What is the treatment for Temporal (Giant Cell) Arteritis?

Treatment of Temporal Arteritis (Giant Cell Arteritis)

Start high-dose oral prednisone (1 mg/kg/day, maximum 60 mg/day) immediately upon clinical suspicion of GCA—do not wait for biopsy confirmation, as vision loss is often irreversible and occurs before treatment initiation. 1, 2

Immediate Treatment Algorithm

For Patients WITHOUT Visual Symptoms or Threatened Vision Loss

• Initiate oral prednisone 1 mg/kg/day (maximum 60 mg/day) as a single morning dose immediately upon clinical suspicion, even before diagnostic confirmation 1, 2
• Daily dosing is superior to alternate-day schedules for achieving remission 2
• Add tocilizumab to glucocorticoids as first-line combination therapy to reduce relapse rates (from 34-62% to significantly lower) and minimize cumulative steroid exposure 3, 1, 2
• If tocilizumab is contraindicated or unavailable, consider methotrexate as an alternative steroid-sparing agent, though evidence is weaker 1, 2

For Patients WITH Visual Symptoms or Threatened Vision Loss

• Administer IV methylprednisolone 500-1000 mg/day for 3 consecutive days immediately, then transition to high-dose oral prednisone (1 mg/kg/day, maximum 60 mg) 3, 1, 2
• This represents a medical emergency—without treatment, the risk of losing the second eye is 50% if one eye is already affected 3, 2
• Vision loss occurs in 15-35% of GCA patients, almost exclusively before glucocorticoid initiation 3, 2

Diagnostic Confirmation While on Treatment

• Arrange temporal artery biopsy within 2 weeks of starting glucocorticoids—treatment does not significantly affect biopsy results within this window 3, 1
• Obtain a long-segment biopsy (≥1 cm) to improve diagnostic yield due to skip lesions 3, 1
• If biopsy is negative but clinical suspicion remains high, obtain noninvasive vascular imaging (ultrasound showing "halo sign," MRI, or PET-CT) to evaluate for large vessel involvement 3, 1, 2
• Elevated inflammatory markers (ESR/CRP) are present in >95% of GCA cases at diagnosis; normal values should raise suspicion for alternative diagnosis 3

Glucocorticoid Tapering Strategy

• Maintain initial high-dose therapy for approximately 1 month until symptoms resolve and inflammatory markers normalize 1, 4, 2
• Begin gradual taper after disease control is achieved, aiming for 10-15 mg/day by 3 months and ≤5 mg/day after 1 year 1, 2
• Guide tapering by clinical symptoms AND normalization of ESR/CRP, not inflammatory markers alone 1, 2
• Avoid alternate-day therapy as it increases relapse risk 2, 5

Adjunctive Therapies

• Prescribe low-dose aspirin (75-150 mg/day) for all patients unless contraindicated to protect against cardiovascular and cerebrovascular events 2
• Implement bone protection with calcium, vitamin D, and bisphosphonates given prolonged glucocorticoid exposure 6
• Consider proton pump inhibitor or H2-receptor antagonist for GI protection 6

Management of Relapses

Relapses occur in 34-62% of patients during glucocorticoid tapering 3

For Relapses WITH Cranial Ischemic Symptoms

• Add tocilizumab (preferred) or methotrexate AND increase glucocorticoid dose 1, 2
• Tocilizumab is superior to methotrexate for relapsing disease with cranial symptoms 4, 2

For Relapses WITH Polymyalgia Rheumatica Symptoms Only

• Increasing glucocorticoid dose alone may be sufficient 2

For Elevated Inflammatory Markers WITHOUT Clinical Symptoms

• Clinical observation and monitoring without escalating immunosuppression is recommended—elevated markers alone may reflect infections or other inflammatory conditions, not active GCA 3, 1

Special Considerations for Large Vessel Involvement

• Obtain noninvasive vascular imaging in all newly diagnosed GCA patients to assess extent of arterial involvement 3, 2
• For active extracranial large vessel involvement, combine oral glucocorticoids with tocilizumab rather than glucocorticoids alone 1, 2
• For severe GCA with worsening limb/organ ischemia, escalate immunosuppressive therapy before considering surgical intervention 2

Long-Term Monitoring

• Implement lifelong clinical monitoring even in apparent remission to detect relapses and glucocorticoid-related adverse effects 1, 2
• Monitor for new-onset headache, jaw claudication, visual changes, and polymyalgia symptoms at each visit 1
• Assess ESR/CRP regularly but do not base treatment decisions on laboratory values alone 1, 2
• Screen for glucocorticoid complications: hypertension, diabetes, osteoporosis, infections, psychosis 6

Critical Pitfalls to Avoid

• Never delay treatment while awaiting biopsy or imaging results—vision loss is permanent and occurs before treatment initiation in the vast majority of cases 3, 1, 2
• Do not rely solely on inflammatory markers to guide treatment—clinical symptoms are paramount, and ESR/CRP can be elevated from other causes 3, 1
• Avoid rapid steroid withdrawal as it leads to disease exacerbation 2
• Do not use infliximab for GCA—it is associated with recurrent ocular symptoms and disease activity 2
• Recognize that PMR symptoms may represent masked or subclinical GCA, particularly in patients with recurrent relapses or inability to taper glucocorticoids 3