尿病患者的感染风险升高：一项丹麦 12 年队列研究

 目标/假设

需要更好地了解 2 型糖尿病患者感染风险升高的潜在机制，以指导风险分层和预防。我们根据胰岛素敏感性和 β 细胞功能指标调查了 2 型糖尿病个体亚组的感染风险。

 方法

我们将 7265 名最近诊断为 2 型糖尿病的个体 （中位病程 1.4 年，IQR 0.5-2.9 年） 分为高胰岛素血症型 （高 β 细胞功能 [HOMA 2-β-细胞功能，HOMA2-B]、低胰岛素敏感性 [HOMA 2-胰岛素敏感性，HOMA2-S]）、经典型 （低 HOMA2-B、低 HOMA2-S） 和胰岛素减少型 （低 HOMA2-B、高 HOMA2-S） 型 2 型糖尿病。对个体进行随访，直到首次接受医院治疗的感染或首次开具抗感染药物处方（社区治疗的感染）。我们使用 Cox 回归分析来估计根据年龄、性别、指数年份、糖尿病病程和治疗、生活方式行为和合并症调整的 HR。

 结果

在研究参与者中，28% 患有高胰岛素血症，63% 患有经典糖尿病，9% 患有胰岛素减少型 2 型糖尿病。3 个亚组医院治疗感染的 10 年风险分别为 42.3% 、 36.8% 和 31.0%。与胰岛素减少亚组相比，高胰岛素血症型 （1.38 [95% CI 1.16， 1.65]） 和经典 2 型糖尿病 （1.20 [95% CI 1.02， 1.42]） 的医院治疗感染校正 HR 升高。所有三个亚组社区治疗感染的 10 年风险均很高，分别为 91.6% 、 90.1% 和 88.3%，对应于高胰岛素血症患者的调整后 HR 为 1.20 （95% CI 1.08， 1.33） 和经典亚组的 1.10 （95% CI 1.00， 1.21）。当进一步调整腹部肥胖、代谢紊乱和低度炎症时，高胰岛素血症亚组的感染风险显着降低。

结论/解释

以较高胰岛素抵抗/高胰岛素血症为特征的 2 型糖尿病患者发生严重感染的风险明显升高。

 图形摘要