The experience of brace treatment in children/adolescents with scoliosis

BACKGROUND: Idiopathic scoliosis is a chronic illness with several different braces used for its treatment. Brace treatment during childhood/adolescence can produce stress. There are studies supporting that it can decrease body-image perception while other studies support that it has no such effect. The purpose of this study was to explore the experience of brace treatment in children/adolescents with scoliosis. The aim was to investigate which feelings are created by the bracing experience in children/adolescents with scoliosis and what are the children/adolescents' with scoliosis opinions of the support provided to them by health-care professionals and by their families. METHODS: We conducted interviews with the help of a semi-structured interview guide in order to address the topic of the experience of brace treatment. A convenient sample of twelve children and adolescents with scoliosis was selected from patients attending follow-up appointments at the Outpatient Scoliosis Clinics of two Greek hospitals. The data was analysed using the method of content analysis. RESULTS: Patients in the sample were 10–16 years old and they were mainly females (71%). Almost all of the participants reported having to deal with stress, denial, fear, anger, and shame. They were satisfied with the information they received regarding their condition and therapy. However, the information was not accompanied by support from the health care professionals. They reported that they were receiving support mainly from their families, friends, and classmates. CONCLUSION: The present study is contributing to the development of a better understanding of significant issues related to the experience of bracing therapy. It is clear that scoliosis children/adolescents have to be provided with support during the long period of bracing. It is apparent that those children/adolescents have unmet needs for care and health professionals and policy makers should try to find a way to address those needs

Risk of venous and arterial thromboembolism in patients with giant cell arteritis and/or polymyalgia rheumatica : A Veterans Health Administration population-based study in the United States

Background: Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are systemic inflammatory diseases that primarily affect elderly women. Objectives: To compare the risk of thromboembolic events and retinal vascular occlusions in GCA and/or PMR with that in osteoarthritis (OA), evaluating a veteran-based population. Methods: A total of 1535 patients with GCA, 10,265 with PMR, and 1203 with overlapping disease, as well as 39,009 age- and sex-matched patients with OA were identified in this retrospective study. The incidence rate ratios (IRRs) of pulmonary embolism (PE), deep venous thrombosis (DVT), arterial thromboembolism, central retinal artery occlusion, and central retinal vein occlusion were calculated and examined over time. The cumulative incidence was plotted and hazard ratios (HRs) of thromboembolic events were calculated, adjusting for independent risk factors of thromboembolism. Results: Patients with GCA and overlapping disease exhibited higher IRRs for all thromboembolic events compared to patients with OA. Patients with GCA had a higher risk of developing DVT and retinal vascular occlusions than those with overlapping disease (HR: 2.01, 95% confidence interval [CI]: 1.35–2.99, p < 0.001; HR: 2.37, 95% CI: 1.23–4.53, p = 0.009, respectively) or PMR alone (HR: 1.89, 95% CI: 1.50–2.41, p < 0.001; HR: 4.68, 95% CI: 3.10–7.07, p < 0.001, respectively). Patients with GCA had a higher risk of developing PE than those with PMR (HR: 1.55, 95% CI: 1.1–2.18, p = 0.01). Conclusion: The risk of thromboembolic events differs between GCA, PMR, and overlapping diseases. Our findings may help predict the risk of thromboembolic events based on disease phenotype

Pathogenesis of giant cell arteritis with focus on cellular populations.

Peer reviewed: TrueGiant cell arteritis (GCA), the most common non-infectious vasculitis, mainly affects elderly individuals. The disease usually affects the aorta and its main supra-aortic branches causing both general symptoms of inflammation and specific ischemic symptoms because of the limited blood flow due to arterial structural changes in the inflamed arteries. The pathogenesis of the GCA is complex and includes a dysregulated immune response that affects both the innate and the adaptive immunity. During the last two decades several studies have investigated interactions among antigen-presenting cells and lymphocytes, which contribute to the formation of the inflammatory infiltrate in the affected arteries. Toll-like receptor signaling and interactions through the VEGF-Notch-Jagged1 pathway are emerging as crucial events of the aberrant inflammatory response, facilitating among others the migration of inflammatory cells to the inflamed arteries and their interactions with the local stromal milieu. The increased use of checkpoint inhibitors in cancer immunotherapy and their immune-related adverse events has fed interest in the role of checkpoint dysfunction in GCA, and recent studies suggest a dysregulated check point system which is unable to suppress the inflammation in the previously immune-privileged arteries, leading to vasculitis. The role of B-cells is currently reevaluated because of new reports of considerable numbers of plasma cells in inflamed arteries as well as the formation of artery tertiary lymphoid organs. There is emerging evidence on previously less studied cell populations, such as the neutrophils, CD8+ T-cells, T regulatory cells and tissue residing memory cells as well as for stromal cells which were previously considered as innocent bystanders. The aim of this review is to summarize the evidence in the literature regarding the cell populations involved in the pathogenesis of GCA and especially in the context of an aged, immune system

Immune complex-mediated neutrophil activation in patients with polymyalgia rheumatica

OBJECTIVE: Neutrophils are important in host defence. However, neutrophils are also linked to inflammation and organ damage. The purpose of this study was to assess whether markers of neutrophil activation are increased in PMR. METHODS: Levels of immune complexes (IC), calprotectin and neutrophil extracellular traps (NETs) were measured in plasma of healthy individuals (n = 30) and patients with PMR (n = 60), at flare and upon treatment with glucocorticoids using ELISA. Plasma-mediated neutrophil activation was assessed in presence of an FcγRIIA inhibitory antibody (IV.3). RESULTS: Plasma levels of calprotectin and NETs were elevated in PMR (P &lt; 0.001). Mechanistically, neutrophil activation was driven by ICs, present in plasma, able to up-regulate neutrophil activation markers CD66b and CD11b (P &lt; 0.0001) in an FcγRIIA-dependent manner (P &lt; 0.01). Of note, circulating levels of IC correlated with plasma induced CD66b and CD11b (r = 0.51, P = 0.004, and r = 0.46, P = 0.01, respectively) and decreased after glucocorticoid therapy. In contrast to NETs, calprotectin significantly decreased after glucocorticoid therapy (P &lt; 0.001) and was higher in PMR without overlapping GCA compared with patients with overlapping disease (P = 0.014). Interestingly, musculoskeletal involvement was associated with elevated levels of calprotectin before initiation of glucocorticoid therapy (P = 0.036). CONCLUSIONS: Neutrophil activation, including NET formation, is increased in PMR, through IC-mediated engagement of FcγRIIA. Clinically, neutrophil activation is associated with musculoskeletal involvement, with calprotectin, but not NETs, being a biomarker of treatment response in PMR patients. In all, IC-mediated neutrophil activation is a central process in PMR pathogenesis identifying potential novel therapeutic targets (FcγRIIA), as well as soluble markers for disease monitoring (calprotectin)

Predictive models for thromboembolic events in giant cell arteritis : A US veterans health administration population-based study

Giant cell arteritis (GCA) that affects older patients is an independent risk factor for thromboembolic events. The objective of this study was to identify predictive factors for thromboembolic events in patients with GCA and develop quantitative predictive tools (prognostic nomograms) for pulmonary embolism (PE) and deep venous thrombosis (DVT). A total of 13,029 patients with a GCA diagnosis were included in this retrospective study. We investigated potential predictors of PE and DVT using univariable and multivariable Cox regression models. Nomograms were then constructed based on the results of our Cox models. We also assessed the accuracy and predictive ability of our models by using calibration curves and cross-validation concordance index. Age, inpatient status at the time of initial diagnosis of GCA, number of admissions before diagnosis of GCA, and Charlson comorbidity index were each found to be independent predictive factors of thromboembolic events. Prognostic nomograms were then prepared based on these predictors with promising prognostic ability. The probability of developing thromboembolic events over an observation period of 5 years was estimated by with time-to-event analysis using the method of Kaplan and Meier, after stratifying patients based on predicted risk. The concordance index of the time-to-event analysis for both PE and DVT was > 0.61, indicating a good predictive performance. The proposed nomograms, based on specific predictive factors, can accurately estimate the probability of developing PE or DVT among patients with GCA

Distinct patterns of angiogenic factor expression as a predictive factor of response to chemotherapy in stage IIIA non-small-cell lung cancer patients.

The expression of various angiogenic factors was assessed in tumour samples of patients with stage III non-small-cell lung cancer (NSCLC) and further evaluated in terms of response to induction paclitaxel-ifosfamide-cisplatin chemotherapy. Freshly isolated lung tumour specimens obtained by bronchoscopy from 70 stage IIIA NSCLC chemotherapy-naïve patients were sampled and analysed for vascular endothelial growth factor receptor (VEGFR)-1, VEGFR-2 and VEGFR-3. Microvessel density was assessed through evaluating the angiogenic markers CD34 and CD105. Immunostaining scores were calculated by multiplying the percentage of labeled cells by the intensity of staining for each examined parameter. The overall mean immunostaining score value from all NSCLC samples was 7.83, 5.56 and 15.86 for VEGFR-1, VEGFR-2 and VEGFR-3, respectively. The overall mean value of the endothelial antigen CD34 was 16.29, whereas the expression of the CD105 antigen in endothelial cells yielded a multivariate distribution. Patients who responded to chemotherapy expressed significantly higher VEGFR-1 and VEGFR-3 mean values compared with non-responders (P&lt;0.001). No significant difference was noted in VEGFR-2 mean values between these two groups (P=0.06). The CD34 mean value was significantly higher in responders (P&lt;0.001), whereas there was no significant difference in CD105 expression between the two groups (P=0.07). Angiogenic marker expression proved to be a potential predictive factor of response to chemotherapy in stage III NSCLC. which merits further investigation