Can Prednisone Cause Hypertension?
Yes, prednisone can cause hypertension and is recognized as a medication that elevates blood pressure, requiring avoidance or limitation when possible, with consideration of alternative routes of administration when feasible. 1
Mechanism and Clinical Evidence
Direct Hypertensive Effects
Systemic corticosteroids including prednisone are explicitly listed among medications that cause elevated blood pressure in the 2017 ACC/AHA Hypertension Guidelines. 1 The FDA label confirms that "average and large doses of hydrocortisone or cortisone can cause elevation of blood pressure, salt and water retention, and increased excretion of potassium," though these effects are noted to be less likely with synthetic derivatives like prednisone except when used in large doses. 2
The mechanisms include:
- Mineralocorticoid-like effects causing sodium retention, plasma volume expansion, and elevated atrial pressures 1
- Direct increase in cellular potassium efflux which shortens atrial action potential duration 1
- Promotion of atherosclerosis, diabetes, and ischemic heart disease with long-term use, all of which are independent risk factors for hypertension 1
Dose and Duration Relationships
The relationship between prednisone and hypertension is complex:
Low-dose therapy: A study of 195 patients on low-dose prednisone/prednisolone showed increased mean systolic and diastolic blood pressure with increased prevalence of hypertension, though the study concluded low-dose therapy does not cause biochemical features of mineralocorticoid excess. 3
Individual susceptibility: Approximately 30% of glucocorticoid-treated patients who developed hypertension showed elevated urinary cortisol metabolite ratios (THFs/THE >1.5), suggesting impaired 11β-hydroxysteroid dehydrogenase type 2 function, with a 3.8-fold increased risk of hypertension regardless of prednisone dose or duration. 4
Paradoxical timing: Hypertension can occur not only during maximum corticosteroid use but also during dose reduction, with diastolic pressures reaching 100-120 mm Hg within 1-8 weeks after reduction begins, occurring at 0-70% of maximum dose. 5
Management Recommendations
Primary Strategy
The ACC/AHA guidelines recommend a hierarchical approach: 1
- Avoid or limit systemic corticosteroid use when possible
- Consider alternative routes of administration (inhaled, topical) when feasible
- Initiate or intensify antihypertensive therapy if systemic use is necessary
Monitoring Requirements
- Blood pressure monitoring should be regular even during short courses 6
- Baseline blood pressure assessment before initiating therapy 1, 6
- Frequent monitoring during dose changes, particularly during reduction phases when paradoxical hypertension may occur 5
- Serum glucose monitoring as hyperglycemia commonly occurs and may contribute to cardiovascular risk 6
Treatment of Steroid-Induced Hypertension
When hypertension develops during corticosteroid therapy:
- Angiotensin-converting enzyme (ACE) inhibitors respond rapidly to steroid-induced hypertension, particularly during dose reduction 5
- Diuretic therapy may be less effective and was resistant in patients with steroid-reduction hypertension 5
- Elevated renin and aldosterone levels were found in patients developing hypertension during steroid reduction, supporting the use of renin-angiotensin system blockade 5
Special Populations and Considerations
Pediatric Patients
Children aged 9-16 years with steroid-requiring asthma can develop severe hypertension (diastolic 100-120 mm Hg) during corticosteroid reduction, even when blood pressures were normal during maximum therapy. 5 Growth velocity monitoring is more sensitive than HPA axis testing for detecting systemic corticosteroid effects. 2
Elderly Patients
The FDA label emphasizes increased risk of diabetes, fluid retention, and hypertension in elderly patients, recommending cautious dose selection starting at the low end of the dosing range. 2
Patients with Rheumatoid Arthritis
Patients treated with prednisone and NSAIDs showed abnormal diurnal blood pressure patterns, with 34% being systolic nondippers and 37% being diastolic excessive dippers, compared to hypertensive controls. 7
Critical Pitfalls to Avoid
- Assuming hypertension only occurs with high doses: Individual susceptibility varies greatly, with some patients developing hypertension on low doses 3, 4
- Discontinuing blood pressure monitoring after dose reduction: Paradoxical hypertension frequently occurs 1-8 weeks after starting dose reduction 5
- Using diuretics as first-line therapy: ACE inhibitors are more effective for steroid-induced hypertension 5
- Ignoring concurrent medications: NSAIDs and other medications may compound the hypertensive effect 7