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Relevant bibliographies by topics / Corticosteroid sensitivity

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Journal articles

Academic literature on the topic 'Corticosteroid sensitivity'

Author: Grafiati

Published: 7 December 2024

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Journal articles on the topic "Corticosteroid sensitivity"

1

Lewis, Brandon W., Devine Jackson, Stephanie A. Amici, 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, no. 6 (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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2

Lewis, Brandon W., Maria L. Ford, Lynette K. Rogers, and Rodney D. Britt. "Oxidative Stress Promotes Corticosteroid Insensitivity in Asthma and COPD." Antioxidants 10, no. 9 (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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3

Tanaka, Takao, Mari Shigeta, and Masahiko Usui. "BCG inoculation and corticosteroid sensitivity." Ocular Immunology and Inflammation 9, no. 3 (2001): 207–10. http://dx.doi.org/10.1076/ocii.9.3.207.3970.

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4

Lauerma, A. I. "Screening for corticosteroid contact sensitivity." Contact Dermatitis 24, no. 2 (1991): 123–30. http://dx.doi.org/10.1111/j.1600-0536.1991.tb01664.x.

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5

Flores, Saul, Ilias Iliopoulos, Rohit S. Loomba, et al. "Glucocorticoid Receptor Polymorphisms in Children Undergoing Congenital Heart Surgery with Cardiopulmonary Bypass." Journal of Pediatric Intensive Care 09, no. 04 (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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6

Kimura, Genki, and Yasuo Kizawa. "Corticosteroid sensitivity in intractable respiratory disease." Folia Pharmacologica Japonica 145, no. 6 (2015): 329. http://dx.doi.org/10.1254/fpj.145.329.

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7

Gaucher, Louis, Leslie Adda, Alice Séjourné, 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 (January 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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8

Notari, Lorella, Roxane Kirton, and Daniel S. Mills. "Psycho-Behavioural Changes in Dogs Treated with Corticosteroids: A Clinical Behaviour Perspective." Animals 12, no. 5 (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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9

Beam, William R., Robert D. Ballard, and Richard J. Martin. "Spectrum of Corticosteroid Sensitivity in Nocturnal Asthma." American Review of Respiratory Disease 145, no. 5 (1992): 1082–86. http://dx.doi.org/10.1164/ajrccm/145.5.1082.

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10

Bittar, Jan, Carlos Kamiya-Matsuoka, Pedro C. Barata, Soo-Hyun Lee-Kim, Adriana Olar, and Ivo W. Tremont-Lukats. "Corticosteroid sensitivity in gliomatosis cerebri delays diagnosis." Practical Neurology 15, no. 4 (2015): 309–11. http://dx.doi.org/10.1136/practneurol-2015-001125.

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