How should I manage an older adult with giant‑cell arteritis on high‑dose glucocorticoids who presents with a hypertensive urgency (systolic ≥180 mm Hg or diastolic ≥120 mm Hg without acute end‑organ injury)?

Management of Hypertensive Urgency in a Patient with Giant Cell Arteritis on High-Dose Glucocorticoids

Treat the hypertensive urgency with standard oral antihypertensive agents while continuing the current glucocorticoid regimen for GCA, because hypertension is a common glucocorticoid-related adverse effect that does not require modification of immunosuppressive therapy. 1

Immediate Blood Pressure Management

• Initiate or intensify oral antihypertensive therapy to achieve gradual blood pressure reduction over 24–48 hours, targeting systolic <160 mm Hg and diastolic <100 mm Hg. 1

• Do not abruptly reduce blood pressure in hypertensive urgency (no end-organ damage), as overly rapid reduction can precipitate ischemic complications in patients with underlying large-vessel vasculitis.

• First-line agents include long-acting calcium channel blockers (amlodipine 5–10 mg daily), ACE inhibitors (lisinopril 10–40 mg daily), or angiotensin receptor blockers (losartan 50–100 mg daily), chosen based on the patient's comorbidities and renal function.

GCA-Specific Considerations

• Continue the current high-dose glucocorticoid regimen without modification unless there are signs of active GCA relapse requiring dose escalation or evidence of inadequate disease control. 2

• Glucocorticoid-induced hypertension occurs in approximately 19% of GCA patients and is an expected adverse effect rather than an indication to reduce immunosuppression. 1, 3

• Assess for signs of GCA disease activity (new headache, jaw claudication, visual symptoms, constitutional symptoms) and check inflammatory markers (ESR, CRP) to distinguish hypertension as a treatment side effect versus a manifestation of active vasculitis. 2

Glucocorticoid-Sparing Strategy

• Add tocilizumab (162 mg subcutaneously weekly) to the current glucocorticoid regimen if the patient is at high risk for steroid-related complications or if this represents new-onset hypertension requiring multiple antihypertensive agents. 1

• Tocilizumab reduces cumulative glucocorticoid exposure and relapse rates, thereby decreasing the long-term burden of steroid-induced hypertension and other metabolic complications. 2, 1

• Methotrexate (15–25 mg weekly) is an alternative steroid-sparing agent if tocilizumab is contraindicated or unavailable, though its glucocorticoid-sparing effect is more modest. 2

Monitoring Protocol

• Measure blood pressure at every clinical visit (ideally weekly initially, then every 2–4 weeks once controlled) to assess response to antihypertensive therapy. 1

• Monitor for other glucocorticoid-related adverse effects including hyperglycemia (fasting glucose or HbA1c), bone loss (DEXA scan, calcium/vitamin D supplementation, bisphosphonate prophylaxis), and infection risk. 1

• Reassess GCA disease activity with clinical examination and inflammatory markers (ESR, CRP) every 4–8 weeks during the glucocorticoid taper phase. 2

Glucocorticoid Tapering Considerations

• Do not accelerate the glucocorticoid taper solely because of hypertension; instead, manage hypertension pharmacologically while following the planned taper schedule guided by GCA disease activity. 2

• The standard taper aims for 15–20 mg/day prednisone by 2–3 months, 10–15 mg/day by 3 months, and ≤5 mg/day by 12 months, adjusted based on clinical symptoms and inflammatory markers. 1

• If the patient experiences a GCA relapse with cranial ischemic symptoms during taper, increase prednisone to 40–60 mg/day and add tocilizumab (preferred) or methotrexate rather than increasing glucocorticoids alone. 2

Critical Pitfalls to Avoid

• Never reduce or discontinue glucocorticoids abruptly in response to hypertensive urgency, as this risks catastrophic GCA relapse with vision loss or stroke. 2, 1

• Do not delay antihypertensive treatment while awaiting rheumatology consultation; initiate blood pressure control immediately and coordinate GCA management subsequently.

• Do not rely solely on inflammatory markers (ESR, CRP) to guide glucocorticoid dosing, as these can be elevated from hypertension-related stress or other non-GCA causes; clinical assessment takes priority. 2

• Avoid using beta-blockers as first-line agents in patients with large-vessel GCA, as they may mask symptoms of limb ischemia or worsen peripheral vascular insufficiency if present.

Long-Term Management

• Implement comprehensive cardiovascular risk reduction including statin therapy (if not already prescribed), smoking cessation, and diabetes screening, as GCA patients have elevated cardiovascular event rates independent of glucocorticoid therapy. 2

• Arrange long-term clinical monitoring even after achieving GCA remission, as relapses occur in 34–75% of patients and glucocorticoid-related complications persist for years. 1