Cattedra di Endocrinologia, Università di Milano, Ospedale San Luca, Istituto Auxologico Italiano IRCCS, Piazzale Brescia 20, Milan, Italy.
Br J Clin Pharmacol. 2011 Jan;71(1):132-6. doi: 10.1111/j.1365-2125.2010.03812.x.
Desmopressin is a known haemostatic agent and is also being used, albeit at lower doses, during the diagnostic work-up of Cushing's syndrome, a condition characterized by excess cortisol concentrations and frequent thromboembolic events. No study has yet evaluated whether administration of desmopressin for diagnostic purposes induces significant, adverse changes in endothelial cell markers in these patients.
Administration of desmopressin to patients with Cushing's disease induces changes in endothelial cell markers comparable with those observed in obese and normal weight subjects. It follows, that desmopressin testing does not induce disease-specific untoward changes in coagulatory markers in patients with endogenous hypercortisolism and its use in this context appears safe.
Desmopressin, a vasopressin analogue, is used for various clinical purposes, including haemostasis and, in recent times, the diagnostic work-up of patients with Cushing's syndrome, a condition associated with a known prothrombotic profile. We decided to evaluate whether and to what extent a diagnostic dose of desmopressin induces significant changes in endothelial parameters in patients with Cushing's disease (CD) and obese and normal weight controls.
Twelve patients with CD, 10 obese and five normal weight controls were studied. Von Willebrand antigen (VWF:Ag), tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) were measured at baseline and up to 4 h after 10 µg desmopressin i.v.
Desmopressin 10 µg transiently increased VWF:Ag and t-PA and decreased PAI-1 in all subjects. The magnitude of the VWF:Ag and t-PA increases after desmopressin was comparable in the three groups (VWF:Ag peak-to-basal ratio 1.9 ± 0.17, 1.5 ± 0.11 and 1.8 ± 0.13 and t-PA peak-to-basal ratio 1.6 ± 0.18, 1.6 ± 0.20 and 1.8 ± 0.24 for CD, obese and controls, respectively, all NS). The PAI-1 decrease observed in patients with CD was comparable with obese (0.7 ± 0.07 and 0.6 ± 0.09, NS) and controls (0.7 ± 0.07 vs. 0.4 ± 0.09, P= 0.08).
Administration of desmopressin to patients with CD for diagnostic purposes induces a transitory increase in VWF:Ag counterbalanced by a decrease in PAI-1 and increase in t-PA. The magnitude of these changes is largely comparable with that observed in obese and normal weight controls. Our data show that testing with desmopressin does not induce disease-specific changes in endothelial markers in patients with CD.
去氨加压素是一种已知的止血剂，并且在库欣综合征的诊断过程中也在使用，尽管剂量较低，但这种疾病的特点是皮质醇浓度过高，经常发生血栓栓塞事件。目前还没有研究评估去氨加压素用于诊断目的是否会导致这些患者的内皮细胞标志物发生显著的、不良的变化。
给予库欣病患者去氨加压素会导致内皮细胞标志物发生变化，与肥胖和正常体重受试者观察到的变化相当。因此，去氨加压素检测不会在内源性皮质醇增多症患者中引起特定于疾病的凝血标志物的不良变化，并且在这种情况下使用似乎是安全的。
去氨加压素，一种血管加压素类似物，用于各种临床用途，包括止血，最近还用于库欣综合征患者的诊断，库欣综合征与已知的促血栓形成特征有关。我们决定评估诊断剂量的去氨加压素是否会引起库欣病（CD）患者以及肥胖和正常体重对照者的内皮参数发生显著变化。
研究了 12 例库欣病患者、10 例肥胖患者和 5 例正常体重对照者。在基线时和静脉注射 10µg 去氨加压素后 4 小时测量血管性血友病因子抗原（VWF：Ag）、组织型纤溶酶原激活物（t-PA）和纤溶酶原激活物抑制剂 1（PAI-1）。
去氨加压素 10µg 可使所有受试者的 VWF：Ag 和 t-PA 短暂增加，并降低 PAI-1。去氨加压素后 VWF：Ag 和 t-PA 的增加幅度在三组之间相似（VWF：Ag 峰-基比值 1.9±0.17、1.5±0.11 和 1.8±0.13，t-PA 峰-基比值 1.6±0.18、1.6±0.20 和 1.8±0.24，均无统计学意义）。CD 患者观察到的 PAI-1 下降与肥胖者（0.7±0.07 和 0.6±0.09，无统计学意义）和对照组（0.7±0.07 与 0.4±0.09，P=0.08）相似。
为诊断目的给予库欣病患者去氨加压素可导致 VWF：Ag 短暂增加，同时 PAI-1 减少和 t-PA 增加。这些变化的幅度与肥胖和正常体重对照组观察到的变化基本相当。我们的数据表明，去氨加压素检测不会在内皮细胞标志物中引起库欣病患者的疾病特异性变化。
