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Effects of Hydrocortisone on the Regulation of Blood Pressure: Results From a Randomized Controlled Trial
Jorien Werumeus Buning1, Martijn van Faassen1, Pauline Brummelman1
1Department of Endocrinology (J.W.B., P.B., R.P.F.D., G.v.d.B., M.M.v.d.K., M.N.K., A.P.v.B.), University of Groningen, University Medical Center Groningen, Groningen, The Netherlands; Department of Laboratory Medicine (M.v.F., A.C.M.K., I.P.K.), University of Groningen, University Medical Center Groningen, Groningen, The Netherlands; Department of Nephrology (C.A.S.), University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Insights
Higher hydrocortisone doses in patients with secondary adrenal insufficiency increase blood pressure and affect key regulatory systems. This highlights the importance of precise hydrocortisone dosing for cardiovascular health.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
Background:
- Patients with secondary adrenal insufficiency face increased cardiovascular risk, potentially linked to higher hydrocortisone replacement doses and unfavorable metabolic profiles.
- Optimizing glucocorticoid replacement is crucial for managing cardiovascular risk in these patients.
Purpose of the Study:
- To investigate the impact of higher versus lower glucocorticoid (hydrocortisone) replacement doses on blood pressure.
- To assess effects on the renin-angiotensin-aldosterone system, 11β-hydroxysteroid dehydrogenase enzyme activity, and circulating (nor)metanephrines.
Main Methods:
- A randomized, double-blind, crossover study involving 47 patients with secondary adrenal insufficiency.
- Patients received either a higher (0.4-0.6 mg/kg/day) or lower (0.2-0.3 mg/kg/day) hydrocortisone dose for 10 weeks, followed by the alternative dose.
Main Results:
- The higher hydrocortisone dose significantly increased systolic and diastolic blood pressure.
- Associated changes included decreased plasma potassium, aldosterone, and renin levels.
- Increased cortisol/cortisone ratios and decreased normetanephrine levels were observed with the higher dose.
Conclusions:
- Elevated hydrocortisone doses, even within the physiological range, significantly impact blood pressure regulation.
- These findings underscore the influence of hydrocortisone dosage on the renin-angiotensin-aldosterone system, 11β-hydroxysteroid dehydrogenase activity, and catecholamine metabolism.
Context:
Cardiovascular risk is increased in patients with secondary adrenal insufficiency, which may be ascribed to an unfavorable metabolic profile consequent to a relatively high hydrocortisone replacement dose.
Objective:
We determined the effects of a higher versus a lower glucocorticoid replacement dose on blood pressure (BP), the renin-angiotensin-aldosterone system, 11β-hydroxysteroid dehydrogenase enzyme activity and circulating (nor)metanephrines.
Design, Setting, And Patients:
Forty-seven patients with secondary adrenal insufficiency from the University Medical Center Groningen participated in this randomized double-blind crossover study.
Interventions:
Patients randomly received 0.2-0.3 mg hydrocortisone/kg body weight followed by 0.4-0.6 mg hydrocortisone/kg body weight, or vice versa, each during 10 weeks.
Main Outcome Measure(S):
BP and regulating hormones were measured.
Results:
The higher hydrocortisone dose resulted in an increase in systolic BP of 5 (12) mm Hg (P = .011), diastolic BP of 2 (9) mm Hg (P = .050), and a median [interquartile range] drop in plasma potassium of -0.1 [-0.3; 0.1] nmol/liter (P = .048). The higher hydrocortisone dose led to decreases in serum aldosterone of -28 [-101; 9] pmol/liter (P = .020) and plasma renin of -1.3 [-4.5; 1.2 ] pg/mL (P = .051), and increased the ratio of plasma and urinary cortisol to cortisone (including their metabolites) (P < .001 for all). Furthermore, on the higher dose, plasma and urinary normetanephrine decreased by -0.101 [-0.242; 0.029] nmol/liter (P < .001) and -1.48 [-4.06; 0.29] μmol/mol creatinine (P < .001) respectively.
Conclusions:
A higher dose of hydrocortisone increased systolic and diastolic BP and was accompanied by changes in the renin-angiotensin-aldosterone system, 11β-hydroxysteroid dehydrogenase enzyme activity, and circulating normetanephrine. This demonstrates that hydrocortisone dose even within the physiological range affects several pathways involved in BP regulation.
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