Stankovic Jelena, Kristensen Kurt, Birkebæk Niels, Jørgensen Jens Otto Lunde, Søndergaard Esben
Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark.
Steno Diabetes Center Aarhus (SDCA), Aarhus University Hospital, Aarhus, Denmark.
Endocr Connect. 2023 Sep 27;12(11). doi: 10.1530/EC-23-0042. Print 2023 Nov 1.
The diagnosis of the polyuria-polydipsia syndrome is challenging. Copeptin is a robust biomarker of arginine vasopressin (AVP) secretion. Arginine, which stimulates growth hormone (GH), has been shown also to stimulate copeptin secretion via unknown mechanisms.
The aim was to investigate copeptin levels in response to three different GH stimulation tests in patients suspected of GH deficiency.
In this cross-sectional study, we measured plasma copeptin levels at baseline and at 60, 105, and 150 min in patients undergoing a stimulation test for growth hormone deficiency with either arginine (n = 16), clonidine (n = 8) or the insulin tolerance test (ITT) (n = 10).
In patients undergoing the arginine test, the mean age was 9 years, and 10 years for clonidine. The ITT was only performed in adult patients (>18 years) with a mean age of 49 years. Copeptin level increased significantly from baseline to 60 min after arginine (P <0.01) and ITT (P < 0.01). By contrast, copeptin level tended to decrease after clonidine stimulation (P = 0.14).
These data support that infusion of arginine increases plasma copeptin levels and reveal a comparable response after an ITT. We hypothesize that the underlying mechanism is abrogation of somatostatin-induced AVP suppression.
多尿-多饮综合征的诊断具有挑战性。 copeptin是精氨酸加压素(AVP)分泌的一种可靠生物标志物。 已证明刺激生长激素(GH)的精氨酸也可通过未知机制刺激copeptin分泌。
目的是研究疑似生长激素缺乏患者在三种不同生长激素刺激试验后的copeptin水平。
在这项横断面研究中,我们测量了接受精氨酸(n = 16)、可乐定(n = 8)或胰岛素耐量试验(ITT)(n = 10)生长激素缺乏刺激试验患者在基线以及60、105和150分钟时的血浆copeptin水平。
接受精氨酸试验的患者平均年龄为9岁,接受可乐定试验的为10岁。ITT仅在平均年龄为49岁的成年患者(> 18岁)中进行。精氨酸和ITT后,copeptin水平从基线到60分钟显著升高(P <0.01)。相比之下,可乐定刺激后copeptin水平有下降趋势(P = 0.14)。
这些数据支持输注精氨酸可增加血浆copeptin水平,并显示ITT后有类似反应。我们推测其潜在机制是消除生长抑素诱导的AVP抑制。