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An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
Published on: February 8, 2019
Vertebral artery involvement in giant cell arteritis: Symptoms, treatment and outcome
Johann Lambeck1, Axel Schläger2, Nils Venhoff3
1Department of Neurology and Neurophysiology, Medical Center, University of Freiburg, Breisacher Strasse 64, 79106 Freiburg, Germany.
Insights
Giant cell arteritis (GCA) affecting the vertebral artery (VA) is uncommon but serious. Early, intensive treatment is crucial due to risks of stroke progression and recurrence in VA+ GCA patients.
Area of Science:
- Neurology
- Vascular Medicine
- Rheumatology
Background:
- Giant cell arteritis (GCA) involving the vertebral artery (VA) is a rare cause of ischemic stroke.
- The long-term clinical and sonographic course of VA+ GCA patients remains poorly understood.
Purpose of the Study:
- To investigate the long-term clinical and sonographic outcomes of patients with GCA and vertebral artery involvement (VA+).
Main Methods:
- A 12-year retrospective analysis of patients with suspected GCA undergoing ultrasound (US).
- Focus on VA+ patients identified via GCA-specific US, with follow-up data extracted from hospital records.
Main Results:
- Of 220 GCA patients, 74 (34%) were VA+. 19% of VA+ patients presented with vertebrobasilar ischemia, more frequent with severe VA occlusive disease.
- Follow-up in 34 VA+ patients showed stable US findings (38%), regression (41%), or progression (21%) of stenosis.
- 12% experienced recurrent vertebrobasilar stroke, with 3 occurring within 30 days of treatment initiation.
Conclusions:
- One-third of cranial GCA cases involve the VA, with significant stroke risk, particularly in severe occlusive disease.
- High rates of stenosis progression and recurrent stroke necessitate prompt, intensive immunosuppressive therapy for VA+ GCA.
Background:
Giant cell arteritis (GCA) of the vertebral artery (VA) is a rare but serious cause of ischemic stroke, however, the long-term clinical and sonographic course of GCA patients with VA involvement (VA+) is poorly understood.
Methods:
All patients with suspected GCA who were consecutively referred to our ultrasound (US) lab over a 12-year-period were analyzed. US examination (GCA-specific) of the cranial and cervical arteries was performed. Patients with a positive US diagnosis of GCA were identified, and further analysis was restricted to VA+ patients. Follow-up data were extracted from our hospital database.
Results:
Among the 785 patients screened for GCA, 220 showed typical US-based findings for GCA, 74 (34 %) of whom were VA+. Fourteen VA+ patients (19 %) had vertebrobasilar ischemia at presentation (11 stroke, 3 TIA). Cerebral ischemia was more frequent in patients with severe compared to moderate VA occlusive disease (35 % vs 9 %; p = 0.0099, OR = 5.39, 95 % CI 1.50-9.42). Two patients died from severe initial stroke. Follow-up data were available for 34 VA+ patients (46 % of all VA+ patients; median period, 740 days), where 13 (38 %) displayed stable US alterations to the VA, 14 (41 %) a regression and 7 (21 %) a progression of stenosis. Four patients (12 %) had vertebrobasilar re-stroke, 3 of them within 30days of treatment initiation.
Conclusion:
One-third-of patients with cranial GCA were VA+, 19 % of whom had vertebrobasilar stroke, of which most had severe VA occlusive disease. Significant rates of stenosis progression and recurrent stroke therefore call for early intensive immunosuppressive treatment.
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