Original articlePathologic Markers Determining Prognosis in Patients With Treated or Healing Giant Cell Arteritis
Section snippets
Methods
This retrospective, consecutive case series was approved by the Houston Methodist Hospital institutional review board (Pro00013783). Clinical history of patients with suspected GCA were reviewed and correlated with a histologic sections of their TABs.
Results
Forty-two patients, 27 (64%) of whom were female, were reviewed. At diagnosis, the median age was 71 years, with a 25th-75th percentile interquartile range (IQR) of 66-79 years. Median follow-up time was 53.6 (25.0-78.9) weeks. Median time between clinical evaluation and TAB was 16.5 (3.0-35.3) days; during this time, patients were on corticosteroids. All suspected patients referred from external ophthalmologists were given oral steroids on the day of presentation at the external
Discussion
Many studies have investigated the correlation between examination findings,4, 5, 6 laboratory findings,11 and histopathologic features9, 10, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21 in the diagnosis of patients with GCA. Genetic polymorphisms in various regulatory elements related to cell types or processes, such as in endothelial cells or angiogenesis, respectively, have been found to increase one's risk for developing GCA and in worsening its severity.22, 23 This study specifically examined
Conclusions
This study provides data supporting the use of CD68 immunohistochemical staining in TABs and demonstrates that patients with greater numbers of CD68+ cells per histologic section were more likely to require additional immunomodulatory therapy and to have more recalcitrant disease. Our data did not show an association between prolonged steroid courses and decreased CD68+cells per slice. Continued future study of the potential use of quantitative immunologic markers (eg, CD68) in the TAB should
References (29)
- et al.
Thrombocytosis in patients with biopsy-proven giant cell arteritis
Ophthalmology
(2002) - et al.
Poor prognosis of visual outcome after visual loss from giant cell arteritis
Ophthalmology
(2005) - et al.
Molecular cloning of CD68, a human macrophage marker related to lysosomal glycoproteins
Blood
(1993) - et al.
Clinicopathologic correlations in giant cell arteritis: a retrospective study of 107 cases
Ophthalmology
(2009) - et al.
Giant cell arteritis: laboratory predictors of a positive temporal artery biopsy
Ophthalmology
(2011) - et al.
Comparison of histopathologic features, clinical symptoms, and erythrocyte sedimentation rates in biopsy-positive temporal arteritis
Ophthalmology
(2005) - et al.
Correlations between histopathological findings and clinical manifestations in biopsy-proven giant cell arteritis
J Autoimmun
(2016) - et al.
A genome-wide association study identifies risk alleles in plasminogen and P4HA2 associated with giant cell arteritis
Am J Hum Genet
(2017) - et al.
Influence of previous corticosteroid therapy on temporal artery biopsy yield in giant cell arteritis
Semin Arthritis Rheum
(2007) - et al.
Tocilizumab for induction and maintenance of remission in giant cell arteritis: a phase 2, randomised, double-blind, placebo-controlled trial
Lancet
(2016)
Epidemiology of giant cell arteritis and polymyalgia rheumatica
Arthritis Rheum
Does this patient have temporal arteritis?
JAMA
Predictors of relapse and treatment outcomes in biopsy-proven giant cell arteritis: a retrospective cohort study
Rheumatology (Oxford)
Risk factors for early visual deterioration in temporal arteritis
J Neurol Neurosurg Psychiatry
Cited by (19)
Consensus statement on the processing, interpretation and reporting of temporal artery biopsy for arteritis
2023, Cardiovascular PathologyEpidemiology and predictors of relapse in giant cell arteritis: A systematic review and meta-analysis
2023, Revue du Rhumatisme (Edition Francaise)Epidemiology and predictors of relapse in giant cell arteritis: A systematic review and meta-analysis
2023, Joint Bone SpineCitation Excerpt :Title and abstract screening yielded 121 articles eligible for full text analysis. In the final analysis, 30 studies were included for the 1-year, 2-year and 5-year CRR of first relapse (2595 patients) [13–40,42,74], 16 studies (1947 patients) [13–15,17,18,22,23,36,37,41–47] for the CRR of second and third relapse, 40 studies (4213 patients) [13,18–20,22,23,25,34,36–38,42,43,45,48–73] for the qualitative synthesis of predictors of relapse, and 16 studies (1961 patients) [13,18,23,36,37,42,45,52,55,56,58,64,66,68,69,71] for the meta-analysis of predictors of relapse. The characteristics of the included studies are presented in Table S3.
Diagnosis of giant cell arteritis using clinical, laboratory, and histopathological findings in patients undergoing temporal artery biopsy
2022, Clinical Neurology and NeurosurgeryCitation Excerpt :Of particular interest is the significance of cluster of differentiation 68 (CD68) staining in GCA specimens. The CD68 marker stains macrophages that invade and destroy the IEL of affected arteries in GCA, which are precursors of epithelioid giant cells that are pathognomonic for active arteritis diagnosis [14]. There is no consensus regarding the significance of CD68-positive staining in the arterial walls of specimens that do not otherwise demonstrate active or classic healed arteritis, such as disruption or destruction of the IEL or transmural inflammatory changes.
High risk and low prevalence diseases: Giant cell arteritis
2022, American Journal of Emergency MedicineCitation Excerpt :Additionally, there is limited literature that suggests GCA may increase the risk of TIA or stroke, though it is unclear what the incidence of these conditions may be in the setting of GCA specifically [75]. Current data suggest stroke may occur in 1.5–7.5% of patients within the first 4 weeks of diagnosis [76-78], and ischemic stroke more commonly displays vertebrobasilar involvement and rarely intracranial involvement [79]. Beyond aortitis, branches of the external carotid artery are typically affected in GCA.
New insights into the pathogenesis of giant cell arteritis: are they relevant for precision medicine?
2021, The Lancet RheumatologyCitation Excerpt :Notably, GM-CSF and M-CSF are early inducers of monocyte differentiation and might promote and sustain these macrophages in the context of giant cell arteritis.62 Using a stratified medicine approach, it is worth noting that macrophage infiltration seems higher in temporal artery biopsies of patients who do not respond to initial steroid tapering compared with patients who do respond, and might predict disease severity in patients with giant cell arteritis.65 In giant cell arteritis, activated dendritic cells througout the arterial wall that express class II MHC and the co-stimulatory molecules CD83, CD80, and CD86 strongly contribute to the activation of CD4+ T lymphocytes.
Stacy Smith is currently at Houston Methodist Neurological Institute, The Woodlands, Texas, USA.