What we have to know about corticosteroids use during Sars-Cov-2 infection

Abstract

Purpose Glucocorticoids (GCs), alone or associated to other drugs, were widely used in the management of patients affected by severe acute respiratory syndrome caused by SARS-CoV-2 infection, during the recent COVID-19 outbreak. This review summarizes the available data on HPA axis impairment in GC-treated SARS-CoV-2 patients, focusing on the risk of adrenal insufficiency and on potential drug interactions during concomitant treatments. Methods Literature on the impact of GCs therapy on HPA axis and on the consequences of coadministration of GCs and other drugs in SARS-CoV-2 patients has been reviewed. Results GC treatment can cause symptoms of hypercortisolism, especially in patients with individual hypersensibility, or hypoadrenalism after drug withdrawal, due to hypothalamic-pituitary-adrenal (HPA) axis suppression, with consequences in terms of increased morbidity and mortality risk. On the other hand, in SARS-CoV-2-infected patient's cortisol secretion could be insufficient also due to critical illness-related corticosteroid insufficiency (CIRCI). In addition, in this clinical context, the co-administration of antiretroviral drugs and corticosteroids may trigger drug-drug interaction and enhance the exposure to the latter ones, metabolized through the CYP450 CYP3A pathway, severely impacting on HPA axis. Conclusion Physicians involved in the management of patients affected by COVID-19 should be aware of the need of an appropriate GC dose tapering, and of potential interaction of GCs with antiviral therapy and drugs used to treat associated co-morbidities.

Cardiovascular protective properties of oxytocin against COVID-19

“…For instance, COVID-19 patients' sera have only limited cross-neutralization [ 26 ], suggesting that recovery from one infection might not protect against the other. In patients with COVID-19, the hypothalamic-pituitary-adrenocortical axis is likely inhibited as stated above, which makes corticosteroid critical for prevention of cytokine storm [ 154 ]; however, corticosteroid delays virus clearing but does not convincingly improve survival or reduce hospitalization duration and the use of mechanical ventilation [ 155 ]. Hydroxychloroquine previously used to treat COVID-19 is known to prolong the QT interval and can have a proarrhythmic propensity [ 36 ].…”

Tele-medicine versus face-to-face consultation in Endocrine Outpatients Clinic during COVID-19 outbreak: a single-center experience during the lockdown period

“…People affected by different endocrine diseases are facing their own disease and the risk of COVID-19 infection; however, the clinical impact of the SARS-CoV-2 in this subset of patients is not already kwon [6][7][8][9][10]. COVID-19 treatment might induce endocrine complications, as adrenal insufficiency secondary to the high-dose glucocorticoid treatment, which is sometimes used in patients with severe disease [11,12]. SARS-CoV-2-related subacute thyroiditis may be an underestimated manifestation of COVID-19 [13], and adrenal infarction can represent a factor of poorer prognosis [14].…”

Challenges and Opportunities from Targeting Inflammatory Responses to SARS-CoV-2 Infection: A Narrative Review

“…Immunosuppression by CSs would be of the greatest benefit within the hyperinflammatory phase of COVID-19, but also harmful during the initial host response to infection because CS-induced suppression of the innate immunity may increase the latent risk of superinfections and delay the clearance of the virus and, thereby, favor disease progression to severe stages. Prolonged use or moderate-to-high doses of CSs can, by themselves, either cause symptoms of iatrogenic hypercortisolism or provoke hypothalamic-pituitary-adrenal (HPA) axis suppression when CS withdrawal is carried without an appropriate dose tapering [ 54 ]. In the first case, any benefits from CS use would be likely outweighed by their known adverse effects [ 55 ], including hyperglycemia that is per se an independent predictor of mortality in hospitalized patients with COVID-19 [ 122 , 123 ].…”

“…In the first case, any benefits from CS use would be likely outweighed by their known adverse effects [ 55 ], including hyperglycemia that is per se an independent predictor of mortality in hospitalized patients with COVID-19 [ 122 , 123 ]. In the second case, CS use may further compromise the HPA axis, which can be already dysfunctional in COVID-19 patients and increase the risk of adrenal insufficiency following CS discontinuation [ 54 , 55 ]. Finally, physicians should be also aware of possible interactions between CSs like dexamethasone and other drugs concomitantly used in COVID-19 patients, in particular those occurring at the level of cytochrome P450 (CYP) enzymes that may significantly influence the concentrations (and thereby the effects) of medications that are CYP substrates [ 54 ].…”

“…On the other hand, use of non-steroidal anti-inflammatory drugs (NSAIDs) and of corticosteroids (CSs) have been repeatedly debated during the SARS-CoV-2 pandemic, because conflicting evidence suggests benefits, harms or even neutral effects. In particular, the main concern is that, even if NSAIDs and CSs can potentially provide an effective brake to inflammatory drive, they can also add further burden to an already compromised patient [ 54 , 55 , 56 , 57 ].…”