COVID-19 and corticosteroids: a narrative review

Batiha, Gaber El‐Saber; Al-Gareeb, Ali I; Saad, Hebatallah M.; Al-Kuraishy, Hayder M

doi:10.1007/s10787-022-00987-z

Cited by 45 publications

(42 citation statements)

References 167 publications

(214 reference statements)

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“…The clinical presentations of PCS are still elusive, comprising different phenotypes and subtypes [ 40 ]. Of interest, PCS may develop in patients with mild-moderate COVID-19 and even in asymptomatic patients [ 41 , 42 ]. As well, PCS may develop in asymptomatic children with COVID-19, resulting in persistent dyspnea and fatigue [ 43 ].…”

Section: Introductionmentioning

confidence: 99%

Pathophysiology of Post-COVID syndromes: a new perspective

Batiha

Al-Kuraishy

Al-Gareeb

et al. 2022

Virol J

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Most COVID-19 patients recovered with low mortality; however, some patients experienced long-term symptoms described as “long-COVID” or “Post-COVID syndrome” (PCS). Patients may have persisting symptoms for weeks after acute SARS-CoV-2 infection, including dyspnea, fatigue, myalgia, insomnia, cognitive and olfactory disorders. These symptoms may last for months in some patients. PCS may progress in association with the development of mast cell activation syndrome (MCAS), which is a distinct kind of mast cell activation disorder, characterized by hyper-activation of mast cells with inappropriate and excessive release of chemical mediators. COVID-19 survivors, mainly women, and patients with persistent severe fatigue for 10 weeks after recovery with a history of neuropsychiatric disorders are more prone to develop PCS. High D-dimer levels and blood urea nitrogen were observed to be risk factors associated with pulmonary dysfunction in COVID-19 survivors 3 months post-hospital discharge with the development of PCS. PCS has systemic manifestations that resolve with time with no further complications. However, the final outcomes of PCS are chiefly unknown. Persistence of inflammatory reactions, autoimmune mimicry, and reactivation of pathogens together with host microbiome alterations may contribute to the development of PCS. The deregulated release of inflammatory mediators in MCAS produces extraordinary symptoms in patients with PCS. The development of MCAS during the course of SARS-CoV-2 infection is correlated to COVID-19 severity and the development of PCS. Therefore, MCAS is treated by antihistamines, inhibition of synthesis of mediators, inhibition of mediator release, and inhibition of degranulation of mast cells.

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Section: Introductionmentioning

confidence: 99%

Pathophysiology of Post-COVID syndromes: a new perspective

Batiha

Al-Kuraishy

Al-Gareeb

et al. 2022

Virol J

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“…Intervention strategies targeting the cytokine storm include traditional anti-inflammatories and immunosuppressives, e.g., corticosteroids such as dexamethasone and cyclosporine, as well as newly developed biologics, e.g., monoclonal antibodies targeting pro-inflammatory cytokines, and recombinant cytokines [ 4 , 5 ]. The current standard of care for hospitalized COVID-19 patients includes strategies to combat the cytokine storm such as dexamethasone and methylprednisolone [ 6 , 7 , 8 , 9 , 10 ], as well as those to address the replication of the virus itself [ 11 , 12 ], such as remdesivir. Any potential regimen that targets both the cytokine storm and viral replication merits further development.…”

Section: Introductionmentioning

confidence: 99%

The Synergistic Inhibition of Coronavirus Replication and Induced Cytokine Production by Ciclesonide and the Tylophorine-Based Compound Dbq33b

et al. 2022

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Ciclesonide is an inhaled corticosteroid used to treat asthma and has been repurposed as a treatment for mildly ill COVID-19 patients, but its precise mechanism of action is unclear. Herein, we report that ciclesonide blocks the coronavirus-induced production of the cytokines IL-6, IL-8, and MCP-1 by increasing IκBα protein levels and significantly decreasing p65 nuclear translocation. Furthermore, we found that the combination of ciclesonide and dbq33b, a potent tylophorine-based coronavirus inhibitor that affects coronavirus-induced NF-κB activation a little, additively and synergistically decreased coronavirus-induced IL-6, IL-8, and MCP-1 cytokine levels, and synergistically inhibited the replication of both HCoV-OC43 and SARS-CoV-2. Collectively, the combination of ciclesonide and dbq33b merits consideration as a treatment for COVID-19 patients who may otherwise be overwhelmed by high viral loads and an NF-κB-mediated cytokine storm.

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Section: Discussionmentioning

confidence: 99%

“…49 Several studies had also shown that although corticosteroids administered to hospitalized patients with COVID-19 did not improve their clinical state after Day 14, they shortened the amount of time it took for radiological findings to improve for all patients regardless of illness severity. [50][51][52] The commencement of the vaccination program also limited our access to patients. The first vaccination program for health-care providers was ongoing when the study started.…”

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confidence: 99%

Lack of Correlation Between Soluble Angiotensin-Converting Enzyme 2 and Inflammatory Markers in Hospitalized COVID-19 Patients with Hypertension

Louisa¹,

Cahyadi²,

Nilasari³

et al. 2022

IDR

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This study aimed to investigate the correlation of plasma soluble angiotensin-converting enzyme 2, sACE2, and several inflammatory markers in COVID-19 patients requiring hospitalization with hypertension. Additionally, we analyzed the effects of renin-angiotensin-aldosterone-system, RAAS, inhibitors on the levels of sACE2 and inflammatory marker levels in patients with COVID-19. Patients and Methods: This cross-sectional study involved patients with COVID-19 who required hospitalization on a stable dose of antihypertensive drugs. The study included three hospitals in Jakarta and Tangerang, Indonesia, between December 2020 and June 2021. We classified eligible subjects into two groups: patients with COVID-19 treated with antihypertensive RAAS inhibitors or non-RAAS inhibitors. Results: We found no correlation between sACE2 and all the inflammatory and coagulation markers studied (high-sensitivity C-reactive protein, IL-6, IL-10, IL6/IL10, tumor necrosis factor-α, neutrophil-to-lymphocyte ratio, and D-dimer) in COVID-19 patients with hypertension. Further analysis showed lower sACE2 concentrations and IL-6/IL-10 ratio in patients treated with RAAS inhibitors vs those treated with non-RAAS inhibitors. Conclusion:We found no correlation between ACE2 and inflammatory markers. Using RAAS inhibitors resulted in a lower sACE2 and IL-6/IL-10 ratio. The type of antihypertensive treatments has a neutral effect on disease severity and outcome in COVID-19 patients with hypertension. However, to firmly-established these effects, our findings should be confirmed in a much larger population.

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COVID-19 and corticosteroids: a narrative review

Cited by 45 publications

References 167 publications

Pathophysiology of Post-COVID syndromes: a new perspective

Pathophysiology of Post-COVID syndromes: a new perspective

The Synergistic Inhibition of Coronavirus Replication and Induced Cytokine Production by Ciclesonide and the Tylophorine-Based Compound Dbq33b

Lack of Correlation Between Soluble Angiotensin-Converting Enzyme 2 and Inflammatory Markers in Hospitalized COVID-19 Patients with Hypertension

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