What is the recommended treatment for steroid‑induced hypertension?

Steroid-Induced Hypertension Treatment

For steroid-induced hypertension, calcium channel blockers (particularly amlodipine 5-10 mg daily) are the preferred first-line antihypertensive agents, followed by ACE inhibitors or ARBs if additional blood pressure control is needed. 1

Pathophysiology and Clinical Recognition

• Steroid-induced hypertension occurs through glucocorticoid receptor activation rather than solely through mineralocorticoid effects, meaning that even synthetic steroids with minimal mineralocorticoid activity (prednisolone, methylprednisolone, dexamethasone) can elevate blood pressure by 6-13 mmHg systolic and 7-11 mmHg diastolic 2
• Blood pressure elevation typically occurs rapidly within 1 week of starting glucocorticoid therapy, particularly at doses ≥20 mg prednisolone equivalent daily 3
• Paradoxically, hypertension may also develop or worsen during steroid dose reduction in patients with asthma, occurring 1-8 weeks after tapering begins, with diastolic pressures reaching 100-120 mmHg 4
• Risk factors include lower serum calcium concentrations and positive family history of essential hypertension 3

First-Line Pharmacologic Management

Calcium Channel Blockers (Preferred)

• Calcium channel blockers are the treatment of choice for cyclosporine-induced hypertension (a related steroid-mediated mechanism), with isradipine and amlodipine specifically preferred because they do not alter drug levels 1
• Start amlodipine 5 mg daily, titrating to 10 mg as needed to achieve target blood pressure <140/90 mmHg (minimum) or <130/80 mmHg (optimal) 1
• Calcium channel blockers provide vasodilation without interfering with steroid metabolism or efficacy 1

ACE Inhibitors or ARBs (Second-Line or Combination)

• ACE inhibitors demonstrate rapid efficacy in steroid-induced hypertension that is resistant to diuretic therapy, likely by counteracting the elevated renin-aldosterone system activation seen in these patients 4
• Lisinopril 10-20 mg daily or losartan 50-100 mg daily can be added if blood pressure remains ≥140/90 mmHg on calcium channel blocker monotherapy 1
• Six of six patients with steroid-induced hypertension during dose reduction had elevated renin levels, and five of six had elevated aldosterone, explaining the superior response to ACE inhibitors over diuretics 4

Agents to Avoid or Use Cautiously

Thiazide Diuretics (Not Recommended as Monotherapy)

• Thiazide diuretics should be avoided in steroid-induced hypertension because they can lead to increased nephrotoxicity when combined with steroids and may worsen steroid-induced hyperglycemia 1
• Diuretics were ineffective in controlling blood pressure elevations during steroid dose reduction in pediatric asthma patients, whereas ACE inhibitors produced rapid response 4
• If a diuretic is absolutely necessary for volume management, potassium-sparing diuretics must be avoided as they act synergistically with steroids to cause hyperkalemia 1

Beta-Blockers (Use Only with Compelling Indication)

• Beta-blockers are not first-line agents for steroid-induced hypertension unless there is a compelling cardiovascular indication such as coronary artery disease, heart failure, or post-myocardial infarction 1
• Beta-1 selective agents may be used in selected patients with concurrent coronary disease 1

Treatment Algorithm

1. Confirm hypertension: Verify blood pressure ≥140/90 mmHg on multiple occasions, ideally with home monitoring ≥135/85 mmHg 1

2. Initiate calcium channel blocker: Start amlodipine 5 mg daily 1

3. Reassess at 2-4 weeks: Check blood pressure and titrate amlodipine to 10 mg if needed 1

4. Add ACE inhibitor or ARB if uncontrolled: Add lisinopril 10-20 mg daily or losartan 50-100 mg daily if blood pressure remains ≥140/90 mmHg 1, 4

5. Consider triple therapy if needed: Add a thiazide-like diuretic (chlorthalidone 12.5-25 mg daily preferred over hydrochlorothiazide) only after optimizing calcium channel blocker and ACE inhibitor/ARB doses, while monitoring for hyperglycemia 1

6. Monitor for steroid-induced hyperglycemia: Check fasting glucose and HbA1c, as steroids commonly cause hyperglycemia requiring management with gliclazide, metformin, or insulin depending on severity 1

Blood Pressure Targets

• Target blood pressure <140/90 mmHg minimum for most patients, with optimal target <130/80 mmHg if well tolerated 1
• For elderly patients (≥65 years), target systolic blood pressure 130-139 mmHg 1
• Reassess within 2-4 weeks after any medication change, aiming to achieve target within 3 months 1

Critical Monitoring Parameters

• Check serum potassium and creatinine 2-4 weeks after initiating ACE inhibitor or ARB, especially if adding to existing therapy 1
• Monitor for steroid-induced hyperglycemia with blood glucose measurements ≥11.1 mmol/L (200 mg/dL) and HbA1c ≥6.5%, which defines steroid-induced diabetes requiring treatment 1
• Screen for secondary hyperglycemia at clinic visits, particularly 2 hours postprandial or 8 hours after prednisolone dosing, as fasting glucose may not capture severity 1

Common Pitfalls to Avoid

• Do not assume mineralocorticoid excess is the sole mechanism—synthetic glucocorticoids without mineralocorticoid activity still cause hypertension through glucocorticoid receptor activation 2
• Do not overlook hypertension during steroid dose reduction—blood pressure may paradoxically rise 1-8 weeks after tapering begins, requiring vigilant monitoring 4
• Do not use thiazide diuretics as first-line therapy—they are ineffective for steroid-induced hypertension and may worsen metabolic complications 1, 4
• Do not combine ACE inhibitors with ARBs—dual renin-angiotensin system blockade increases adverse events without additional benefit 1
• Do not delay treatment intensification—steroid-induced hypertension requires prompt management within 2-4 weeks to reduce cardiovascular risk 1