Can COVID-19 Be a Potential Risk Factor for Voriconazole-Induced Hyperkalemia?

Hmida, S. Ben; Bougharriou, I.; Chaabouni, H.; Ghozzi, H.; Zghal, K.; Benjemaa, M.

doi:10.21601/ejbms/11285

Cited by 1 publication

(1 citation statement)

References 15 publications

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“…However, there are contradicting findings on concurrent use of voriconazole and lopinavir/ritonavir, as some studies have found that the area under the concentration-time curve (AUC) and maximum concentration ( C max ) of voriconazole decreased; while, other studies have shown an unexpected increase in voriconazole concentration when co-administered with lopinavir/ritonavir in patients with COVID-19 [ 104 ]. Voriconazole can induce severe hyperkalaemia in patients with COVID-19 with severe inflammation, when serum voriconazole level was elevated or when voriconazole–drug interaction occurs [ 105 ]. Among the experimental COVID-19 therapies, voriconazole was found to interact with atazanavir and hydroxychloroquine [ 106 ].…”

Section: Drugs Used To Treat Covid-19mentioning

confidence: 99%

Role of Cytochrome P450 2C9 in COVID-19 Treatment: Current Status and Future Directions

Lim

Bishtawi

Lim

2023

Eur J Drug Metab Pharmacokinet

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The major human liver drug metabolising cytochrome P450 (CYP) enzymes are downregulated during inflammation and infectious disease state, especially during coronavirus disease 2019 (COVID-19) infection. The influx of proinflammatory cytokines, known as a ‘cytokine storm’, during severe COVID-19 leads to the downregulation of CYPs and triggers new cytokine release, which further dampens CYP expression. Impaired drug metabolism, along with the inevitable co-administration of drugs or ‘combination therapy’ in patients with COVID-19 with various comorbidities, could cause drug–drug interactions, thus worsening the disease condition. Genetic variability or polymorphism in CYP2C9 across different ethnicities could contribute to COVID-19 susceptibility. A number of drugs used in patients with COVID-19 are inducers or inhibitors of, or are metabolised by, CYP2C9, and co-administration might cause pharmacokinetic and pharmacodynamic interactions. It is also worth mentioning that some of the COVID-19 drug interactions are due to altered activity of other CYPs including CYP3A4. Isoniazid/rifampin for COVID-19 and tuberculosis co-infection; lopinavir/ritonavir and cobicistat/remdesivir combination therapy; or multi-drug therapy including ivermectin, azithromycin, montelukast and acetylsalicylic acid, known as TNR4 therapy, all improved recovery in patients with COVID-19. However, a combination of CYP2C9 inducers, inhibitors or both, and plausibly different CYP isoforms could lead to treatment failure, hepatotoxicity or serious side effects including thromboembolism or bleeding, as observed in the combined use of azithromycin/warfarin. Further, herbs that are CYP2C9 inducers and inhibitors, showed anti-COVID-19 properties, and in silico predictions postulated that phytochemical compounds could inhibit SARS-CoV-2 virus particles. COVID-19 vaccines elicit immune responses that activate cytokine release, which in turn suppresses CYP expression that could be the source of compromised CYP2C9 drug metabolism and the subsequent drug–drug interaction. Future studies are recommended to determine CYP regulation in COVID-19, while recognising the involvement of CYP2C9 and possibly utilising CYP2C9 as a target gene to tackle the ever-mutating SARS-CoV-2.

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Section: Drugs Used To Treat Covid-19mentioning

confidence: 99%