Managing Hypertension in Patients on Corticosteroid Therapy
Recognition and Monitoring
Corticosteroids cause hypertension through both glucocorticoid and mineralocorticoid effects, requiring close blood pressure monitoring during both initiation and dose reduction of therapy. 1, 2
- Monitor blood pressure before starting corticosteroid therapy and at least every 4 weeks during treatment, as hypertension can develop within 24 hours of initiation 3, 4
- Be aware that hypertension may paradoxically develop or worsen during corticosteroid dose reduction, particularly 1-8 weeks after tapering begins 5
- Check serum electrolytes (sodium and potassium) periodically, though hypertension occurs independent of mineralocorticoid effects and sodium retention 1, 3
- The risk increases with cumulative corticosteroid exposure: incidence rates rise from 44.4 per 1000 person-years in non-users to 55.6 per 1000 person-years with cumulative prednisolone-equivalent doses ≥3055 mg 6
Blood Pressure Targets
Target blood pressure should be <130/80 mmHg for most patients on corticosteroids, though <140/90 mmHg is acceptable for elderly or frail patients. 7
- For patients with diabetes or chronic kidney disease on corticosteroids, maintain BP <130/80 mmHg 8
- For elderly patients with multiple comorbidities, individualize targets to 140/90 mmHg based on frailty status 9
First-Line Pharmacological Management
Initiate antihypertensive therapy with an ACE inhibitor or ARB as first-line treatment, as these agents specifically counteract the renin-angiotensin system activation caused by corticosteroids. 5
- Start with an ACE inhibitor (such as lisinopril) or ARB (such as losartan) at low doses, as patients developing hypertension during corticosteroid reduction show elevated renin and aldosterone levels 5
- For patients requiring immediate blood pressure control (BP ≥160/100 mmHg), initiate combination therapy with an ACE inhibitor/ARB plus either a thiazide-like diuretic (chlorthalidone or indapamide) or a dihydropyridine calcium channel blocker (amlodipine) 8, 7
- Use once-daily dosing and single-pill combinations to improve adherence 9
Resistant Hypertension Algorithm
If blood pressure remains uncontrolled on three agents (ACE inhibitor/ARB, calcium channel blocker, and thiazide-like diuretic), add a mineralocorticoid receptor antagonist such as spironolactone. 8
Step-by-step escalation:
- Step 1: Optimize lifestyle modifications (sodium restriction <2400 mg/day, weight loss, exercise) and ensure adherence to three-drug regimen at maximum tolerated doses 8, 1
- Step 2: Substitute chlorthalidone or indapamide for the prior diuretic if not already using these thiazide-like agents 8
- Step 3: Add spironolactone (start 25 mg daily) or eplerenone, monitoring potassium and creatinine closely 8
- Step 4: If heart rate >70 bpm, add a beta-blocker (metoprolol succinate or bisoprolol) 8
- Step 5: Add hydralazine 25 mg three times daily, titrating upward 8
- Step 6: Consider referral to hypertension specialist 8
Critical Pitfalls and Caveats
- Avoid relying on diuretics alone: While corticosteroids cause sodium retention, the hypertensive effect is primarily glucocorticoid-mediated and occurs even without volume expansion 3, 4
- Do not use spironolactone as monotherapy: Although it blocks mineralocorticoid receptors, it does not prevent cortisol-induced hypertension when used alone 4
- Monitor during dose reduction: Hypertension during corticosteroid tapering is resistant to diuretics but responds rapidly to ACE inhibitors 5
- Avoid combining ACE inhibitors with ARBs: This combination increases adverse events without additional benefit 8
- Monitor potassium carefully: When combining ACE inhibitors/ARBs with mineralocorticoid receptor antagonists, check serum potassium and creatinine at least annually, or more frequently if eGFR <60 mL/min 8
- Use the lowest effective corticosteroid dose: Minimize cumulative exposure by using the lowest dose for the shortest duration necessary to control the underlying condition 1
Corticosteroid-Specific Considerations
- Fludrocortisone has marked mineralocorticoid activity and requires particularly careful blood pressure and electrolyte monitoring 2
- Synthetic glucocorticoids (prednisolone, methylprednisolone, triamcinolone, dexamethasone) all cause hypertension despite minimal mineralocorticoid activity, with blood pressure increases of 6-13 mmHg systolic 3
- Low-dose corticosteroid therapy (<10 mg/day prednisolone equivalent) may not cause hypertension in all patients, but monitoring remains essential 10