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Artigos de revistas sobre o assunto "Corticosteroid sensitivity"
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Lewis, Brandon W., Devine Jackson, Stephanie A. Amici, Joshua Walum, Manel Guessas, Sonia Guessas, Elise Coneglio et al. "Corticosteroid insensitivity persists in the absence of STAT1 signaling in severe allergic airway inflammation". American Journal of Physiology-Lung Cellular and Molecular Physiology 321, n.º 6 (1 de dezembro de 2021): L1194—L1205. http://dx.doi.org/10.1152/ajplung.00244.2021.
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Corticosteroid insensitivity in asthma limits the ability to effectively manage severe asthma, which is characterized by persistent airway inflammation, airway hyperresponsiveness (AHR), and airflow obstruction despite corticosteroid treatment. Recent reports indicate that corticosteroid insensitivity is associated with increased interferon-γ (IFN-γ) levels and T-helper (Th) 1 lymphocyte infiltration in severe asthma. Signal transducer and activator of transcription 1 (STAT1) activation by IFN-γ is a key signaling pathway in Th1 inflammation; however, its role in the context of severe allergic airway inflammation and corticosteroid sensitivity remains unclear. In this study, we challenged wild-type (WT) and Stat1−/− mice with mixed allergens (MA) augmented with c-di-GMP [bis-(3′-5′)-cyclic dimeric guanosine monophosphate], an inducer of Th1 cell infiltration with increased eosinophils, neutrophils, Th1, Th2, and Th17 cells. Compared with WT mice, S tat1−/− had reduced neutrophils, Th1, and Th17 cell infiltration. To evaluate corticosteroid sensitivity, mice were treated with either vehicle, 1 or 3 mg/kg fluticasone propionate (FP). Corticosteroids significantly reduced eosinophil infiltration and cytokine levels in both c-di-GMP + MA-challenged WT and Stat1−/− mice. However, histological and functional analyses show that corticosteroids did not reduce airway inflammation, epithelial mucous cell abundance, airway smooth muscle mass, and AHR in c-di-GMP + MA-challenged WT or Stat1−/− mice. Collectively, our data suggest that increased Th1 inflammation is associated with a decrease in corticosteroid sensitivity. However, increased airway pathology and AHR persist in the absence of STAT1 indicate corticosteroid insensitivity in structural airway cells is a STAT1 independent process.
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Lewis, Brandon W., Maria L. Ford, Lynette K. Rogers e Rodney D. Britt. "Oxidative Stress Promotes Corticosteroid Insensitivity in Asthma and COPD". Antioxidants 10, n.º 9 (24 de agosto de 2021): 1335. http://dx.doi.org/10.3390/antiox10091335.
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Corticosteroid insensitivity is a key characteristic of patients with severe asthma and COPD. These individuals experience greater pulmonary oxidative stress and inflammation, which contribute to diminished lung function and frequent exacerbations despite the often and prolonged use of systemic, high dose corticosteroids. Reactive oxygen and nitrogen species (RONS) promote corticosteroid insensitivity by disrupting glucocorticoid receptor (GR) signaling, leading to the sustained activation of pro-inflammatory pathways in immune and airway structural cells. Studies in asthma and COPD models suggest that corticosteroids need a balanced redox environment to be effective and to reduce airway inflammation. In this review, we discuss how oxidative stress contributes to corticosteroid insensitivity and the importance of optimizing endogenous antioxidant responses to enhance corticosteroid sensitivity. Future studies should aim to identify how antioxidant-based therapies can complement corticosteroids to reduce the need for prolonged high dose regimens in patients with severe asthma and COPD.
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Tanaka, Takao, Mari Shigeta e Masahiko Usui. "BCG inoculation and corticosteroid sensitivity". Ocular Immunology and Inflammation 9, n.º 3 (janeiro de 2001): 207–10. http://dx.doi.org/10.1076/ocii.9.3.207.3970.
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Lauerma, A. I. "Screening for corticosteroid contact sensitivity". Contact Dermatitis 24, n.º 2 (fevereiro de 1991): 123–30. http://dx.doi.org/10.1111/j.1600-0536.1991.tb01664.x.
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Flores, Saul, Ilias Iliopoulos, Rohit S. Loomba, Amy M. Opoka, Rashmi D. Sahay, Lin Fei e David S. Cooper. "Glucocorticoid Receptor Polymorphisms in Children Undergoing Congenital Heart Surgery with Cardiopulmonary Bypass". Journal of Pediatric Intensive Care 09, n.º 04 (29 de abril de 2020): 241–47. http://dx.doi.org/10.1055/s-0040-1709658.
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AbstractWe conducted a candidate gene association study to test the hypothesis that different gene polymorphisms will be associated with corticosteroid responsiveness and study outcomes among children undergoing congenital heart surgery. This is a prospective observational cohort study at a large, tertiary pediatric cardiac center on children undergoing corrective or palliative congenital heart surgery. A total of 83 children were enrolled. DNA was isolated for three polymorphisms of interest namely N363 (rs56149945) and 9β (rs6198) associated with increased sensitivity to corticosteroids and BclI (rs41423247) associated with decreased sensitivity to corticosteroids. Duration of inotropic use, low cardiac output scores (LCOS), and vasoactive inotrope scores were examined in relation to these three polymorphisms. Using Kaplan–Meier analysis, heterozygous individuals showed longer transcriptional intermediary factor (TIF) compared with wild type for N363 polymorphism (p = 0.05). In multivariable Cox regression, heterozygous alleles for 9β polymorphism showed significantly shorter TIF compared with wild type (hazard ratio = 2.04 [1.08–3.87], p = 0.03). The relationship between lower LCOS scores and alleles groups was significant for 9β heterozygous polymorphism only (1.5 [1–2.2], p = 0.01) in comparison to wild type and homozygous. The presence of heterozygote alleles for the increased corticosteroid sensitivity is associated with longer TIF compared with wild type. Conversely, the presence of heterozygous alleles for the decreased sensitivity to corticosteroids is associated with shorter TIF compared with wild type.
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Kimura, Genki, e Yasuo Kizawa. "Corticosteroid sensitivity in intractable respiratory disease". Folia Pharmacologica Japonica 145, n.º 6 (2015): 329. http://dx.doi.org/10.1254/fpj.145.329.
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Gaucher, Louis, Leslie Adda, Alice Séjourné, Camille Joachim, Guillaume Chaby, Claire Poulet, Sophie Liabeuf et al. "Impact of the corticosteroid indication and administration route on overall survival and the tumor response after immune checkpoint inhibitor initiation". Therapeutic Advances in Medical Oncology 13 (janeiro de 2021): 175883592199665. http://dx.doi.org/10.1177/1758835921996656.
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Background: Based on their indications, systemic corticosteroids appear to negatively affect clinical outcomes in immune checkpoint inhibitor (ICI)-treated patients. There are few data on the influence of topical and inhaled corticosteroids on the ICIs’ effectiveness. Methods: In a single-center study, we retrospectively investigated the impact of systemic corticosteroids according to their indication [an immune-related adverse event (irAE) or another indication] on overall survival (OS) and the tumor response in all consecutive patients after initiation of ipilimumab, nivolumab or pembrolizumab over a 9-year period. The impacts of topical and inhaled corticosteroids were also examined. Results: Three hundred and seventy-two patients were included. The mean ± standard deviation age was 64.0 ± 12.1 years. The most frequently prescribed ICI was nivolumab (in 58.3% of the patients) and the most frequent indications were lung cancer (44.6%) and melanoma (29.6%). Systemic corticosteroid use for an irAE did not have a negative impact on OS [adjusted hazard ratio (HR) [95% confidence interval (CI)] 1.04 (0.56–1.95), p = 0.902] or the best overall tumor response [adjusted odds ratio (OR) (95% CI) 1.69 (0.52–6.56), p = 0.413], while systemic corticosteroid use for another indication was associated with shorter OS [adjusted HR (95% CI) 1.34 (1.05–2.03), p = 0.046] and a poor best overall tumor response [adjusted OR (95% CI) 2.04 (1.07–5.80), p = 0.039] with a cumulative dose cut-off of 3215 mg prednisolone equivalent (specificity 71.4%; sensitivity 65.3%) and a time cut-off of 132 days (specificity 71.4%; sensitivity 89.8%). The use of topical corticosteroids was associated with a longer OS; this was probably due to dermatological irAEs. Inhaled corticosteroid use did not influence OS. Conclusion: Systemic corticosteroid use for an irAE does not impact OS or the tumor response, whereas use for other indications (themselves often associated with a worse prognosis) does. Topical and inhaled steroids do not have a negative impact on OS.
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Notari, Lorella, Roxane Kirton e Daniel S. Mills. "Psycho-Behavioural Changes in Dogs Treated with Corticosteroids: A Clinical Behaviour Perspective". Animals 12, n.º 5 (26 de fevereiro de 2022): 592. http://dx.doi.org/10.3390/ani12050592.
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Arousal and distress are often important factors in problematic behaviours, and endogenous corticosteroids are important mediators in the associated stress responses. Exogenous corticosteroid treatments have been reported to change behaviour in human patients and laboratory animals, with similar changes also noted in pet dogs. These behaviours not only potentially adversely impact the welfare of the dogs, but also the quality of life of their owners. Indeed, corticosteroids can bias sensitivity towards aversion in dogs. A decrease in behaviours associated with positive affective states, such as play and exploratory behaviours, together with an increase in aggression and barking have also been described in dogs. According to the available literature, human patients with pre-existing psychiatric disorders are more at risk of developing behavioural side effects due to corticosteroid treatments. It is reasonable to consider that the same may happen in dogs with pre-existing behavioural problems. In this paper, the possible behavioural side effects of exogenous corticosteroids are summarised to help inform and support veterinarians prescribing these drugs.
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Beam, William R., Robert D. Ballard e Richard J. Martin. "Spectrum of Corticosteroid Sensitivity in Nocturnal Asthma". American Review of Respiratory Disease 145, n.º 5 (maio de 1992): 1082–86. http://dx.doi.org/10.1164/ajrccm/145.5.1082.
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Bittar, Jan, Carlos Kamiya-Matsuoka, Pedro C. Barata, Soo-Hyun Lee-Kim, Adriana Olar e Ivo W. Tremont-Lukats. "Corticosteroid sensitivity in gliomatosis cerebri delays diagnosis". Practical Neurology 15, n.º 4 (28 de abril de 2015): 309–11. http://dx.doi.org/10.1136/practneurol-2015-001125.
Texto completo da fonteTeses / dissertações sobre o assunto "Corticosteroid sensitivity"
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Mercado, Nicolas. "Restoration of corticosteroid sensitivity in severe asthma". Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/4388.
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Severe asthma accounts for a small number of asthmatics but represents a disproportionate cost to health care systems. The underlying mechanism in severe asthma remains unknown and most of the cost is the result of inadequate treatment. Although the disease presents a very heterogeneous profile it displays a certain degree of resistance to corticosteroid therapy. It is hypothesized that corticosteroid insensitivity can be reversed pharmacologically. We investigated the effects of drugs which are currently used for treatment of asthma on glucocorticoid sensitivity in peripheral blood mononuclear cells (PBMCs) from patients with mild, moderate and severe asthma and healthy volunteers. Long acting β2 receptor agonists (LABAs) were found to be able to reverse corticosteroid insensitivity in some severe asthmatic patients. These patients showed a defect of glucocorticoid receptor (GR) nuclear translocation with hyperphosphorylation of GR. Furthermore, LABAs were found to inhibit GR phosphorylation through inhibition of p38MAPKγ phosphorylation. Other severe asthmatic patients were also found to be 'responders' to theophylline, another current add-on treatment, and showed a defect in histone deacetylase activity. Further studies were conducted in order to find additional molecular abnormalities which may define novel add-on treatments to reverse corticosteroid resistance. Using simple laboratory methods in peripheral blood mononuclear cells (PBMCs) by one blood sampling, analysis of GR nuclear translocation potential, GR dependent transrepression (IL-8, IL-2 inhibition) and GR-dependent transactivation (Histone-4 lysine-5 acetylation, GILZ expression) revealed a heterogeneous population in severe asthma. Low levels of corticosteroid response were associated with a decrease in lung function in severe asthma. The use of possible add-on treatments such as an IKK2 inhibitor, a PI3K inhibitor, macrolides and a p38MAPKα/β inhibitor as well as existing treatments (theophylline and formoterol) confirmed that different molecular mechanisms were involved in severe asthma and is possible to choose the best add-on treatment individually for each patient. Particularly, a p38MAPKα/β inhibitor was broadly effective in severe asthma. This screening might be useful in determining the underlying phenotype of each individual patient. In the last chapter, I evaluated the effects of nortriptyline hydrochloride (NH), which is a well-known compound but recently identified as a novel add-on treatment to corticosteroids. Studies using PBMCs showed that there were 'responders' and 'non-responders' to NH in severe asthma. Analysis by correlation with other compounds suggested that NH can modify PI3K signalling. In fact NH inhibited phosphorylation of Akt, a surrogate marker of PI3K under oxidative stress, and restored HDAC activity defective under oxidative stress. This new combination will be one of choice for the treatment of severe asthma. This thesis gives new insights on phenotyping of severe asthma patients and novel add-on treatments to corticosteroids, possibly leading to future tailor-made treatment.
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Spears, Mark. "Reduced corticosteroid sensitivity in smokers with asthma : potential mechanisms and treatment". Thesis, University of Glasgow, 2009. http://theses.gla.ac.uk/1100/.
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Smokers with asthma display reduced responses to both inhaled and oral corticosteroids with associated increased symptoms, accelerated decline in lung function and increased use of health care services. Little work has been undertaken to address the possible causes of this reduced response and to find effective replacement therapies. Therefore this thesis was carried out with the aim of identifying potential mechanisms and new therapies for this group. The oral bronchodilator theophylline has been suggested as a treatment for corticosteroid insensitivity due to its ability to increase HDAC activity in-vitro. I undertook an exploratory proof of concept clinical trial based on the hypothesis that low dose theophylline would restore corticosteroid sensitivity in smokers with asthma through theophylline induced recovery of HDAC activity. Low dose oral theophylline added to inhaled corticosteroid increased pre-bronchodilator lung function and reduced symptoms of asthma whilst low dose theophylline given alone reduced symptoms but had no effect on pre-bronchodilator lung function. This research provides a foundation for future studies designed to examine the efficacy of theophylline in smokers with asthma. Agonists of the nuclear hormone receptor peroxisome proliferator activated receptor-γ (PPARγ) have been demonstrated to be effective at reducing inflammation in both in-vitro and animal models of asthma. Therefore to examine the hypothesis that PPARγ stimulation would reduce the inflammation present in smokers with asthma I undertook an exploratory, proof of concept clinical trial using the PPARγ agonist rosiglitazone. Treatment with rosiglitazone was associated with a trend to improvement in FEV1 and improvement in a marker of small airway lung function and as such may provide an alternative treatment for small airways obstruction in conditions such as asthma and chronic obstructive airways disease. This trial will enable powering of future confirmatory studies. Altered cytokine profiles, specifically the combination of increased interleukin (IL)-2 and 4, are observed in asthmatic subjects with corticosteroid insensitivity. Based on this work I examined the hypothesis that the altered response to corticosteroids in smokers with asthma was associated with an altered cytokine milieu including raised levels of IL-2 and 4. Smokers with asthma, characterised as corticosteroid resistant by oral corticosteroid trial, demonstrated significantly raised sputum supernatant IL-6 levels and raised levels of a number of other sputum cytokines compared to non smokers with asthma. This altered phenotype suggests cigarette smoking in asthma may be associated with a deviation to Th1 mediated inflammation and could provide an explanation for the reduced corticosteroid response of smokers with asthma. The cell type/s responsible for both this shift in immunological phenotype and production of increased levels of sputum cytokines is unclear and will require further study. Previous in-vitro and in-vivo research has identified altered histone acetylation patterns in subjects with relative corticosteroid resistance. Therefore I examined the hypothesis that smokers with asthma displayed reduced responses to corticosteroids as a result of a cigarette smoke induced reduction in histone de-acetylase (HDAC) activity. Smokers with asthma provided sputum macrophages and blood for peripheral blood borne monocytes to examine total HDAC activity. Sputum and blood macrophage total HDAC activity was equivalent in smokers and non-smokers with asthma. Therefore reduced blood total HDAC activity does not appear to explain the altered corticosteroid response in this group. However the number of sputum macrophages obtained may have been too low to allow conclusive examination of this endpoint. Another consideration is that contamination of the sample due to the technique used may be altering the signal obtained. Further work either through modification of sputum induction techniques to increase macrophage number or bronchoscopic sampling is required to conclusively address the role of alveolar macrophage HDAC activity in the reduced corticosteroid response displayed by smokers with asthma. Exhaled nitric oxide has been exploited as a useful exploratory and confirmatory endpoint in asthma. However exhaled nitric oxide, measured using standard flow rates and methodology, is unhelpful in smokers with asthma as cigarette smoking is associated with a marked reduction in exhaled nitric oxide levels in the majority of subjects. Recent research has demonstrated that measurement of exhaled nitric oxide at multiple flow rates followed by mathematical modelling reveals increased levels of alveolar nitric oxide that were unaltered by current smoking. Therefore to examine the hypothesis that smokers with asthma display altered levels of alveolar nitric oxide and flow independent parameters compared to non-smokers with asthma I carried out a cross-sectional study. Alveolar nitric oxide, determined by linear modelling, was significantly reduced in smokers with asthma compared to non smokers with asthma. The concentrations observed were within the range for normal subjects and therefore this method does not overcome the problems inherent in measuring exhaled nitric oxide at standard flows. The use of non-linear modelling did demonstrate parity between smokers and non-smokers with asthma for alveolar nitric oxide. Nitric oxide flux was lower in smokers with asthma when derived by both linear and non-linear modelling and displayed sensitivity to oral corticosteroids. Therefore nitric oxide flux is worthy of further investigation as an exploratory endpoint in smokers with asthma. In conclusion treatment of smokers with asthma with low dose theophylline alone, the combination of low dose theophylline and inhaled corticosteroid and the PPARγ agonist rosiglitazone was associated with clinical improvements and further clinical trials to assess the role for these treatments in the management of smokers with asthma are justified. Smokers with asthma display an altered sputum cytokine profile with raised levels of the proinflammatory cytokine IL-6, equivalent blood total HDAC activity and reduced alveolar nitric oxide compared to non-smokers with asthma. Sputum HDAC activity requires further development before it can be confidently employed as a method of assessing total pulmonary HDAC activity.
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Laulhé, Margaux. "Sensibilité aux hormones glucocorticoïdes : recherche des facteurs impliqués dans la variabilité inter-individuelle". Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL078.
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Les corticoïdes de synthèse, dérivés des hormones glucocorticoïdes, représentent un traitement incontournable pour de nombreuses pathologies. Ils sont utilisés par environ 3% de la population mondiale, principalement dans le traitement des maladies inflammatoires, telles que l'asthme ou la polyarthrite rhumatoïde. Bien que la corticothérapie soit un traitement très efficace, elle entraine de nombreux effets secondaires, métaboliques, osseux et hormonaux, en particulier une insuffisance corticotrope post-corticothérapie, qu'il est difficile de prévoir. En effet, il existe une variabilité inter-individuelle dans la sensibilité aux corticoïdes encore mal comprise. Dans ce travail de thèse, nous nous sommes intéressés aux facteurs génétiques impliqués dans cette variabilité inter-individuelle. D'abord, nous nous sommes intéressés à plusieurs variants du gène NR3C1 codant le récepteur glucocorticoïde (GR). Le GR est le principal récepteur relayant les effets des glucocorticoïdes au niveau cellulaire. Nous avons caractérisé in vitro 3 variants du gène NR3C1. Nous avons évalué l'activité transcriptionnelle du GR, l'expression des gènes cibles et la translocation nucléaire en réponse à différents agonistes. Pour les 2 premiers variants, nous avons mis en évidence une diminution de l'activité transcriptionnelle du GR, associée à une diminution du transfert nucléaire et de l'expression des gènes cibles. Ils entrainaient une modification de la structure du GR et étaient responsable du phénotype de résistance primaire aux hormones glucocorticoïdes. Nous avons également caractérisé le variant N363S en établissant un modèle cellulaire et un modèle murin génétiquement modifiés pour exprimer le variant. En effet, ce variant est retrouvé chez 2% de la population et est associé à une augmentation de la sensibilité aux glucocorticoïdes. L'étude du modèle murin n'a pas mis en évidence de phénotype particulier lié à l'expression du variant à l'état basal en l'absence de glucocorticoïdes. L'étude du phénotype sous glucocorticoïdes est en cours. Ensuite, nous nous sommes intéressés aux gènes codant les enzymes CYP3A4 et CYP3A5. Les enzymes CYP3A4/5 sont impliquées dans le métabolisme des hormones glucocorticoïdes, mais surtout dans le métabolisme lié au premier passage hépatique des corticothérapies inhalées. Nous avons mis en évidence deux variants entrainant une perte de fonction des cytochromes CYP3A4 et CYP3A5 chez un patient ayant présenté un syndrome d'hypersensibilité aux glucocorticoïdes après une corticothérapie inhalée à dose modérée. L'absence ou la diminution d'activité des CYP3A4/5 pourrait constituer un facteur de risque facilement dépistable des complications induites par la corticothérapie en particulier inhalée.Enfin, nous avons étudié l'impact d'un traitement prolongé par dexaméthasone sur la fonction de la cellule corticotrope hypophysaire. Nous avons traité les cellules corticotropes AtT-20/D16v, qui représentent un modèle bien caractérisé pour l'étude du rétrocontrôle négatif de l'axe corticotrope par les glucocorticoïdes. L'analyse du transcriptome des cellules après traitement par dexaméthasone pendant 7 jours montre une altération importante et prolongée dans le temps, puisque le transcriptome n'est pas complètement restauré après 7 jours d'arrêt du traitement. Nous avons mis en évidence une expression différentielle de certains gènes qui sont surexprimés au moment de la récupération par rapport aux conditions traitée et contrôle, suggérant un rôle de ces gènes dans la récupération de l'axe corticotrope.Nous pensons qu'une meilleure compréhension des facteurs impliqués dans la variabilité inter-individuelle dans la sensibilité aux glucocorticoïdes et dans la récupération de l'axe corticotrope permettra d'améliorer la prise en charge des patients traités par les hormones glucocorticoïdes dans une démarche de médecine personnaliséeBecause of their anti-inflammatory properties, corticosteroids are an essential treatment for numerous diseases. Corticosteroids are used by about 3% of the global population, mainly to treat inflammatory diseases such as asthma or rheumatoid arthritis. Although corticosteroid therapy is highly effective, it leads to numerous side effects, including metabolic dysregulations, bone resorption, and hormonal deficiencies. Corticosteroid-induced adrenal insufficiency is one of the most frequent side effects. As sensitivity to corticosteroids is highly variable between individuals and remains poorly understood, evaluating the individual risk of side effects susceptibility is difficult. This thesis focused on the genetic factors involved in the inter-individual variability of corticosteroid sensitivity.First, we investigated several variants of the NR3C1 gene encoding the glucocorticoid receptor (GR). The GR mediates the effects of glucocorticoids at the cellular level. We characterized 3 NR3C1 variants in vitro by assessing the transcriptional activity of the GR, target genes expression, and nuclear translocation in response to agonists. For the first 2 variants, we demonstrated a decreased transcriptional activity of the GR, which was associated with reduced nuclear translocation and target gene expression. These variants resulted in a structural modification of the GR and are responsible for the primary glucocorticoid resistance phenotype. We also characterized the N363S variant by developing a genetically modified cell and mouse model. The N363S variant is found in 2% of the population and is associated with increased glucocorticoid sensitivity. Characterization of the mouse model revealed no specific phenotype associated with the variant expression under basal conditions. Evaluation of the phenotype under corticoid treatment is currently ongoing. Next, we focused on the genes encoding the CYP3A4 and CYP3A5 enzymes. The CYP3A4/5 enzymes are involved in glucocorticoid hormone metabolism, particularly in the hepatic first-pass metabolism of inhaled corticosteroids. We identified a homozygous loss-of-function variant of the CYP3A4 gene together with a homozygous loss-of-function polymorphism of the CYP3A5 gene in a patient presenting with glucocorticoid hypersensitivity after moderate-dose inhaled corticosteroid therapy. Absence or reduction of CYP3A4/5 activity may constitute a risk factor that can be evaluated to prevent inhaled corticosteroid-induced complications.Finally, we studied the effect of prolonged dexamethasone treatment on pituitary corticotroph cells function. We treated AtT-20/D16v corticotroph cells, a well-characterized model for studying negative feedback regulation of the hypothalamic-pituitary-adrenal (HPA) axis by glucocorticoids. Transcriptome analysis of cells after 7 days of dexamethasone treatment showed significant and persistent modifications, as the transcriptome did not normalize 7 days after dexamethasone withdrawal. We identified differential expression of specific genes that were overexpressed during the recovery period compared to both treated and control conditions, suggesting a role for these genes in HPA axis recovery.Overall, we believe that a better understanding of genetic factors involved in inter-individual variability in sensitivity to glucocorticoids and corticotropic axis recovery will improve the management of patients treated with corticosteroids to achieve a personalized medicine approach
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Meyer, E., E. W. Smith e J. M. Haigh. "Sensitivity of different areas of the flexor aspect of the human forearm to corticosteroid-induced skin blanching". 1992. http://eprints.ru.ac.za/399/1/Pub54.pdf.
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The intensity of corticosteroid-induced blanching has been found to vary at different areas of the flexor aspect of the human forearm. A retrospective analysis of 38,880 observations of skin blanching in 56 volunteers was conducted to assess the sensitivity of forearm skin to betamethasone 17-valerate. The mid-forearm appears to be more sensitive to the blanching response than do the areas close to the wrist or elbow. These results indicate that each preparation under evaluation should be applied to several sites along the forearm when using the human skin blanching assay in order to obtain an accurate comparative assessment of corticosteroid release from topical delivery vehicles.
Capítulos de livros sobre o assunto "Corticosteroid sensitivity"
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Humphreys, Hilary. "Case 26". In Oxford Case Histories in Infectious Diseases and Microbiology, editado por Hilary Humphreys, 173–78. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198846482.003.0026.
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Clinical signs suggestive of meningitis such as Kernig’s sign have low sensitivity in adults and fever, headache, neck stiffness, and altered mental status are the common clinical manifestations. Where possible, a sample of cerebrospinal fluid (CSF) should be taken and a combination of a third-generation cephalosporin and vancomycin started as empiric treatment. Amoxicillin should be added in the elderly or others at risk of listeriosis. Corticosteroids administered with antibiotics may reduce mortality from meningitis due to Streptococcus pneumoniae and severe hearing loss in children due to Haemophilus influenzae. Those over 65 years of age and patients in other risk groups should be vaccinated against invasive pneumococcal disease. Increasingly, there are recommendations that both the polysaccharide vaccine (PPV23) and conjugated vaccines (e.g. PCV13) should be used to maximize protection.
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Cătălin Jianu, Dragoș, Silviana Nina Jianu, Georgiana Munteanu, Traian Flavius Dan, Anca Elena Gogu e Ligia Petrica. "An Integrated Approach to the Role of Neurosonology in the Diagnosis of Giant Cell Arteritis". In Giant-Cell Arteritis [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96379.
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Giant cell arteritis (GCA) is a primary vasculitis that affects especially extracranial medium-sized arteries, such as superficial temporal arteries (TAs). Three findings are important for the ultrasound (US) diagnosis of TA: „dark halo” sign, which represents vessel wall edema, stenosis, and acute occlusions. US has a high sensitivity to detect vessel wall thickening in the case of large vessels GCA. The eye involvement in GCA is frequent and consists in arteritic anterior ischemic optic neuropathies or central retinal arterial occlusion, with abrupt, painless, and severe loss of vision of the involved eye. Because findings of TAs US do not correlate with eye complications in GCA, color Doppler imaging of the orbital vessels is of critical importance (it reveals low end diastolic velocities, and high resistance index), in order to quickly differentiate the mechanism of eye involvement (arteritic, versus non-arteritic). The former should be treated promptly with systemic corticosteroids to prevent further visual loss of the fellow eye.
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Levy, Deborah M., e Gail S. Ross. "Cognitive and Psychiatric Manifestations of Childhood-Onset Systemic Lupus Erythematosus". In Cognitive and Behavioral Abnormalities of Pediatric Diseases. Oxford University Press, 2010. http://dx.doi.org/10.1093/oso/9780195342680.003.0009.
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Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the production of autoantibodies directed against multiple organ systems. Individuals with SLE may have disease of only one organ system or of many organ systems at one time during a “flare” of disease activity. Systemic lupus erythematosus is characterized by multiple flares and remissions, and flares may lead to end-organ damage. The diagnosis of SLE is generally made by fulfilling four out of 11 of the American College of Rheumatology (ACR) 1997 Revised Classification Criteria for SLE (Hochberg 1997). Although the 1997 revised criteria have not been validated, the earlier 1982 criteria (Tan et al. 1982) have a sensitivity of 96% and specificity of 100%in childhood-onsetSLE(cSLE) (Ferraz et al. 1994). See Table 3.1 for these criteria. Systemic lupus erythematosus has a prevalence rate of 500 per million persons in the U.S. population (Klippel 1997) but may be as high as 130 per 100,000 persons (Uramoto et al. 1999). Approximately 15% of all SLE has its onset in childhood (prior to 18 years of age). Systemic lupus erythematosus occurs more commonly in non-Caucasians, with greater severity of SLE in children and adult Latino and African Americans than in non-Latino Caucasians (Michet et al. 1979).The female predominance of SLE in adulthood (10:1 female-to-male ratio) is less pronounced in childhood, and the ratio prior to puberty is more likely to be 5:1 or even 3:1.The majority of cSLE cases have onset in the peripubertal age period (10–15 years), which continues to suggest a link between estrogen and other hormones on the development of SLE. Childhood-onset SLE differs from adult-onset SLE in that the frequency of renal disease is higher, and the incidence and prevalence of neuropsychiatric SLE (NPSLE) is probably greater (Tucker et al. 1995; Sibbit et al. 2002). Children require aggressive immunosuppression, which on a dose per kilogram of body weight is generally higher than that required by an adult to treat a similar disease manifestation. Immunosuppression often includes corticosteroids. At least in adults, corticosteroids do not appear to cause cognitive impairment (Carbette et al. 1986; Denburg et al. 1997; Carlomagno et al. 2000).
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Brucato, Antonio, e Stefano Maggiolini. "Pericardial effusion". In ESC CardioMed, editado por Yehuda Adler, 1572–75. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0377.
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Pericardial effusion is classified according to its onset—acute, subacute, or chronic (>3 months)—distribution (circumferential or loculated), and haemodynamic impact. Concerning the size, we propose a simple semiquantitative echocardiographic assessment: mild (<10 mm), moderate (10–20 mm), and large (>20 mm), evaluated as the largest telediastolic echo-free space in two-dimensional mode. Symptoms vary according to the speed of accumulation; slow accumulation may induce no or minor symptoms. In the presence of chronic, large pericardial effusions, appropriate tests for neoplasms, tuberculosis, and hypothyroidism should be considered. Chest computed tomography scanning is helpful in reaching an aetiological diagnosis (neoplasms, lymphomas, pneumonia, tuberculosis). High values of proteins, albumin, and lactate dehydrogenase are usually considered indicative of an exudate, as in pleural fluid, but this may not be true for pericardial fluid, and cytology has a sensitivity of only 50% for neoplasm. Mycobacterium cultures and a genome search for tuberculosis with the polymerase chain reaction in pericardial fluid are mandatory if pericardiocentesis is performed. If inflammatory signs are present, the clinical management should be that of pericarditis and a trial of non-steroidal anti-inflammatory drugs, colchicine, or low-dose corticosteroids, or a combination of these, may be tried. In about 60% of cases, the effusion is associated with a known disease, and the therapy should be targeted. When pericardiocentesis is performed in large effusions, prolonged pericardial drainage of up to 30 mL/24 h has been suggested to prevent recurrences, although evidence to support this is scarce. Prognosis is related to the aetiology, and idiopathic effusions may have a good prognosis especially if the effusion is mild to moderate.
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Brucato, Antonio, e Stefano Maggiolini. "Pericardial effusion". In ESC CardioMed, editado por Yehuda Adler, 1572–75. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0377_update_001.
Texto completo da fonteResumo:
Pericardial effusion is classified according to its onset—acute, subacute, or chronic (>3 months)—distribution (circumferential or loculated), and haemodynamic impact. Concerning the size, we propose a simple semiquantitative echocardiographic assessment: mild (<10 mm), moderate (10–20 mm), and large (>20 mm), evaluated as the largest telediastolic echo-free space in two-dimensional mode. Symptoms vary according to the speed of accumulation; slow accumulation may induce no or minor symptoms. In the presence of chronic, large pericardial effusions, appropriate tests for neoplasms, tuberculosis, and hypothyroidism should be considered. Chest computed tomography scanning is helpful in reaching an aetiological diagnosis (neoplasms, lymphomas, pneumonia, tuberculosis). High values of proteins, albumin, and lactate dehydrogenase are usually considered indicative of an exudate, as in pleural fluid, but this may not be true for pericardial fluid, and cytology has a sensitivity of only 50% for neoplasm. Mycobacterium cultures and a genome search for tuberculosis with the polymerase chain reaction in pericardial fluid are mandatory if pericardiocentesis is performed. If inflammatory signs are present, the clinical management should be that of pericarditis and a trial of non-steroidal anti-inflammatory drugs, colchicine, or low-dose corticosteroids, or a combination of these, may be tried. In about 60% of cases, the effusion is associated with a known disease, and the therapy should be targeted. When pericardiocentesis is performed in large effusions, prolonged pericardial drainage of up to 30 mL/24 h has been suggested to prevent recurrences, although evidence to support this is scarce. Prognosis is related to the aetiology, and idiopathic effusions may have a good prognosis especially if the effusion is mild to moderate.
Trabalhos de conferências sobre o assunto "Corticosteroid sensitivity"
1
Allam, Venkata sita rama raju, Ian Adcock, Kian Fan Chung, Eric Morand, James Harris e Maria Sukkar. "MIF antagonism restores corticosteroid sensitivity in a murine model of severe asthma". In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa979.
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He, Z., Y. Bin, Y. Liang, J. Zhang, M. Li e X. Zhong. "Erythromycin Restores Corticosteroid Sensitivity Induced by CSE Through Inhibition of JNK/C-JUN Pathway". In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4531.
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To, M., N. Honda, K. Haruki e Y. To. "Metformin: A potential drug candidate to restore poor corticosteroid sensitivity in obese asthmatic patients". In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.4344.
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Soares, Izadora Fonseca Zaiden, João Nicoli Ferreira dos Santos e Lis Gomes Silva. "Dramatic cognitive improvement with acetylcholinesterase inhibitor in cerebral amyloid angiopathyrelated inflammation". In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.578.
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Context: Cerebral amyloid angiopathy (CAA) is characterized by progressive deposition of amyloid-ß fibrils in the walls of small arterioles and capillaries of the leptomeninges and cerebral cortex. A rare subtype of CAA is CAA-related inflammation (CAA-RI), which exhibits marked perivascular or transmural inflammatory infiltration in brain tissue. The major clinical features of CAA-RI are rapidly progressive dementia, behavioral changes, headache, seizures, or stroke-like signs. Conclusive diagnosis requires histopathological confirmation, but validated clinicoradiological criteria for the diagnosis of probable CAA-RI have good sensitivity (82%) and specificity (97%). Treatment with high dose corticosteroids with or without other immunosuppressive therapy is recommended. We report a case of probable CAA-RI that did not respond to corticosteroid therapy but had a surprising improvement with acetylcholinesterase inhibitor. Case report: A 77-year-old illiterate woman presented with a history of subacute onset of seizures and behavioral changes. Her medical history was positive for a hearing loss due to a toxic exposure in childhood, and a cured breast cancer. The neurological examination showed attention impairment, disorientation, and incoherent speech. CSF showed a mildly elevated protein count. Brain MRI met criteria for probable CAA-RI. She had a poor response with high doses of corticosteroids, but after a trial with Donepezil she showed important cognitive and functional improvement. Conclusion: This result attracts attention to the importance of the cholinergic pathway in the etiology and pathological mechanisms of CAA. Randomized Controlled Trials would be required to confirm our hypothesis and to find new therapeutic options for CAA.
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Bantulà Fonts, Marina, Jordi Roca-Ferrer, César Picado Vallés, Valeria Tubita, Irina Bobolea, Antonio Valero, Joaquim Mullol, Joan Bartra e Ebymar Arismendi. "1,25-dihydroxyvitamin D3 effect on corticosteroid sensitivity in obese asthmatic patients before and after bariatric surgery". In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.315.
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Harshman, T., M. L. Ford, B. W. Lewis, K. Heyob e R. D. Britt. "JAK1 Inhibition Reduces Airway Inflammation and Increases Corticosteroid Sensitivity in a Severe Allergic Airway Inflammation Mouse Model". In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a4455.
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Thomas, A., S. Siddiqui e Y. Amrani. "P21 Evaluating the clinical impact of corticosteroid sensitivity and insensitivity of peripheral blood mononuclear cells in severe asthma". In British Thoracic Society Winter Meeting 2017, QEII Centre Broad Sanctuary Westminster London SW1P 3EE, 6 to 8 December 2017, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2017. http://dx.doi.org/10.1136/thoraxjnl-2017-210983.163.
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Lowe, Alexander P. P., Anthony T. Nials, William R. Ford, Emma J. Kidd e Kenneth J. Broadley. "Decreased Sensitivity To Inhaled Corticosteroid Of Functional And Inflammatory Asthmatic Responses After Ovalbumin Combined With LPS In Guinea Pigs". In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5641.
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Moura, Fernanda Maria Gonçalves de Sousa, Deborah Inayara Mendes Tenorio de Albuquerque, Andreas Batista Schelp, Thiago Ivan Vilchez Santillan, Marcella Canato Toloi e Herval Ribeiro Soares Neto. "Fibrocartilaginous embolism causing spinal cord infartion: case report Fernanda Mari". In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.523.
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A 41-year-old male presented with strength, sensitivity and sphincters deficits of acute evolution after a mild car accident, characterized by paraplegia and areflexia of the lower limbs, hypoesthesia with sensory level at T6 and preserved artresthesia. A major diagnostic evaluation was carried out with neuroxias imaging tests, extensive laboratory investigation and exclusion of occult neoplasia. Cerebrospinal fluid was normal. Magnetic resonance imaging of the thoracic spine revealed signal alteration between T4-T7 without enhancement after contrast injection. A short course of intravenous corticosteroid therapy was attempted without any clinical improvement. Due to the acute presentation, history of minimal trauma, absence of findings in laboratory investigations, no other risk factors, clinical and images compatible with anterior spinal cord infarction, Fibrocartilaginous Embolism (FCE) was defined as a probable etiology. FCE is a rare cause of spinal cord infarction and consists in the migration of fibrocartilaginous nucleus pulposus material through the nearby vasculature into one of the spinal cord vessels, usually at the thoracic level and affects the territory of the anterior spinal artery. It can be associated with minor trauma and other causes. The probable diagnosis of FCE is based on data from the clinical history, exclusion of other alternative diagnoses and neuroradiological findings, such as changes in the spinal cord signal in the vascular territory and degenerative changes in the vertebral disc. Definitive diagnosis is possible only with biopsy. Treatment is supportive with physical rehabilitation. Although rare, FCE should be considered as a differential diagnosis in cases of unexplained medullary infarction in young patients without cardiovascular risk factors. The case in question is important and exemplifies that a high diagnostic suspicion is necessary to elucidate these cases.
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Wang, Julie, James Ho, Wilson Yee, Thomas Mok, Johnny Chan, T. Yao, Sidney Tam et al. "Association Of Inhaled Corticosteroids With Insulin Resistance, Adiponectin And High-Sensitivity C Reactive Protein In Adults With Asthma". In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1777.
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