Treating Patients with Giant Cell Arteritis Is Complicated by Relapses

Summary and Comment |
July 16, 2015

Treating Patients with Giant Cell Arteritis Is Complicated by Relapses

  1. Jonathan S. Coblyn, MD

More relapses occurred during therapy than afterward.

  1. Jonathan S. Coblyn, MD

Patients with giant cell arteritis (GCA) often are treated successfully with steroids, but tapering steroids can be difficult. In addition, relapses are common in GCA patients, and no steroid-sparing secondary therapies are uniformly successful. In this multicenter longitudinal study, U.S. investigators evaluated the frequency and features of relapses in 128 patients with GCA who were followed for a median 21 months. All patients (80% women; mean age at diagnosis, 70) met modified 1990 American College of Rheumatology criteria for GCA (Arthritis Rheum 1990; 33:1122), which do not require temporal artery biopsy for diagnosis; in this study, biopsy was done in 103 patients and was consistent with GCA in 80 patients. Relapse was defined as either new disease activity after a period of remission or worsening disease activity.

During follow-up, 59 relapses occurred in 44 patients (34%). The most common GCA symptoms at the time of relapse were headache (42%) and polymyalgia rheumatica (51%); ischemic symptoms (limb claudication, jaw or tongue claudication, and vision problems) were noted in 29%. Most relapses (73%) occurred while patients were still taking glucocorticoids (median prednisone dose at the time of relapse, 7.5 mg daily); only 11 relapses (17%) occurred after stopping prednisone. Of note, erythrocyte sedimentation rates and C-reactive protein levels were normal in eight relapses. Other medications patients were taking at the time of relapse included methotrexate (13 relapses), anti–tumor necrosis factor therapies (2 relapses), and mycophenolate mofetil (2 relapses).


This study highlights the difficulties associated with treating GCA patients. Patients relapse frequently, and relapse can occur even with normal inflammatory markers. Despite the success of steroids in treating patients with this disease, we need new biomarkers to help identify relapses and newer therapies for treating patients who relapse.

Editor Disclosures at Time of Publication

  • Disclosures for Jonathan S. Coblyn, MD at time of publication Consultant / Advisory board CVS Health (member, Pharmacy and Therapeutics Committee)


Reader Comments (1)

Marc Sapir MD, MPH Physician, Family Medicine/General Practice, retired

In the 2010 article cited, 3 of 5 positive criteria for diagnosing GCA were adequate to achieve a sensitivity of over 90%. As a result more people are being diagnosed without ever receiving a temporal biopsy. I had one such patient and was perplexed at the time that no biopsy was done because she was a patient with many diffuse somatic symptoms that I, who had known her for years, found non-specific.. In the current study (reviewed here) 80 of 103 patients biopsied had positive results. That is, over 20% were biopsy negative, presumably false negatives. However, why should all of the criteria in the paradigm be treated as equal? We used to be taught that giant cells on biopsy is the singular most objective criterion for this diagnosis. Many patients with other types of headaches have bi-temporal symptoms. The fact that the diagnosis is often made by a neurologist who has seen the patients but a few times increases the possibility of misreading subjective elements. Giving up the old requirement of temporal artery biopsy may subject 10-20% of people diagnosed by 3/5 who do not have GCA to long term steroid therapy and the attendant hazards of that treatment.

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