Giant Cell Arteritis Patients Research Articles

Decreased Immunity to Varicella Zoster Virus in Giant Cell Arteritis.

Herpes zoster, which can have a major impact on quality of life, results from reactivation of a latent varicella zoster virus (VZV) infection. We hypothesized that giant cell arteritis (GCA) patients are at increased risk of herpes zoster because of treatment with high-dose glucocorticoids and advanced age. Aim of the study, therefore, was to determine cell-mediated and humoral immunity to VZV in patients with GCA, patients with closely related disease polymyalgia rheumatica (PMR; treated with lower doses of glucocorticoids) and healthy controls (HCs). Cell-mediated immunity to VZV was determined by performing interferon-γ (IFNγ) enzyme-linked immunospot and intracellular cytokine flow cytometry measurements in 11 GCA and 15 PMR patients and in 26 age/sex-matched HCs. Immunoglobulin G antibodies to VZV glycoprotein (VZV-IgG) were measured in serum samples of 35 GCA and 26 PMR patients at different times of follow-up and in 58 age and sex-matched HCs by an enzyme-linked immunosorbent assay. The number of VZV-specific IFNγ spot-forming cells was significantly lower in GCA patients on treatment, than in age-matched HCs (p = 0.029), but was not different in PMR patients on treatment. Similar levels of VZV-IgG were found in GCA and PMR patients at baseline, compared to HCs. The finding of a decreased cell-mediated immunity to VZV, known to be of great importance in defense to the virus, indicates an increased herpes zoster risk in GCA patients compared to an already at-risk elderly population. Herpes zoster vaccination is, therefore, of special importance in GCA patients, and would ideally be administered at time of diagnosis. Interestingly, as VZV was suggested to be the trigger in GCA pathogenesis, similar levels of VZV-IgG were found in GCA patients at time of diagnosis and age-matched HCs, indicating that GCA patients did not experience herpes zoster substantially more often in the months preceding diagnosis than controls.

Positron Emission Tomography/Computerized Tomography in Newly Diagnosed Patients with Giant Cell Arteritis Who Are Taking Glucocorticoids.

Large vessel uptake on positron emission tomography/computerized tomography (PET/CT) supports the diagnosis of giant cell arteritis (GCA). Its value, however, in patients without arteritis on temporal artery biopsy and in those receiving glucocorticoids remains unknown. We compared PET/CT results in GCA patients with positive (TAB+) and negative temporal artery biopsies (TAB-), and controls. Patients with new clinically diagnosed GCA starting treatment with glucocorticoids underwent temporal artery biopsy and PET/CT. Using a visual semiquantitative approach, 18F-fluorodeoxyglucose (FDG) uptake was scored in 8 vascular territories and summed overall to give a total score in patients and matched controls. Twenty-eight patients with GCA and 28 controls were enrolled. Eighteen patients with GCA were TAB+. Mean PET/CT scores after an average of 11.9 days of prednisone were higher in patients with GCA compared to controls, for both total uptake (10.34 ± 2.72 vs 7.73 ± 2.56; p = 0.001), and in 6 of 8 specific vascular territories. PET/CT scores were similar between TAB+ and TAB- patients with GCA. The optimal cutoff for distinguishing GCA cases from controls was a total PET/CT score of ≥ 9, with an area under the receiver-operating characteristic curve of 0.75, sensitivity 71.4%, and specificity 64.3%. Among patients with GCA, these measures correlated with greater total PET/CT scores: systemic symptoms (p = 0.015), lower hemoglobin (p = 0.009), and higher platelet count (p = 0.008). Vascular FDG uptake scores were increased in most patients with GCA despite exposure to prednisone; however, the sensitivity and specificity of PET/CT in this setting were lower than those previously reported.

Aortitis in giant cell arteritis: diagnosis with FDG PET/CT and agreement with CT angiography

To assess the detection rate of aortitis in giant cell arteritis (GCA) with fluorodeoxyglucose positron emission tomography/computed tomography (PET) and to compare the findings with CT angiography (CTA). Fifty-two GCA patients and 27 controls were included. GCA patients had a PET scan at diagnosis (35/52) or during relapse (17/52). Concomitant CTA was performed in 35/52 patients. Aortitis was defined as FDG uptake higher than the liver for PET and wall thickness≥3mm for CTA. Agreement between PET and CTA was evaluated by the kappa coefficient and Spearman correlation coefficient. Aortitis was diagnosed using PET in 40% (14/35) of patients at diagnosis and in 0% of controls (0/27). Agreement was perfect between PET and CT at a patient-based level, and very good at a vascular segment-based level (kappa: 0.72 to 1). PET was positive in 35% (6/17) of patients scanned during GCA relapse, showing aortitis (n=4) and/or articular uptake (n=4). Discrepancies between PET and CT were observed only in relapsing GCA (n=3). Correlation between the maximum standardized uptake value and wall thickness was moderate at diagnosis (r: 0.57 to 0.7) and not statistically significant during relapse. The detection rate of aortitis in GCA patients using PET is 40%, approximately in the range of CTA rates, suggesting that the two techniques have similar sensitivity. PET seems valuable in relapsing GCA, allowing the detection of vascular and articular activities.

Repetitive 18F-FDG-PET/CT in patients with large-vessel giant-cell arteritis and controlled disease

Objective18F-FDG PET/CT can detect large-vessel involvement in giant-cell arteritis (GCA) with a good sensitivity. In patients with clinically and biologically controlled disease, we aimed to assess how vascular uptakes evolve on repetitive FDG-PET/CT. Patients and methodsAll included patients had to satisfy the 4 following criteria: 1) diagnosis of GCA was retained according to the criteria of the American College of Rheumatology or based on the satisfaction of 2 criteria associated with the demonstration of large-vessel involvement on FDG-PET/CT; 2) all patients had a positive PET/CT that was performed at diagnosis before treatment or within the first 10days of treatment; 3) another FDG-PET/CT was performed after at least 3months of controlled disease without any relapse; 4) patients were followed-up at least for 12months. ResultsTwenty-five patients (17 [68%] women, median age: 69 [65–78]) with large-vessel inflammation on a baseline FDG-PET/CT and with repetitive imaging during the period with controlled disease were included and followed-up for 62 [25–95] months. Four repeated procedures revealed total extinction of vascular uptakes at 11.5 [8–12] months after the first FDG-PET/CT. Eight PET/CT revealed decreased numbers of vascular uptakes, and 10 procedures revealed no changes. The 3 remaining procedures indicated worsening of the numbers of vascular uptakes in the absence of relapse. ConclusionsOur study revealed long-term persistent vascular uptake on repeated FDG-PET/CT in >80% of our GCA patients with large-vessel inflammation and clinical-biological controlled disease. Prospective studies are required to confirm these findings.

What is the impact of giant cell arteritis on patients’ lives? A UK qualitative study

ObjectivesClinical management of giant cell arteritis (GCA) involves balancing the risks and burdens arising from the disease with those arising from treatment, but there is little research on the nature...

Involvement of Monocyte Subsets in the Immunopathology of Giant Cell Arteritis

Monocytes/macrophages are critical in systemic and local inflammation in giant cell arteritis (GCA) and possibly in clinically overlapping polymyalgia rheumatica (PMR). Therefore, we aimed to understand the contribution of monocyte subsets and the CX3CR1-CX3CL1 and CCR2-CCL2 migratory pathways, to the pathology of GCA. Peripheral blood monocytes were enumerated in samples from newly-diagnosed, untreated GCA and PMR patients and after prednisone-induced remission. The distribution of classical (CD14brightCD16neg) and the more pro-inflammatory, intermediate (CD14brightCD16+) and non-classical (CD14dimCD16+) monocyte subsets was analysed by flow cytometry. The phenotype of macrophages in temporal artery biopsies (TABs) from GCA patients was studied by immunohistochemistry and immunofluorescence. A clear monocytosis was seen in newly diagnosed GCA and PMR patients caused by elevated numbers of classical monocytes. Prednisone treatment suppressed numbers of non-classical monocytes. Both chemokine CX3CL1 and CCL2 were highly expressed in the TAB. Most macrophages in the TAB of GCA patients expressed non-classical monocyte markers CD16 and CX3CR1 whereas co-localisation of CD16 with classical monocyte marker CCR2 was infrequent. In conclusion, we report an altered distribution of monocyte subsets in both GCA and PMR patients. The majority of macrophages in TABs of GCA patients were CD68 + CD16 + CX3CR1 + CCR2− and thereby resembled the phenotype of non-classical monocytes.

The role of colour doppler ultrasonography of facial and occipital arteries in patients with giant cell arteritis: A prospective study

ObjectiveColour Doppler Sonography (CDS) in giant cell arteritis (GCA) allows the study of involvement of cranial arteries other than the temporal arteries, which are inconvenient to biopsy, such as the facial (FaA), and occipital (OcA) arteries. We aimed to estimate the frequency of the FaA, and OcA involvement in GCA; and to explore the clinical characteristics of these subgroups of patients. MethodsFrom 1 January 2014 to 31 December 2016 we prospectively performed a CDS of the FaA, and OcA in addition to the temporal (TA), and the extracranial supra-aortic arteries in all newly diagnosed patients suspected of having GCA. All the arteries were evaluated in two planes for the highly specific halo sign. ResultsDuring the 36-month observation period we performed a CDS of the cranial and extra-cranial arteries in 93 GCA patients. We observed the halo sign on the FaA, and OcA in 38 (40.9%), and 29 (31.2%) cases, respectively. The FaA, or OcA were affected in 4/22 (18.2%) patients with a negative TA CDS. FaA involvement significantly correlated with jaw claudication and with severe visual manifestations, including permanent visual loss. ConclusionsA fifth of patients with a negative CDS of the TAs had signs of vasculitis on the CDS of the FaA, or OcA. The addition of FaA and OcA CDS to the routine CDS of the TAs could identify 4.3% more patients and thus further improve the sensitivity of the CDS in the suspected GCA.

Association between giant cell arteritis and thyroid dysfunction in a "real life" population.

Giant cell arteritis is a systemic autoimmune disorder which involves inflammation of medium to large vessels. The association between giant cell arteritis and autoimmune thyroid disorders has been investigated numerous times in the literature with inconsistent results. Our objective was to evaluate whether a genuine association exists between giant cell arteritis and thyroid dysfunction, which is often due to immune-mediated thyroid disease. Utilizing the medical database of Clalit Health Services, we compared the proportion of hypo and hyperthyroidisim between patients with giant cell arteritis and age-matched and gender-matched controls in a cross-sectional study. Univariate analysis was performed using Chi-square and student t-test and a multivariate analysis was performed using a logistic regression model. Five thousand six hundred and sixty three giant cell arteritis patients and 23,308 age-matched and gender-matched controls were included in the study. The proportion of hypothyroidism amongst giant cell arteritis patients was increased in comparison with controls (18.2 vs. 6.91%, respectively, p-value < 0.001), as was hyperthyroidism (2.56 and 1.19% respectively, p-value < 0.001). Giant cell arteritis demonstrated an independent association with hypothyroidism on multivariate analysis (Odd Ratios 1.297, 95% Confidence Intervals 1.19-1.42), yet not with hyperthyroidism. Giant cell arteritis patients have a higher proportion of hypothyroidism in comparison with matched controls. Physicians treating giant cell arteritis patients should consider screening for thyroid dysfunction on a regular basis.

Temporal artery biopsy in the diagnosis of giant cell arteritis: Does the end justify the means?

BackgroundEarly temporal artery biopsy is recommended in all patients with suspected cranial GCA (Giant Cell Arteritis) by the BSR (British Society of Rheumatology) and BHPR (British Health Professionals in Rheumatology) guidelines. This should be performed within one week ideally.AimTo assess ACR (American College of Rheumatology) score at presentation and whether temporal artery biopsy result affects clinical management of the clinically suspected GCA patient.MethodCase records of all temporal artery biopsies performed within January 2012 until December 2014 were analysed for size and result of biopsy and this was correlated to clinical management following result.Results129 temporal arteries were biopsied with a total of 17 positive biopsy results. 10 biopsy samples were insufficient to confirm or refute GCA. 8 patients within the biopsies negative for GCA had their prednisolone therapy stopped. 5 patients had unknown follow up, with the remainder (89, 87.3%) of the patients continued prednisolone management for treatment of GCA for at least 6 weeks.ConclusionOverall 13.2% of our biopsies were positive for GCA and 87.3% of biopsy negative patients continued prednisolone therapy on clinical grounds. In the face of new diagnostic tests (high resolution MRI (Magnetic Resonance Imaging), colour duplex USS (Ultra Sound Scan) and PET (Positive Emission Topography) can we justify invasive surgery to all patients on histological grounds when the results may not alter management? Further investigation is needed directly comparing newer imaging modalities to histology.

Tocilizumab for giant cell arteritis with corticosteroid-resistant progressive anterior ischemic optic neuropathy

BackgroundGiant cell arteritis is an inflammatory disorder of the medium- and large-size arteries. Permanent visual loss related to arteritic anterior ischemic optic neuropathy is among the most serious complications of this disease and initial treatment usually consists of high dose corticosteroids. There is no consensus in the literature concerning the optimal therapeutic approach in giant cell arteritis patients with corticosteroid-resistant arteritic anterior ischemic optic neuropathy. Case reportA 73-year-old Caucasian female with biopsy-proven giant cell arteritis developed an acute visual loss of the right eye due to arteritic anterior ischemic optic neuropathy. Despite 5 daily methylprednisolone pulses, systemic symptoms persisted and rapid involvement of the controlateral eye was documented. Therefore, tocilizumab (humanised monoclonal antibody binding the human interleukin-6 receptor) was introduced as a potential salvage therapy with a swift consecutive resolution of the systemic symptoms and stabilization of the ophthalmic lesions. ConclusionsAlthough a late effect of steroids pulses cannot be formally ruled out in this dramatic situation, tocilizumab likely offered a decisive effect in preventing bilateral blindness and may have contributed to steroid tapering. Tocilizumab may represent a new early effective second-line treatment option in corticosteroid-resistant anterior ischemic optic neuropathy. More data are needed to confirm this observation and to evaluate the safety profile of this treatment.

Épidémiologie et histoire naturelle de l’artérite à cellules géantes (Horton)

Knowledge of the natural history and epidemiology of giant cell arteritis (GCA) is growing. With the recent conceptual change, GCA is no longer considered a disease with mandatory cranial symptoms but, rather, a larger disease spectrum also including idiopathic aortitis in people older than 50 and polymyalgia rheumatica with large-vessel involvement. The incidence peak between age 70 and 80 years, greater frequency in females and greater occurrence in Nordic countries are well-established epidemiological characteristics. Conversely, the notion that the incidence of GCA is increasing is challenged by several recent population-based studies suggesting a trend reversal for about 15 to 20 years. The known link with the allele HLA-DRB1*04 was confirmed by a genome-wide association study that also found associations with two other genetic polymorphisms. Recent studies indicating a link with varicella zoster virus infection have invigorated the hypothesis of an infectious cause for GCA. Smoking is the most solidly recognized environmental risk factor, but other traditional cardiovascular risk factors do not seem to predispose to GCA. Evidence is mounting that overall mortality in GCA patients is at best slightly higher than expected in relation to general population mortality data, but GCA is associated with an increase in morbidity and mortality specifically related to aortic aneurysm or other cardiovascular causes. Further studies are needed to integrate the current knowledge into a single etiological model.

Quality of life of patients treated for giant cell arteritis: a case-control study.

The objective of the study was to assess the quality of life (QOL) of patients with giant cell arteritis (GCA), following high dose of corticosteroids (CS). Thirty patients with GCA who had stopped CS or who were under long-term low dose of CS were included and matched to 60 controls. QOL was measured by the SF-36 score and a specific questionnaire. GCA patients had no impairment of QOL compared to controls according to SF-36. Most of them (57%) estimated that their general condition was improved following treatment. Patients with GCA complications or CS therapy side effects had no significant impairment of their QOL compared with patients without complications or adverse effects. Only the patients who had gained weight had a lower score on the domain "Vitality" (VT; p=0.013). Walking difficulties were the most frequent complaints. They were associated with impaired scores on the physical summary score (p=0.0340) and on the "General Health" (GH; p=0.005) and "Physical Functioning" (PF, p=0.0298) domains. Falls among GCA patients were associated with altered scores on the domain VT (p=0.0058) and on the mental summary score if they had fallen at least three times (p=0.0460). GCA patients following high dose of CS or under long-term low doses of CS have no significant impairment of their QOL compared to controls. GCA complications, including visual impairment, do not seem to have any major impact on QOL.

Incidence, Prevalence, and Survival of Biopsy-Proven Giant Cell Arteritis in Northern Italy During a 26-Year Period.

To investigate the epidemiology and mortality in patients with biopsy-proven giant cell arteritis (GCA) in northern Italy. All patients with incident temporal-artery biopsy-positive GCA, diagnosed between 1986 and 2012 and living in the Reggio Emilia area, were identified by using a pathology register and by reviewing all histopathologic specimens. For each patient, we identified 1 comparison subject from the same geographic area, matched for age and sex. Mortality rates and specific causes of death were reported. There were 285 incident cases of biopsy-proven GCA (210 women) during the 26-year study period. The overall age- and sex-adjusted incidence per 100,000 persons ages ≥50 years was 5.8 (95% confidence interval [95% CI] 5.1, 6.5). Incidence was significantly higher in women (7.8 [95% CI 6.7, 8.9]) than in men (3.3 [95% CI 2.6, 4.1]) (P < 0.0001). Annual age- and sex-adjusted incidence rates significantly increased by 15.9% per 3 years from 1986 to 2000, then significantly fell by -4.8% per 3 years from 2001-2012. The prevalence of GCA on December 31, 2012 was 87.9 (95% CI 75.8, 101.4). No significant differences in the mortality rates were observed between GCA patients (4.9 per 100 person-years [95% CI 4.1, 5.8]) and non-GCA subjects (5.6 [95% CI 4.7, 6.6]). No significant differences in causes of death were observed comparing GCA patients to non-GCA subjects. This large population-based study of biopsy-proven GCA confirmed the lower incidence of GCA in Mediterranean countries and did not observe any increased mortality risk.

Risk of ocular manifestations in patients with giant cell arteritis: a nationwide study in Sweden

Objective: No large-scale nationwide study has determined the risk of ocular manifestations in patients with giant cell arteritis (GCA). The aim was to study the incidence and risk factors of ocular manifestations in patients with GCA in Sweden.Method: A national cohort was created by linking Swedish nationwide registers. GCA patients were identified from the Swedish Hospital Inpatient and Outpatient Registers between 2002 and 2010, and were followed until the development of ocular manifestations. Standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) were calculated for ocular manifestations in patients with GCA compared to those without GCA.Results: We identified 3737 males and 8311 females with GCA. A total of 1618 individuals had subsequent ocular manifestations, representing 13.4% of the GCA patients. The overall SIR of ocular manifestations was 6.96 (95% CI 6.63–7.31). The risk for disorders of the optic nerve or visual tract was particularly high (SIR = 51.68, 95% CI 46.12–57.73). Men with GCA had a higher risk than women, and GCA patients without polymyalgia rheumatica (PMR) symptoms had a higher risk than those with PMR symptoms. Living outside big cities was negatively associated with ocular manifestations in GCA patients, whereas hypertension and diabetes were associated with an increased risk of ocular manifestations.Conclusion: The overall risk of ocular manifestations was higher in GCA patients than in the general population, especially for men and for those without PMR symptoms.

No detection of varicella-zoster virus in temporal arteries of patients with giant cell arteritis.

Data on the presence of varicella-zoster virus (VZV) in temporal arteries of patients with giant cell arteritis (GCA) are controversial. We analyzed VZV infection in temporal arteries from Italian patients with temporal artery biopsy (TAB)-positive GCA, TAB-negative GCA, and controls. A total of 79 formalin-fixed, paraffin-embedded (FFPE) TABs performed between 2009 and 2012 at a single institution from 34 TAB-positive GCA patients, 15 TAB-negative GCA patients, and 30 controls were retrieved. Six 5-μm sections of all FFPE TABs were cut. The first section was analyzed by immunohistochemistry using mouse monoclonal anti-VZVgE IgG1 antibody. DNA was extracted from the remaining five sections and analyzed by real-time polymerase chain reaction (PCR) for the presence of VZV DNA. For 10 of the 34 TAB-positive GCA patients, an additional 2-mm piece of frozen TAB was available. DNA was extracted from the entire 2-mm length frozen specimen and analyzed by PCR for the presence of VZV DNA. Thirty additional 5-μm sections were cut from the FFPE TABs of these 10 patients and analyzed by immunohistochemistry for the presence of VZV antigen. Immunohistochemical analysis detected VZV antigen in 1/34 (3%) TAB-positive GCA, 0/15 TAB-negative GCA, and 0/30 controls, and in none of the 300 sections cut from the 10 FFPE TABs positive for GCA for which the frozen specimens were available. DNA obtained from all TABs was amplifiable. VZV DNA was neither found in any of the FFPE TABs nor found in frozen TABs. Our data do not support in Italian patients a possible role for VZV infection in the etiopathogenesis of GCA.

Immunoinhibitory checkpoint deficiency in medium and large vessel vasculitis

Giant cell arteritis (GCA) causes autoimmune inflammation of the aorta and its large branches, resulting in aortic arch syndrome, blindness, and stroke. CD4+ T cells and macrophages form organized granulomatous lesions in the walls of affected arteries, destroy the tunica media, and induce ischemic organ damage through rapid intimal hyperplasia and luminal occlusion. Pathogenic mechanisms remain insufficiently understood; specifically, it is unknown whether the unopposed activation of the immune system is because of deficiency of immunoinhibitory checkpoints. Transcriptome analysis of GCA-affected temporal arteries revealed low expression of the coinhibitory ligand programmed death ligand-1 (PD-L1) concurrent with enrichment of the programmed death-1 (PD-1) receptor. Tissue-residing and ex vivo-generated dendritic cells (DC) from GCA patients were PD-L1lo, whereas the majority of vasculitic T cells expressed PD-1, suggesting inefficiency of the immunoprotective PD-1/PD-L1 immune checkpoint. DC-PD-L1 expression correlated inversely with clinical disease activity. In human artery-SCID chimeras, PD-1 blockade exacerbated vascular inflammation, enriched for PD-1+ effector T cells, and amplified tissue production of multiple T-cell effector cytokines, including IFN-γ, IL-17, and IL-21. Arteries infiltrated by PD-1+ effector T cells developed microvascular neoangiogenesis as well as hyperplasia of the intimal layer, implicating T cells in the maladaptive behavior of vessel wall endogenous cells. Thus, in GCA, a breakdown of the tissue-protective PD1/PD-L1 checkpoint unleashes vasculitic immunity and regulates the pathogenic remodeling of the inflamed arterial wall.

Giant Cell Arteritis-related Stroke: A Retrospective Multicenter Case-control Study.

Our aim was to describe patients with giant cell arteritis (GCA)-related stroke and to compare them with a control group of GCA patients without stroke. We created a retrospective multicenter cohort of patients with (1) GCA diagnosed according to the American College of Rheumatology criteria between 1995 and 2015, and (2) stroke occurring at the time of GCA diagnosis or occurring within 4 weeks of starting GCA therapy. The control group consisted of GCA patients without stroke. Forty patients [21 women (53%), median age 78 (60-91) yrs] with GCA-related stroke were included and were compared with 200 control patients. Stroke occurred at GCA diagnosis in 29 patients (73%), whereas it occurred after diagnosis in 11 patients. Vertebrobasilar territory was involved in 29 patients (73%). Seven patients died within a few hours or days following stroke. Compared with the control group, stroke patients had more ophthalmic ischemic symptoms [25 (63%) vs 50 (25%), p < 0.001]. Conversely, they demonstrated lower biological inflammatory variables [C-reactive protein: 61 (28-185) mg/l vs 99 (6-400) mg/l, p = 0.04] and less anemia [22/37 (59%) vs 137/167 (79%), p = 0.03] than patients without stroke. Multivariate logistic regression revealed that the best predictors for the occurrence of stroke were the presence of ophthalmic ischemic symptoms at diagnosis (OR 5, 95% CI 2.14-12.33, p = 0.0002) and the absence of anemia (OR 0.39, 95% CI 0.16-0.99, p = 0.04). Stroke, especially in the vertebrobasilar territory, is more likely to occur in patients with GCA who experience recent ophthalmic ischemic symptoms and who exhibit low inflammatory variables.

Estimating the Cost of Illness of Giant Cell Arteritis in the United States.

IntroductionGiant cell arteritis (GCA) is a chronic vasculitis affecting approximately 230,000 Americans. Limited data exist on the healthcare resource utilization and costs attributable to GCA. The objective of this study was to estimate the cost of illness in patients with GCA in the US.MethodsA cohort of patients with a new GCA diagnosis was identified from a large US claims database between 1 January 2008 and 31 December 2012. Newly diagnosed GCA patients were defined by two claims with GCA (ICD-9 446.5) as one of the listed diagnoses during the study period and no GCA diagnosis in the 12 months prior. Subjects without a GCA diagnosis were matched 5:1 to cases. One-year healthcare costs were compared among cases and controls, adjusting for covariates using generalized linear models.ResultsA cohort of 1293 GCA patients and 6465 controls was identified. The mean age was 73 years, and 69% were females. Mean Charlson Comorbidity Index was 1.9 for GCA patients and 1.0 for controls. Mean 1-year cost for GCA patients was $34,065 [standard deviation (SD) $52,411], and mean 1-year cost for controls was $12,890 (SD $37,345). After multivariate adjustment, the difference in 1-year cost between GCA patients and controls was $16,431 (95% CI $13,821–$19,041).ConclusionsPatients with GCA experience substantially higher healthcare costs in the first year following diagnosis compared to patients without GCA. These results add to the limited evidence available to inform researchers, clinicians, and policymakers on the cost burden of GCA in the US.FundingGenentech Inc.

COMPARAÇÃO DA PREVALÊNCIA DE COMORBIDADES EM PACIENTES COM ARTERITE DE TAKAYASU E ARTERITE DE CÉLULAS GIGANTES

Introduction: Vasculitis are associated with high morbi-mortality caused by cardiovascular disease, through accelerated atherosclerosis. This process has a multifactorial risk factors, which could be related to aspects of the inflammatory disease itself, to the use of steroids and to the presence of traditional risk factors of cardiovascular diseases. Objective: Analyze if patients with large vessels vasculitis (LVV) have higher frequency of comorbidities and compare the prevalence between Takayasu arteritis (TAA) and giant cell arteritis (GCA). Method: 45 medical records of patients who had LVV were analyzed in a retrospective study in Florianopolis, Brazil. Demographic data were collected, as well as related to clinical tidings. These data were compared between the vasculitis groups (TAA and GCA) through analysis on SPSS 18.0, t-student test and chi-squared test or Fisher’s exact test, p ≤ 0,05. Project was approved by Human Research Ethics Committee of the related institutions. Results: Among the 45 patients, 22 had TAA and 23 had GCA. 84,4% of the patients were women. The percentage of systemic arterial hypertension, diabetes mellitus and dyslipidemia on TAA were 77,3%, 9,1% and 95,5%, respectively. In the same order these comorbidities were found in GCA patients in 87%, 39,1% and 100%. The control of dyslipidemia was not satisfactory in both groups. Lipid profile did not have a significant difference between TAA and GCA. Conclusion: Patients with GCA have higher prevalence of diabetes mellitus when compared to general population and to TAA. The higher prevalence of systemic arterial hypertension and dyslipidemia found in LVV combined with endothelial inflammation due to vasculitis can contribute to accelerate atherosclerosis and should be evaluated and well treated.

Temporal Trends of Venous Thromboembolism Risk Before and After Diagnosis of Giant Cell Arteritis.

Giant cell arteritis (GCA) and the use of glucocorticoids have both been associated with increased risk of venous thromboembolism (VTE). However, the possibility of confounding by indication has not been investigated. We undertook this study to examine the temporal risk of VTE in GCA patients before and after GCA diagnosis, accounting for confounders including glucocorticoid treatment. We conducted a matched cohort study using an electronic medical record database representative of the UK population (1990-2013). We calculated age-, sex-, and entry time-matched and multivariate relative risks (RRs) of VTE, comparing 6,441 patients with new-onset GCA (defined by corresponding diagnosis codes and prescribed glucocorticoid treatment) to 63,985 controls before and after GCA diagnosis. Analysis before GCA diagnosis was stratified by oral glucocorticoid use to account for confounding. There were 27 incident VTE events during the 12 months preceding GCA diagnosis and 195 afterward. Compared to controls, during the 12, 9, 6, and 3 months preceding GCA diagnosis, the age-, sex-, and entry time-matched RRs for VTE among patients with imminent GCA not treated with glucocorticoids were 1.8, 2.2, 2.4, and 3.6, respectively. In the first 3, 6, 12, 24, 48, and 96 months after GCA diagnosis, the corresponding RRs were 9.9, 7.7, 5.9, 4.4, 3.3, and 2.4. Multivariate analyses including several common VTE risk factors showed similar trends. The risk of VTE increases shortly before GCA diagnosis, peaks at the time of diagnosis, and then progressively declines thereafter. This risk is apparent in patients with imminent GCA unexposed to oral glucocorticoids, suggesting a role for inflammation-associated thrombosis that is independent of glucocorticoid use.