Estatinas e COVID-19: Suspender ou não Suspender? Eis a Questão!

Ferrari, Filipe; Santos, Raul D.

doi:10.36660/abc.20200949

Cited by 4 publications

(2 citation statements)

References 28 publications

(36 reference statements)

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“…Statins, as hypolipidemic drugs may decrease the infectivity of SARS-CoV-2 by disrupting lipid rafts and lowering membrane cholesterol levels [26]. However statins are not only associated with lowering lipid levels, they also exert pleiotropic effects such as attenuating inflammation and atherosclerotic plaque stabilization which may be crucial in patients with atherosclerosis and COVID-19 [27]. The issue of atherosclerotic plaque stability should be more investigated in patients with SARS-CoV-2 infection.…”

Section: Lipids In Sars-cov-2 Infectionmentioning

confidence: 99%

“…Despite evidence that lower cholesterol concentrations are associated with more severe course of COVID-19, there is, however, no evidence that statins may worsen prognosis. On the contrary, these drugs may reduce the pro-inflammatory and pro-thrombotic mechanisms that characterize more severe cases of COVID-19 [27]. Currently, there is no evidence to support discontinuation of statins in patients with COVID-19, except when important elevations of hepatic enzymes, rhabdomyolysis, or drug-attributed risk of life occur.…”

Section: The Safety Of Statinsmentioning

confidence: 99%

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COVID-19: Direct and Indirect Mechanisms of Statins

Pawlos

Niedzielski

Gorzelak-Pabiś

et al. 2021

IJMS

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The virus responsible for the current COVID-19 pandemic is severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2): a new virus with high infectivity and moderate mortality. The major clinical manifestation of COVID-19 is interstitial pneumonia, which may progress to acute respiratory distress syndrome (ARDS). However, the disease causes a potent systemic hyperin-flammatory response, i.e., a cytokine storm or macrophage activation syndrome (MAS), which is associated with thrombotic complications. The complexity of the disease requires appropriate intensive treatment. One of promising treatment is statin administration, these being 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors that exert pleiotropic anti-inflammatory effects. Recent studies indicate that statin therapy is associated with decreased mortality in COVID-19, which may be caused by direct and indirect mechanisms. According to literature data, statins can limit SARS-CoV-2 cell entry and replication by inhibiting the main protease (Mpro) and RNA-dependent RNA polymerase (RdRp). The cytokine storm can be ameliorated by lowering serum IL-6 levels; this can be achieved by inhibiting Toll-like receptor 4 (TLR4) and modulating macrophage activity. Statins can also reduce the complications of COVID-19, such as thrombosis and pulmonary fibrosis, by reducing serum PAI-1 levels, attenuating TGF-β and VEGF in lung tissue, and improving endothelial function. Despite these benefits, statin therapy may have side effects that should be considered, such as elevated creatinine kinase (CK), liver enzyme and serum glucose levels, which are already elevated in severe COVID-19 infection. The present study analyzes the latest findings regarding the benefits and limitations of statin therapy in patients with COVID-19.

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Section: Lipids In Sars-cov-2 Infectionmentioning

confidence: 99%

Section: The Safety Of Statinsmentioning

confidence: 99%

COVID-19: Direct and Indirect Mechanisms of Statins

Pawlos

Niedzielski

Gorzelak-Pabiś

et al. 2021

IJMS

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Lipid homeostasis and mevalonate pathway in COVID-19: Basic concepts and potential therapeutic targets

Proto

Fiore

Piscopo

et al. 2021

Progress in Lipid Research

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Despite encouraging progresses achieved in the management of viral diseases, efficient strategies to counteract infections are still required. The current global challenge highlighted the need to develop a rapid and cost-effective strategy to counteract the SARS-CoV-2 pandemic. Lipid metabolism plays a crucial role in viral infections. Viruses can use the host lipid machinery to support their life cycle and to impair the host immune response. The altered expression of mevalonate pathway-related genes, induced by several viruses, assures survival and spread in host tissue. In some infections, statins, HMG-CoA-reductase inhibitors, reduce cholesterol in the plasma membrane of permissive cells resulting in lower viral titers and failure to internalize the virus. Statins can also counteract viral infections through their immunomodulatory, anti-inflammatory and anti-thrombotic effects. Beyond statins, interfering with the mevalonate pathway could have an adjuvant effect in therapies aimed at mitigating endothelial dysfunction and deregulated inflammation in viral infection. In this review we depicted the historical and current evidence highlighting how lipid homeostasis and mevalonate pathway targeting represents a valid approach to rapidly neutralize viruses, focusing our attention to their potential use as effective targets to hinder SARS-CoV-2 morbidity and mortality. Pros and cons of statins and Mevalonate-pathway inhibitors have been also dissected.

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Epicardial and pericoronary adipose tissue in severe COVID-19 infection

Duyuler

Demirtaş

et al. 2021

Acta Cardiologica

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Estatinas e COVID-19: Suspender ou não Suspender? Eis a Questão!

Cited by 4 publications

References 28 publications

COVID-19: Direct and Indirect Mechanisms of Statins

COVID-19: Direct and Indirect Mechanisms of Statins

Lipid homeostasis and mevalonate pathway in COVID-19: Basic concepts and potential therapeutic targets

Epicardial and pericoronary adipose tissue in severe COVID-19 infection

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