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Use of Corticosteroids in the Severely Ill Patient

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Abstract

Besides primary and secondary adrenal insufficiency, many medical conditions benefit from the use of corticosteroids because of their anti-inflammatory and immunosuppressive activity. Several mechanisms are involved in the suppression of inflammation by the glucocorticoids, and many remain to be elucidated. Glucocorticoids inhibit the recruitment of leukocytes and monocyte-macrophages into affected areas and the synthesis of a great variety of chemotactic substances and other factors that mediate increased capillary permeability, vasodilatation, and contraction of various nonvascular smooth muscles. All natural and synthetic glucocorticoids act by binding a specific cytoplasmic glucocorticoid receptor. The complex glucocorticoid receptor has the ability to enter the nucleus of the cell and bind specific sites of DNA and control transcription of glucocorticoid-regulated genes. At present the list of substances whose synthesis or release is inhibited by glucocorticoids includes arachidonic acid and its metabolites (prostaglandins and leukotrienes), platelet activating factor (PAF), the nitric-oxide pathway, tumor necrosis factor (TNF) and many interleukins. Glucocorticoids can thus control the synthesis or release of substances involved in onset and evolution of inflammation [1–7].

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© 2000 Springer-Verlag Italia

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Antonelli, M., Passariello, M. (2000). Use of Corticosteroids in the Severely Ill Patient. In: Gullo, A. (eds) Anesthesia, Pain, Intensive Care and Emergency Medicine — A.P.I.C.E.. Springer, Milano. https://doi.org/10.1007/978-88-470-2286-7_56

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  • DOI: https://doi.org/10.1007/978-88-470-2286-7_56

  • Publisher Name: Springer, Milano

  • Print ISBN: 978-88-470-0095-7

  • Online ISBN: 978-88-470-2286-7

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