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Relapses common in patients with giant cell arteritis
Relapses in patients with giant cell arteritis are common, may occur during treatment and commonly used serum markers of inflammation may appear at normal values during relapse, according to recently published research.
Researchers studied 102 women and 26 men with giant cell arteritis (GCA) enrolled in the Vasculitis Clinical Research Consortium Longitudinal Study of GCA, a multicenter, longitudinal, observational study. Patients’ mean age at diagnosis was 69.9 years at diagnosis. All patients were evaluated quarterly, and 49 reported at least one prior relapse before enrollment. Glucocorticoids were used by 118 of 128 patients, methotrexate was used by 19 patients, azathioprine by three patients, cyclophosphamide by two patients and one patient took mycophenolate motefil as GCA treatments.
A diagnosis of GCA required minimum age above 50 years with two or more symptoms, including headache, temporal artery abnormalities, erythrocyte sedimentation rate (ESR) at or above 40 mm/h by Westergren method, abnormal temporal artery seen on biopsy and/or large vessel vasculitis seen by biopsy or angiography.
During the follow-up period, 44 patients experienced 59 relapses. Temporal artery biopsies showed a positive diagnosis in 34 of the patients; six patients had negative diagnoses, and biopsy was not performed in four patients. More than one relapse was experienced by 10 of the patients, including six patients who had two relapses, three patients who had three relapses and one who had four.
On the day of evaluation, disease was still active in 43 of the 44 patients, with low activity in 28 patients and moderate activity in 15 patients. More than half (52%) of the patients who experienced relapse reported a history of relapse prior to enrollment, compared with 31% of patients with no relapse history.
The most common symptoms in relapse were headache and polymyalgia rheumatic, and three patients (7%) developed new visual symptoms.
Glucocorticoids were in use by 43 of 44 patients who experienced a relapse, and methotrexate was in use at the time of 13 relapses. Anti-tumor necrosis factor alpha treatments were in use during two relapses, and mycophenolate motefil was in use during two relapses. In eight relapses, ESR and C-reactive protein (CRP) were at normal values, but ESR and CRP data were only available for 39 relapse incidents. Mean ESR was 31 mm/h, and mean CRP was 16.3 mg/L.
The establishment of more reliable biomarkers and more effective treatments for GCA are needed, the researchers concluded. - by Shirley Pulawski
Disclosure: Kermani was supported by the Vasculitis Clinical Research Consortium (VCRC), which received support from the U.S. National Institute of Arthritis and Musculoskeletal and Skin Diseases (U54AR057319), the U.S. National Center for Research Resources (U54 RR019497), the U.S. Office of Rare Diseases Research, and the U.S. National Center for Advancing Translational Science. The VCRC is part of the Rare Diseases Clinical Research Network.
Perspective
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Giant cell arteritis (GCA) is not an uncommon disorder among elderly patients and generally responds promptly to therapy with glucocorticoids, however, relapses are not uncommon. Retrospective studies have suggested relapse rates as high as 62%. Furthermore, in an often-quoted autopsy study from the 1970s, virtually all patients with GCA were noted to have active disease even though they were thought to be in remission at the time of death.
Kermani and colleagues from the Vasculitis Clinical research Consortium have performed a prospective study looking for relapse in 128 patients with GCA who were followed for a median of 21.4 months. They noted 59 relapses in 44 patients. More importantly, nearly one-third of the relapses were associated with ischemic symptoms with the majority still on glucocorticoids. Most impressive to me was that in 215 of the relapses both erythrocyte sedimentation rate and C-reactive protein were normal, thus compromising both the positive and negative predictive value of these often ordered tests.
My conclusion is we need better biomarkers for this disease, especially a biomarker that is at least exquisitely sensitive to help rule out flares. Secondly, as per my Perspective a few weeks ago, this again makes me think we are certainly not curing GCA and we may just be suppressing a dysfunctional host response to something. Did someone say varicella zoster virus?