Acute Lateral Medullary Infarct due to Giant Cell Arteritis: A Case Study.
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ABSTRACT:
SUBMITTER: Dardick JM
PROVIDER: S-EPMC6756979 | biostudies-literature | 2019 Oct
REPOSITORIES: biostudies-literature
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Acute Lateral Medullary Infarct due to Giant Cell Arteritis: A Case Study.
Dardick Joseph M JM Esenwa Charles C CC Zampolin Richard L RL Ustun Berrin B Ayesha Bibi B Kirchoff-Torres Kathryn F KF Liberman Ava L AL
Stroke 20190909 10
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Project description:BackgroundThe etiology of giant cell arteritis (GCA) and its predictors are incompletely understood. Previous studies have indicated reduced risk of future development of GCA in individuals with obesity and/or diabetes mellitus. There is limited information on blood lipids before the onset of GCA. The objective of the study was to investigate the relation between apolipoprotein levels and future diagnosis of GCA in a nested case-control analysis.MethodsIndividuals who developed GCA after inclusion in a population-based health survey (the Malmö Diet Cancer Study; N = 30,447) were identified by linking the health survey database to the local patient administrative register and the national patient register. A structured review of medical records was performed. Four controls for every validated case, matched for sex, year of birth, and year of screening, were selected from the database. Anthropometric measures, self-reported physical activity, based on a comprehensive, validated questionnaire, and non-fasting blood samples had been obtained at health survey screening. Concentrations of apolipoprotein A-I (ApoA-I) and apolipoprotein B (ApoB) in stored serum were measured using an immunonephelometric assay. Potential predictors of GCA were examined in conditional logistic regression models.ResultsThere were 100 cases with a confirmed clinical diagnosis of GCA (81% female; mean age at diagnosis 73.6 years). The median time from screening to diagnosis was 12 years (range 0.3-19.1). The cases had significantly higher ApoA-I at baseline screening compared to controls (mean 168.7 vs 160.9 mg/dL, odds ratio [OR] 1.57 per standard deviation (SD); 95% confidence interval [CI] 1.18-2.10) (SD 25.5 mg/dL). ApoB levels were similar between cases and controls (mean 109.3 vs 110.4 mg/dL, OR 0.99 per SD; 95% CI 0.74-1.32) (SD 27.1 mg/dL). The ApoB/ApoA1 ratio tended to be lower in cases than in controls, but the difference did not reach significance. The association between ApoA-I and GCA development remained significant in analysis adjusted for body mass index and physical activity (OR 1.48 per SD; 95% CI 1.09-1.99).ConclusionSubsequent development of GCA was associated with significantly higher levels of ApoA-I. These findings suggest that a metabolic profile associated with lower risk of cardiovascular disease may predispose to GCA.
| S-EPMC10821258 | biostudies-literature
Project description:Giant cell arteritis (GCA) and Takayasu Arteritis (TAK) are two systemic granulomatous vasculitides affecting medium- and large-sized arteries. Similarities in GCA and TAK regarding the clinical presentation, the systemic inflammatory response and the distribution of the arterial lesions, have triggered a debate over the last decade about whether GCA and TAK represent two different diseases, or are age-associated different clinical phenotypes of the same disease. On the other hand, there are differences regarding epidemiology, several clinical features (eg, polymyalgia rheumatica in GCA) and treatment. The aim of this review is to present the latest data regarding this question and to shed some light on the differences and similarities between GCA and TAK regarding epidemiology, genetics, pathogenesis, histopathology, clinical presentation, imaging and treatment. The existing data in literature support the opinion that GCA and TAK are different clinical entities.
| S-EPMC7362112 | biostudies-literature
Project description: Not available
| S-EPMC9105486 | biostudies-literature
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| S-EPMC8406620 | biostudies-literature
Project description:ObjectiveIdentify predictors of treatment failure in patients with giant cell arteritis (GCA) receiving tocilizumab in combination with glucocorticoids and in patients with GCA receiving only glucocorticoids.MethodsPosthoc analysis of the Giant-Cell Arteritis Actemra trial including 250 patients who received tocilizumab every week plus a 26-week prednisone taper (n=100), tocilizumab every-other-week plus a 26-week prednisone taper (n=49) or placebo plus a 26-week (n=50) or 52-week (n=51) prednisone taper in the intention-to-treat population. Responders for this analysis were patients who maintained remission (no GCA signs/symptoms and no erythrocyte sedimentation rate elevation) through week 52. Treatment failure was defined as inability to achieve remission by week 12 or relapse between weeks 12 and 52. Predictors investigated in univariate and multivariable analyses included patient characteristics, disease-related and treatment-related factors and patient-reported outcomes (PROs).Results149 patients received tocilizumab plus prednisone (TCZ/PDN) and 101 received placebo plus prednisone (PBO+PDN). After adjustment for confounders, treatment failure was significantly less likely in the TCZ/PDN group than the PBO/PDN group (OR, 0.2; 95% CI, 0.1 to 0.3; p<0.0001). Risk for treatment failure was significantly higher in women than men in the PBO/PDN group (OR, 5.2; 95% CI, 1.6 to 17.2; p=0.007) but not in the TCZ/PDN group. Predictors of treatment failure in the TCZ/PDN group included lower baseline prednisone doses and worse PROs at baseline.ConclusionThe strongest risk factors for treatment failure in GCA are treatment with prednisone alone and female sex. Lower starting prednisone doses and impaired PROs are associated with failure to respond to tocilizumab.Trial registration numberNCT01791153.
| S-EPMC8522464 | biostudies-literature
Project description:Glucocorticoids have been the mainstay of treatment in giant cell arteritis (GCA) for the past 70 years. Conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs) have largely failed to show significant clinical efficacy or reduction of the glucocorticoid burden in GCA. Tocilizumab is the first biologic to make a substantial impact in GCA treatment. With the current understanding of GCA pathogenesis implicating multiple cytokines, notably interleukin (IL) 6, IL-12, IL-23, IL-1β, and the role of janus kinases (JAKs) and the signal transducer and activator of transcription (STAT) pathway in these cytokines, many biologics are currently being investigated in GCA. This review article looks at the existing evidence for biologic agents in GCA. In addition to tocilizumab, the potential role of ustekinumab, abatacept, JAK inhibitors and other promising biologics in GCA are discussed in detail. A treatment algorithm based on the best evidence to date is also presented.
| S-EPMC7797292 | biostudies-literature
Project description:Giant cell arteritis (GCA) is the most frequent primary large-vessel vasculitis in individuals older than 50. Glucocorticoids (GCs) are considered the cornerstone of treatment. GC therapy is usually tapered over months according to clinical symptoms and inflammatory marker levels. Considering the high rate of GC-related adverse events in these older individuals, immunosuppressive treatments and biologic agents have been proposed as add-on therapies. Methotrexate was considered an alternative option, but its clinical impact was limited. Other immunosuppressants failed to demonstrate a significant favourable benefit/risk ratio. The approval of tocilizumab, an anti-interleukin 6 (IL-6) receptor inhibitor brought significant improvement. Indeed, tocilizumab had a noticeable effect on cumulative GCs' dose and relapse prevention. After the improvement in pathophysiological knowledge, other targeted therapies have been proposed, with anti-IL-12/23, anti-IL-17, anti-IL-1, anti-cytotoxic T-lymphocyte antigen 4, Janus kinase inhibitors or anti-granulocyte/macrophage colony stimulating factor therapies. These therapies are currently under evaluation. Interestingly, mavrilimumab, ustekinumab and, to a lesser extent, abatacept have shown promising results in phase 2 randomised controlled trials. Despite this recent progress, the value, specific condition and optimal application of each treatment remain undecided. In this review, we discuss the scientific rationale for each treatment and the therapeutic strategy.
| S-EPMC8999932 | biostudies-literature
Project description:Objectives:The EULAR core dataset for observational studies in GCA does not include glycated haemoglobin (HbA1c). A multivariable score to stratify the pre-test probability of GCA also does not include HbA1c. There have been contradictory reports about diabetes mellitus being a risk factor for GCA. We report the first study analysing the relationship of pre-diagnosis HbA1c with the risk of GCA. Methods:This was a single-centre retrospective case-control study conducted in Norfolk, UK. All GCA cases were diagnosed with imaging or biopsy. Each case was assigned two age- and sex-matched controls. The primary outcome measure was the glycaemic status (HbA1c categorized into euglycaemia, pre-diabetes or diabetes mellitus) at diagnosis between cases and controls. The HbA1c was compared between two groups using the Mann-Whitney U test. The glycaemic categorization was compared using the ?2 test. Results:One hundred and twelve cases and 224 controls were included. The median (interquartile range) of HbA1c of cases and controls was 40 (37, 43) and 41 (39, 47) mmol/mol (P?<?0.001), respectively. Ten of 112 cases and 52 of 224 controls had diabetes mellitus. The ?2 test demonstrated a significant interaction between glycaemic state and GCA (P?=?0.006). Individuals with diabetes mellitus had an odds ratio (95% CI) of 0.32 (0.13, 0.74) (P?=?0.008) of having GCA compared with euglycaemic individuals. Conclusion:HbA1c in the diabetic range reduces the probability of GCA. HbA1c should be considered in any multivariable score to calculate the risk of GCA, and in future development of diagnostic and classification criteria. There is a need for an epidemiological study looking at the possibility of a protective nature of diabetes mellitus against GCA or whether it is only a mimic.
| S-EPMC7380559 | biostudies-literature
Project description:To compare patterns of arteriographic lesions of the aorta and primary branches in patients with Takayasu's arteritis (TAK) and giant cell arteritis (GCA).Patients were selected from two North American cohorts of TAK and GCA. The frequency of arteriographic lesions was calculated for 15 large arteries. Cluster analysis was used to derive patterns of arterial disease in TAK versus GCA and in patients categorised by age at disease onset. Using latent class analysis, computer derived classification models based upon patterns of arterial disease were compared with traditional classification.Arteriographic lesions were identified in 145 patients with TAK and 62 patients with GCA. Cluster analysis demonstrated that arterial involvement was contiguous in the aorta and usually symmetric in paired branch vessels for TAK and GCA. There was significantly more left carotid (p=0.03) and mesenteric (p=0.02) artery disease in TAK and more left and right axillary (p<0.01) artery disease in GCA. Subclavian disease clustered asymmetrically in TAK and in patients ?55 years at disease onset and clustered symmetrically in GCA and patients >55 years at disease onset. Computer derived classification models distinguished TAK from GCA in two subgroups, defining 26% and 18% of the study sample; however, 56% of patients were classified into a subgroup that did not strongly differentiate between TAK and GCA.Strong similarities and subtle differences in the distribution of arterial disease were observed between TAK and GCA. These findings suggest that TAK and GCA may exist on a spectrum within the same disease.
| S-EPMC3729734 | biostudies-literature
Project description:ObjectiveTo identify and validate, using computer-driven methods, patterns of arterial disease in Takayasu arteritis (TAK) and giant cell arteritis (GCA).MethodsPatients with TAK or GCA were studied from the Diagnostic and Classification Criteria for Vasculitis (DCVAS) cohort and a combined North American cohort. Case inclusion required evidence of large-vessel involvement, defined as stenosis, occlusion, or aneurysm by angiography/ultrasonography, or increased 18 F-fluorodeoxyglucose (FDG) uptake by positron emission tomography (PET) in at least 1 of 11 specified arterial territories. K-means cluster analysis identified groups of patients based on the pattern of arterial involvement. Cluster groups were identified in the DCVAS cohort and independently validated in the North American cohort.ResultsA total of 1,068 patients were included (DCVAS cohort: TAK = 461, GCA = 217; North American cohort: TAK = 225, GCA = 165). Six distinct clusters of patients were identified in DCVAS and validated in the North American cohort. Patients with TAK were more likely to have disease in the abdominal vasculature, bilateral disease of the subclavian and carotid arteries, or focal disease limited to the left subclavian artery than GCA (P < 0.01). Patients with GCA were more likely to have diffuse disease, involvement of bilateral axillary/subclavian arteries, or minimal disease without a definable pattern than TAK (P < 0.01). Patients with TAK were more likely to have damage by angiography, and patients with GCA were more likely to have arterial FDG uptake by PET without associated vascular damage.ConclusionArterial patterns of disease highlight both shared and divergent vascular patterns between TAK and GCA and should be incorporated into classification criteria for large-vessel vasculitis.
| S-EPMC7035996 | biostudies-literature