ECE2020 Audio ePoster Presentations Hot topics (including COVID-19) (110 abstracts)
Obstructive sleep apnea in primary aldosteronism is associated with cortisol cosecretion
Daniel Heinrich 1 , Christian Adolf 1 , Laura Handgriff 1 , Holger Schneider 1 , Nina Nirschl 1 , Elisabeth Obster 1 , Lisa Sturm 1 , Xiao Wang 1 , Martin Bidlingmaier 1 , Moritz Wildgruber 2 , Roland Ladurner 3 , Felix Beuschlein 4 & Martin Reincke 1
1Klinikum der Universität München, Medizinische Klinik und Poliklinik IV, Munich, Germany; 2Klinik und Poliklinik für Radiologie, Klinikum der Universität München, Munich, Germany; 3Klinik für Allgemein-, Viszeral- und Transplantationschirurgie, Campus Innenstadt, Klinikum der Universität München, Munich, Germany; 4Klinik für Endokrinologie, Diabetologie und Klinische Ernährung, Universitätsspital Zürich, Zurich, Germany
Background: Primary aldosteronism (PA) is a secondary form of arterial hypertension that – in case of unilateral disease – can be cured by surgery. Multiple studies have shown that PA patients are at higher risk to suffer from cardiovascular events and to develop metabolic diseases. Two thirds of patients with PA suffer from obstructive sleep apnea (OSA). A bi-directional, pathophysiological interplay between OSA and PA has been proposed, with focus on overnight rostral fluid shift and the metabolic syndrome. Cortisol cosecretion – a newly identified trait of PA patients – is associated with metabolic risk parameters, independently of mineralocorticoid excess.
Objective: While the connection between the extent of cortisol oversecretion and OSA in overt Cushing’s disease has been established, the role of cortisol cosecretion has not been investigated in the relationship of PA and OSA.
Methods and results: We report the results of 31 PA patients who were screened for OSA and hypercortisolism (1-mg overnight dexamethasone suppression test, 24-hour urinary free cortisol determination and late-night salivary cortisol measurement) before initiation of treatment. Serum cortisol values after dexamethasone suppression tests were significantly higher in OSA patients (1.6 µg/dl [1.3; 2.5] vs 1 [1; 1.2], P = 0.002) and increased with OSA severity (moderate and severe OSA, 2.0 µg/dl [1.5; 2.5] in comparison to mild OSA, 1.4 µg/dl [1.2; 1.9] or no OSA, 1 µg/dl [1; 1.2], P = 0.016). When adjusting these results for BMI, age, systolic blood pressure and HbA1c values the results remained significant (P = 0.042).
Conclusions: The main finding of our study is the association of OSA with biochemical evidence of cortisol cosecretion in patients with PA. In this concept, PA induces fluid retention and rostral fluid shift leading to OSA in vulnerable subjects (male, obese patients), inducing increased night-time hypoxia and stress including hypothalamic pituitary adrenal axis activation. This observation can explain the strong links found between cortisol cosecretion, obesity, the metabolic syndrome and primary aldosteronism. Further interventional studies are warranted to determine long-term outcome of CPAP treatment on cortisol cosecretion for this patient cohort.
Volume 70
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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