Journal of clinical medicine · 2023
Plasma-Metanephrines in Patients with Autoimmune Addison's Disease with and without Residual Adrenocortical Function.
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Åkerman Anna-Karin, Sævik Åse Bjorvatn, Thorsby Per Medbøe, Methlie Paal, Quinkler Marcus, Jørgensen Anders Palmstrøm, Höybye Charlotte, Debowska Aleksandra J, Nedrebø Bjørn Gunnar, Dahle Anne Lise, Carlsen Siri, Tomkowicz Aneta, Sollid Stina Therese, Nermoen Ingrid, Grønning Kaja, Dahlqvist Per, Grimnes Guri, Skov Jakob, Finnes Trine, Wahlberg Jeanette, Holte Synnøve Emblem, Simunkova Katerina, Kämpe Olle, Husebye Eystein Sverre, Øksnes Marianne, Bensing Sophie
Аннотация
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.
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.