Glucocorticoid excess and COVID-19 disease
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Glucocorticoid excess and COVID-19 disease Valentina Guarnotta 1 & Rosario Ferrigno 2 & Marianna Martino 3 & Mattia Barbot 4 & Andrea M. Isidori 5 Carla Scaroni 4 & Angelo Ferrante 6 & Giorgio Arnaldi 3 & Rosario Pivonello 2 & Carla Giordano 1
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Accepted: 28 September 2020 # The Author(s) 2020
Abstract The pandemic of coronavirus disease (COVID-19), a disease caused by severe acute respiratory syndrome coronavirus 2 (SARSCoV-2), is causing high and rapid morbidity and mortality. Immune system response plays a crucial role in controlling and resolving the viral infection. Exogenous or endogenous glucocorticoid excess is characterized by increased susceptibility to infections, due to impairment of the innate and adaptive immune system. In addition, diabetes, hypertension, obesity and thromboembolism are conditions overrepresented in patients with hypercortisolism. Thus patients with chronic glucocorticoid (GC) excess may be at high risk of developing COVID-19 infection with a severe clinical course. Care and control of all comorbidities should be one of the primary goals in patients with hypercortisolism requiring immediate and aggressive treatment. The European Society of Endocrinology (ESE), has recently commissioned an urgent clinical guidance document on management of Cushing’s syndrome in a COVID-19 period. In this review, we aim to discuss and expand some clinical points related to GC excess that may have an impact on COVID-19 infection, in terms of both contagion risk and clinical outcome. This document is addressed to all specialists who approach patients with endogenous or exogenous GC excess and COVID-19 infection. Keywords Cushing’s syndrome . SarsCoV2 . Glucocorticoid . Infections . Cortisol . Immune system
1 Introduction Severe acute respiratory syndrome due to coronavirus SARSCoV2, or COVID-19, has recently been identified to be a cause of severe pneumonia, with potential evolution to acute respiratory distress syndrome (ARDS), further complicated by cardiovascular and renal injury, particularly in older patients with metabolic comorbidities, such as obesity, hypertension and diabetes, in which higher morbidity and mortality have
* Giorgio Arnaldi [email protected]
been observed [1, 2]. Metabolic alterations are common clinical features of Cushing’s syndrome (CS), a complex and challenging disease characterized by chronic glucocorticoid (GC) excess [3–5]. CS can be exogenous, resulting from chronic administration of corticosteroids, or endogenous, due to adrenal overproduction of cortisol. In around 80% of cases, endogenous CS is caused by excessive adrenal stimulation from abnormally elevated ACTH levels, due to an ACTH-secreting pituitary tumour (Cushing’s Disease, CD)
3
Clinica di Endocrinologia e Malattie del Metabolismo, Dipartimento di Scienze Cliniche e Molecolari (DISCLIMO), Università Politecnica delle Marche, Ospedali Riuniti di Ancona, Via Conca 71, 60126 Ancona, Italy
4
Endocrinology Unit, Department of Medicine, DIME University-Hospital of Padova, Padua, Italy
5
Department of
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