Clinical Research, Steno Diabetes Center Copenhagen, University of Copenhagen, DK-2730 Herlev, Denmark.
Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, DK-2900 Hellerup, Denmark.
J Clin Endocrinol Metab. 2024 Oct 15;109(11):2735-2744. doi: 10.1210/clinem/dgae278.
People with type 1 diabetes (T1D) are at increased risk of thrombosis compared to the general population; however, the underlying mechanisms remain unclear. Hypoglycemia induced at rest can induce coagulation activation, but little is known about the hemostatic effects of exercise-related hypoglycemia in people with T1D.
We compared hemostatic profiles of individuals with T1D with healthy controls and explored hemostatic effects of hypoglycemia, induced with or without exercise, in participants with T1D.
Thrombelastography was used for a baseline hemostatic comparison between fifteen men with T1D and matched healthy controls. In addition, the participants with T1D underwent two euglycemic-hypoglycemic clamp days in a randomized, crossover fashion. Hypoglycemia was induced with the participants at rest (Hypo-rest) or during exercise (Hypo-exercise). Thrombelastography provides data on the rate of coagulation activation (R-time), the rate of clot formation (K-time, α-Angle), the maximum clot amplitude (MA), the functional fibrinogen contribution to the clot strength (MA-FF) and the fibrinolysis (LY-30).
The T1D group exhibited a faster rate of coagulation activation (shorter R-time) and a faster clot formation (greater α-Angle) compared with the controls. During the clamp experiments, Hypo-exercise induced an increased clot strength (MA) with a mean difference from baseline of 2.77 mm (95% CI, 2.04-3.51) accompanied with a decreased fibrinolysis (LY-30) of -0.45 percentage point (-0.60 to -0.29). Hypo-rest resulted in increased functional fibrinogen (MA-FF) of 0.74 mm (0.13-1.36) along with an increased fibrinolysis (LY-30) of 0.54 percentage point (0.11-0.98).
Individuals with T1D exhibit a hypercoagulable hemostatic profile compared with healthy controls and exercise-related hypoglycemia may increase the susceptibility to thrombosis via both procoagulant and antifibrinolytic effects.
与普通人群相比，1 型糖尿病（T1D）患者发生血栓的风险增加；然而，潜在机制仍不清楚。静息时发生的低血糖可诱导凝血激活，但人们对 T1D 患者与运动相关的低血糖相关的止血作用知之甚少。
我们比较了 T1D 个体与健康对照者的止血特征，并探讨了 T1D 患者在静息和运动时低血糖诱导对止血的影响。
采用血栓弹力图对 15 名 T1D 男性患者和匹配的健康对照者进行基线止血比较。此外，T1D 患者以随机交叉的方式进行两次正常血糖-低血糖钳夹试验。低血糖通过患者静息（Hypo-rest）或运动时（Hypo-exercise）诱发。血栓弹力图提供了凝血激活速率（R-time）、血凝块形成速率（K-time，α-Angle）、最大血凝块幅度（MA）、纤维蛋白原对血凝块强度的功能贡献（MA-FF）和纤溶（LY-30）的数据。
与对照组相比，T1D 组的凝血激活速度（较短的 R-time）和血凝块形成速度（较大的α-Angle）更快。在钳夹试验中，Hypo-exercise 导致血凝块强度（MA）增加，与基线相比平均差异为 2.77mm（95%CI，2.04-3.51），同时纤溶（LY-30）减少 0.45 个百分点（-0.60 至-0.29）。Hypo-rest 导致功能纤维蛋白原（MA-FF）增加 0.74mm（0.13-1.36），同时纤溶（LY-30）增加 0.54 个百分点（0.11-0.98）。
与健康对照者相比，T1D 个体表现出高凝止血特征，运动相关的低血糖可能通过促凝和抗纤维蛋白溶解作用增加血栓形成的易感性。
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