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Review
. 2020 Jan 3:10:1.
doi: 10.1186/s13601-019-0303-6. eCollection 2020.

Benefits and harm of systemic steroids for short- and long-term use in rhinitis and rhinosinusitis: an EAACI position paper

Affiliations
Review

Benefits and harm of systemic steroids for short- and long-term use in rhinitis and rhinosinusitis: an EAACI position paper

Valerie Hox et al. Clin Transl Allergy. .

Erratum in

Abstract

Because of the inflammatory mechanisms of most chronic upper airway diseases such as rhinitis and chronic rhinosinusitis, systemic steroids have been used for their treatment for decades. However, it has been very well documented that-potentially severe-side-effects can occur with the accumulation of systemic steroid courses over the years. A consensus document summarizing the benefits of systemic steroids for each upper airway disease type, as well as highlighting the potential harms of this treatment is currently lacking. Therefore, a panel of international experts in the field of Rhinology reviewed the available literature with the aim of providing recommendations for the use of systemic steroids in treating upper airway disease.

Keywords: Glucocorticosteroids; Rhinitis; Rhinosinusitis.

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Conflict of interest statement

Competing interestsGS: Honoraria for articles, speaker and advisory boards: ALK, Astra Zeneca, Brittania Pharmaceuticals, Capnia, Church & Dwight, Circassia, Groupo Uriach, GSK, Meda/Mylan, Merck, MSD, Ono Pharmaceuticals, Oxford Therapeutics, Sanofi-Aventis, UCB. Travel funding: ALK, Bayer, GSK, Meda. Chair of BSACI Rhinitis guidelines, EAACI Ethics Committee, Rhinology & Laryngology Research Fund. Chair of Data Monitoring Board for Acarizax paediatric AR trial. CH: Reimbursed for Advisory Board work for sanofi, Smith and Nephew and speakers bureau for Medtronic. CB: Advisory board of Sanofi, GSK, Novartis, Astra-Zeneca, Mylan and reimbursed for presentations and travel. TVZ: Consultant for Medtronic and 3NT. STS: has acted as paid consultant for ERT and Roche Products. All these are outside the submitted work. All other authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
The hypothalamic–pituitary–adrenal axis. Stress stimuli induce the production of CRH by the hypothalamus. CRH induces the production of ACTH by the pituitary gland which stimulates the production of glucocorticoids (cortisol) in the adrenal gland cortex. Cortisol acts on many cells, tissues, and organs including the immune system. The excessive release of cortisol as well as proinflammatory cytokines have a negative feedback on the central nervous system by inhibiting this circadian cycle. CRH corticotrophin releasing hormone, ACTH adrenocorticotrophin hormone
Fig. 2
Fig. 2
Molecular mechanisms of glucocorticoid action. After crossing the cell membrane by passive diffusion, glucocorticoids bind to GRα, associated heat-shock proteins (HSP) are released, and the ligand bound receptor translocates into the nucleus. Through the activation of MAP kinase (MAPKs) intracellular cascade, inflammatory stimuli induce the production of transcription factors. A GRα dimer can bind glucocorticoid responsive elements (GRE) on the promoter region of target genes and activate anti-inflammatory gene (MKP-1, GILZ, TTP, lipocortin-1) transcription. B Binding of GRα to a negative GRE (nGRE) leads to gene (POMC, osteocalcin) repression. C Protein–protein interactions between GRα and transcription factors (AP-1, NF-κB) repress the transcription of pro-inflammatory genes (COX-2, TNF-α, VEGF, IL-8). D GRα can alter mRNA or protein stability of inflammatory mediators

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