Endocrine Abstracts

Background: The differential diagnosis of the polyuria-polydipsia syndrome is challenging. The water-deprivation test is the current gold standard, but the test is cumbersome, and the diagnostic performance is poor. Copeptin, which is a split product of the vasopressin pre-propeptide, appears to be a robust biomarker in the circulation and a promising tool for the diagnosis of patients with polyuria and polydipsia, especially when measured in conjunction with intravenous infusion of arginine. With this study we aimed to clarify underlying mechanisms of copeptin secretion.

Methods: Using a cross-sectional study-design, we included patients referred to Aarhus University Hospital with suspicion of growth hormone deficiency, who underwent arginine (n=16), insulin tolerance test (n=12) or clonidine (n= 8) stimulatory tests. Baseline copeptin was measured and repeated at 60, 105 and 150 minutes.

Results: 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). Arginine and the ITT induced a similar response in copeptin level from baseline to 60 min (P<0.01).

Conclusion: The present data support that arginine infusion and the ITT induce a similar increase in plasma copeptin level after 60 min. Clonidine tended to decrease copeptin levels. We hypothesize that abrogation of somatostatin-induced copeptin-suppression could be a possible explanatin.