What is the recommended steroid regimen (initial dose, route, and taper) and adjunct therapy for a patient with suspected giant‑cell (temporal) arteritis, with or without visual symptoms?

Steroid Dosing for Temporal Arteritis (Giant Cell Arteritis)

Immediate Treatment Based on Clinical Presentation

For patients with suspected GCA and visual symptoms or threatened vision loss, immediately administer IV pulse methylprednisolone 500-1000 mg/day for 3 consecutive days, followed by high-dose oral prednisone 1 mg/kg/day (maximum 60-80 mg/day). 1, 2 Do not delay oral glucocorticoid treatment while arranging IV therapy—start oral prednisone immediately if IV administration will be delayed. 1

For patients with suspected GCA without visual symptoms or cranial ischemia, start high-dose oral prednisone 40-60 mg/day (or 1 mg/kg/day, maximum 60 mg) immediately upon clinical suspicion, even before biopsy confirmation. 3, 2 This should be given as a single morning dose using daily dosing rather than alternate-day scheduling. 2

The rationale for immediate treatment is compelling: visual loss occurs in 15-35% of GCA patients, primarily before therapy initiation, and if one eye is affected, the risk of losing vision in the second eye approaches 50% without treatment. 1 Visual recovery is uncommon once vision loss has occurred, making prevention through immediate treatment paramount. 1

Diagnostic Workup (Do Not Delay Treatment)

Arrange temporal artery biopsy as soon as possible, ideally within 2 weeks of starting glucocorticoids, as biopsy remains diagnostic even after steroid initiation within this window. 3, 2 Request a long-segment biopsy (>1 cm) to improve diagnostic yield due to skip lesions. 3, 2

Do not delay treatment while awaiting biopsy results—the risk of permanent vision loss outweighs the minimal impact of early steroid therapy on biopsy sensitivity. 3, 1

Glucocorticoid Tapering Strategy

Initial High-Dose Phase

Maintain the initial high dose (40-60 mg/day) for approximately 1 month until symptoms resolve and inflammatory markers (ESR/CRP) normalize. 3, 2

Structured Taper Schedule

• By 2-3 months: Reduce to 15-20 mg/day 3, 2
• By 3 months: Target 10-15 mg/day 3
• By 12 months: Aim for ≤5 mg/day 3, 2

Guide tapering by clinical symptoms and normalization of inflammatory markers rather than following a rigid timeline. 2 Avoid alternate-day dosing during taper, as this increases relapse risk. 3

Total Treatment Duration

Most patients require 1-2 years of glucocorticoid therapy, though some may need longer treatment due to relapsing disease or secondary adrenal insufficiency. 3, 2 Relapses occur in 34-75% of GCA patients during steroid tapering. 2

Adjunctive Steroid-Sparing Therapy

Add tocilizumab (162 mg subcutaneously weekly) to glucocorticoids as first-line therapy, particularly for patients at high risk of steroid-related complications. 3, 2 Tocilizumab reduces relapse rates, allows faster steroid tapering, and minimizes total glucocorticoid exposure. 2

Consider methotrexate as an alternative steroid-sparing agent if tocilizumab is contraindicated, though evidence supporting its efficacy is more modest. 3, 2 For relapsing disease with cranial ischemic symptoms, tocilizumab is preferred over methotrexate. 2

Management of Disease Relapse

Major Relapse (Cranial Ischemic Symptoms)

• Immediately increase prednisone to 40-60 mg/day 2
• Add tocilizumab as steroid-sparing agent (preferred over methotrexate for cranial symptoms) 2

Minor Relapse (Constitutional Symptoms Only)

• Increase glucocorticoid dose modestly and slow taper 2
• Consider adding or optimizing steroid-sparing agent 2

Isolated Elevation of Inflammatory Markers Without Symptoms

Clinical observation and monitoring without escalation of immunosuppressive therapy is appropriate, as clinical assessment takes priority over laboratory values alone. 2

Critical Supportive Care

All patients should receive bone protection therapy (calcium, vitamin D, bisphosphonates as indicated) in accordance with local guidelines, given the high risk of glucocorticoid-induced osteoporosis. 3, 4 Consider peptic ulcer prophylaxis with proton pump inhibitors. 4

Monitor aggressively for glucocorticoid-related adverse events, which occur in 86% of patients with long-term therapy. 3 Each 1 gram increase in cumulative glucocorticoid dose significantly increases the likelihood of adverse events. 5

Common Pitfalls to Avoid

Never delay treatment while awaiting biopsy confirmation or specialist consultation—vision loss can be permanent and irreversible. 3, 1 The window for preventing blindness is narrow, and clinical suspicion alone warrants immediate high-dose glucocorticoids. 3

Do not use infliximab for GCA—it is associated with recurrent ocular symptoms and markers of disease activity. 3

Do not rely solely on inflammatory markers to guide treatment decisions—clinical symptoms should take precedence, as isolated ESR/CRP elevation without symptoms does not warrant treatment escalation. 2

Consider adding low-dose aspirin or antiplatelet therapy for patients with critical cranial involvement, as this may decrease cranial ischemic complications. 3, 6