Search Results

You are looking at 1 - 1 of 1 items for

  • Author: Jelena Stankovic x
Clear All Modify Search
Jelena Stankovic Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark

Search for other papers by Jelena Stankovic in
Google Scholar
PubMed
Close
,
Kurt Kristensen Steno Diabetes Center Aarhus (SDCA), Aarhus University Hospital, Aarhus, Denmark
Department of Pediatrics, Aarhus University Hospital, Aarhus, Denmark

Search for other papers by Kurt Kristensen in
Google Scholar
PubMed
Close
,
Niels Birkebæk Department of Pediatrics, Aarhus University Hospital, Aarhus, Denmark

Search for other papers by Niels Birkebæk in
Google Scholar
PubMed
Close
,
Jens Otto Lunde Jørgensen Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark

Search for other papers by Jens Otto Lunde Jørgensen in
Google Scholar
PubMed
Close
, and
Esben Søndergaard Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark
Steno Diabetes Center Aarhus (SDCA), Aarhus University Hospital, Aarhus, Denmark

Search for other papers by Esben Søndergaard in
Google Scholar
PubMed
Close

Background

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.

Aim

The aim was to investigate copeptin levels in response to three different GH stimulation tests in patients suspected of GH deficiency.

Methods

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).

Results

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).

Conclusion

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.

Open access