ECE2020 Audio ePoster Presentations Adrenal and Cardiovascular Endocrinology (121 abstracts)
Residual corticosteroid production in autoimmune addison´s disease
Åse Bjorvatn Saevik 1,2 , Anna-Karin Åkerman 3,4 , Paal Methlie 1,2,5 , Marcus Quinkler 6 , Anders Palmström Jörgensen 7 , Charlotte Höybye 3,8 , Aleksandra J Debowska 9 , Bjørn Gunnar Nedrebø 1,10 , Anne Lise Dahle 10 , Siri Carlsen 11 , Aneta Tomkowicz 12 , Stina Therese Sollid 13 , Ingrid Nermoen 14 , Kaja Grønning 14 , Per Dahlqvist 15 , Guri Grimnes 16,17 , Jakob Skov 3 , Trine Finnes 18 , Susanna F Valland 18 , Jeanette Wahlberg 19 , Synnøve Emblem Holte 20 , Katerina Simunkova 1 , Olle Kämpe 2,8,21 , Eystein Sverre Husebye 1,2,5,21 , Sophie Bensing 3,8 & Marianne Øksnes 1,2,5,21
1University of Bergen, Department of Clinical Science, Bergen, Norway; 2University of Bergen, KG Jebsen center for Autoimmune Disorders, Bergen, Norway; 3Karolinska Institutet, Department of Molecular Medicine and Surgery, Sweden; 4Örebro University Hospital, Department of Medicine, Örebro, Sweden;5Haukeland University Hospital, Department of Medicine, Bergen, Norway; 6Endocrinology in Charlottenburg, Berlin, Germany; 7Oslo University Hospital, Department of Endocrinology, Oslo, Norway; 8Karolinska University Hospital, Department of Endocrinology, Metabolism and Diabetes, Stockholm, Sweden; 9Vestfold Hospital Trust, Department of Medicine, Tønsberg, Norway; 10Haugesund Hospital, Department of Internal Medicine, Haugesund, Norway; 11Stavanger University Hospital, Department of Endocrinology, Stavanger, Norway; 12Sørlandet Hospital, Kristiansand, Department of Medicine, Kristiansand, Norway; 13Drammen Hospital, Vestre Viken Health Trust, Department of Medicine, Drammen, Norway; 14Akershus University Hospital, Department of Endocrinology, Lørenskog, Norway; 15Umeå University, Department of Public Health and Clinical Medicine, Umeå, Sweden; 16University Hospital of North Norway, Division of Internal Medicine, Tromsø, Norway; 17Tromsø Endocrine Research Group, UiT the Arctic University of Norway, Department of Clinical Medicine, Tromsø, Norway; 18Innlandet Hospital Trust, Section of Endocrinology, Hamar, Norway; 19Linköping University, Department of Endocrinology and Department of Health, Medicine and Caring Sciences, Linköping, Sweden; 20Sørlandet Hospital, Arendal, Department of Medicine, Arendal, Norway; 21Karolinska Institutet, Department of Medicine (Solna), Karolinska University Hospital, Stockholm, Sweden
Background: Previous research show that autoimmune adrenal insufficiency develops gradually over time and inexorably results in a total inability to produce adrenal steroids. However, growing evidence suggest that a few patients preserve some steroid producing capacity.
Aim: To explore the frequency of residual cortisol production and possible clinical consequences in patients with autoimmune Addison´s disease (AAD).
Material and Methods: We performed a two-staged clinical multicenter study. Study subjects submitted a medication-fasting morning blood sample for analysis of adrenocortical steroids by liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. Before sampling, patients abstained from cortisone acetate or hydrocortisone and fludrocortisone for at least 18 and 24 hours, respectively. Residual glucocorticoid (GC) production was defined as quantifiable serum cortisol and 11-deoxycortisol, and residual mineralocorticoid (MC) production as quantifiable serum aldosterone and corticosterone. Clinical variables included demographics, replacement therapy, frequency of adrenal crises, clinical biochemistry, and quality of life. Peak cortisol response was evaluated by a standard 250 µg cosyntropin test.
Results: Fifty-eight of 192 patients (30.2%) had residual GC production, more common in men (n = 33, P < 0.002) and in shorter disease duration (median 6 [0−44] vs 13 [0−53] years, P < 0.001). Residual MC production was found in 26 (13.5%) patients and associated with shorter disease duration (median 5.5 [0.5–26.0] vs 13 [0–53] years, P < 0.004), lower fludrocortisone replacement dosage (median 0.075 [0.050–0.120] vs 0.100 [0.028–0.300] mg, P < 0.005), and higher plasma renin concentration (median 179 [22–915] vs 47.5 [0.6–658.0] mIE/l, P < 0.001). None had a normal cosyntropin response, but peak cortisol strongly correlated with unstimulated cortisol (r = 0.753, P < 0.000) and plasma ACTH (r = −0.694, P < 0.001). No differences in HRQoL or other clinical parameters were seen.
Conclusion: In patients with AAD one-third have residual production of glucocorticoids, more common in men and patients with shorter disease duration. In the future, these patients could be candidates for regenerative therapy.
Volume 70
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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