ECE2016 Guided Posters Pituitary - Clinical (10 abstracts)
Effects of hydrocortisone substitution on blood pressure – results from an RCT
Jorien Werumeus Buning 1 , Martijn van Faassen 2 , Pauline Brummelman 1 , Robin P F Dullaart 1 , Gerrit van den Berg 1 , Melanie M van der Klauw 1 , Michiel N Kerstens 1 , Anneke C Muller Kobold 2 , Ido P Kema 2 , Bruce H R Wolffenbuttel 1 & André P van Beek 1
1Department of Endocrinology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands; 2Department of Laboratory Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Background: Patients with secondary adrenal insufficiency show increased risk of cardiovascular disease. Higher doses of glucocorticoid replacement are related to an unfavourable metabolic profile. In the absence of randomized controlled trials assessing the effect of hydrocortisone dose on haemodynamics and blood pressure regulation, we determined effects of a higher vs a lower glucocorticoid replacement dose on blood pressure, the renin-angiotensin-aldosterone system (RAAS) and sympathetic activity.
Materials and methods: Forty-seven patients treated for secondary adrenal insufficiency participated in this randomized double blind cross-over study (Clinicaltrials.gov identifier: NCT01546922). Patients were randomized to receive 0.2–0.3 mg hydrocortisone/kg body weight followed by 0.4–0.6 mg hydrocortisone/kg body weight or vice versa, both for 10 weeks. Each treatment period was followed by a study visit including measurement of blood pressure and collection of fasting blood samples.
Results: The higher dose of hydrocortisone resulted in a mean (S.D.) increase in body weight of 0.5 (1.7) kg (P=0.045), an increase in systolic blood pressure of 5 (12) mmHg (P=0.011) and a borderline significant increase in diastolic blood pressure of 2 (9) mmHg (P=0.050). A median [interquartile] plasma potassium decrease was observed of −0.1 [−0.3; 0.1] mmol/l (P=0.048). Furthermore, the higher dose of hydrocortisone led to a decrease in plasma renin concentrations of −1.4 [−4.7; 1.2] pg/ml (P=0.015), a decrease in aldosterone levels of −27 [−101; 9] pmol/l (P=0.020) and a decrease in aldosterone-to-renin ratio (ARR) of −2.6 [−5.6; 1.4] pmol/ng (P=0.047). In addition, a decrease of −0.104 [−0.242; 0.016] (P=0.001) nmol/l in plasma normetanephrine concentration was found on the higher dose of hydrocortisone, while metanephrines remained unchanged.
Conclusion: The higher dose of hydrocortisone led to an increase in systolic and diastolic blood pressure accompanied by a suppression of the RAAS and in sympathetic activity. This suggests that hydrocortisone affects multiple pathways involved in blood pressure regulation even at concentrations generally considered to be physiological.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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