Plasma-metanephrines in patients with autoimmune Addison’s disease with and without residual adrenocortical functionEndocrinology in Charlottenburg, Berlin, Germany.
Department of Endocrinology, Oslo University Hospital, Oslo, Norway.
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; Department of Endocrinology, Karolinska University Hospital, Stockholm, Sweden.
Department of Medicine, Vestfold Hospital Trust, Tønsberg, Norway.
Department of Clinical Science, University of Bergen, Bergen, Norway; Department of Internal Medicine, Haugesund Hospital, Haugesund, Norway.
Department of Internal Medicine, Haugesund Hospital, Haugesund, Norway.
Department of Endocrinology, Stavanger University Hospital, Stavanger, Norway.
Department of Medicine, Sørlandet Hospital, Kristiansand, Norway.
Department of Medicine, Drammen Hospital, Vestre Viken Health Trust, Drammen, Norway.
Department of Endocrinology, Akershus University Hospital, Lørenskog, Norway.
Department of Endocrinology, Akershus University Hospital, Lørenskog, Norway.
Division of Internal Medicine, University Hospital of North Norway, Tromsø, Norway; Tromsø Endocrine Research Group, Department of Clinical Medicine, UiT the Arctic University of Norway, Tromsø, Norway.
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
Section of Endocrinology, Innlandet Hospital Trust, Hamar, Norway.
Department of Medicine, Örebro University Hospital, Örebro, Sweden; School of Medical Sciences, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Department of Medicine, Sørlandet Hospital, Arendal, Norway.
Department of Clinical Science, University of Bergen, Bergen, Norway.
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; Department of Endocrinology, Karolinska University Hospital, Stockholm, Sweden; Department of Medicine (Solna), Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
Department of Clinical Science, University of Bergen, Bergen, Norway; K.G. Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway; Department of Medicine, Haukeland University Hospital, Bergen, Norway; Department of Medicine (Solna), Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
Department of Clinical Science, University of Bergen, Bergen, Norway; K.G. Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway; Department of Medicine, Haukeland University Hospital, Bergen, Norway; Department of Medicine (Solna), Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; Department of Endocrinology, Karolinska University Hospital, Stockholm, Sweden.
Vise andre og tillknytning
2023 (engelsk)Inngår i: Journal of Clinical Medicine, E-ISSN 2077-0383, Vol. 12, nr 10, artikkel-id 3602Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]
Purpose: Residual adrenocortical function, RAF, has recently been demonstrated in one-third of patients with autoimmune Addison’s disease (AAD). Here, we set out to explore any influence of RAF on the levels of plasma metanephrines and any changes following stimulation with cosyntropin.
Methods: We included 50 patients with verified RAF and 20 patients without RAF who served as controls upon cosyntropin stimulation testing. The patients had abstained from glucocorticoid and fludrocortisone replacement > 18 and 24 h, respectively, prior to morning blood sampling. The samples were obtained before and 30 and 60 min after cosyntropin stimulation and analyzed for serum cortisol, plasma metanephrine (MN), and normetanephrine (NMN) by liquid-chromatography tandem-mass pectrometry (LC-MS/MS).
Results: Among the 70 patients with AAD, MN was detectable in 33%, 25%, and 26% at baseline, 30 min, and 60 min after cosyntropin stimulation, respectively. Patients with RAF were more likely to have detectable MN at baseline (p = 0.035) and at the time of 60 min (p = 0.048) compared to patients without RAF. There was a positive correlation between detectable MN and the level of cortisol at all time points (p = 0.02, p = 0.04, p < 0.001). No difference was noted for NMN levels, which remained within the normal reference ranges.
Conclusion: Even very small amounts of endogenous cortisol production affect MN levels in patients with AAD.
sted, utgiver, år, opplag, sider
2023. Vol. 12, nr 10, artikkel-id 3602
Emneord [en]
Addison’s disease, adrenal cortex, adrenal medulla, catecholamines, metanephrines, residual function
HSV kategori
Identifikatorer
URN: urn:nbn:se:umu:diva-209380DOI: 10.3390/jcm12103602ISI: 000997093500001Scopus ID: 2-s2.0-85160573677OAI: oai:DiVA.org:umu-209380DiVA, id: diva2:1764458
Forskningsfinansiär
The Research Council of Norway, 288022Novo Nordisk Foundation, NNF18OC00341302023-06-082023-06-082023-09-05bibliografisk kontrollert