Acute Gouty Arthritis During Favipiravir Treatment for Coronavirus Disease 2019

Hase, Ryota; Kurata, Rika; Ishida, Keiko; Kurita, Takashi; Muranaka, Emiri; Mito, Haruki

doi:10.2169/internalmedicine.5377-20

Cited by 17 publications

(15 citation statements)

References 6 publications

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“…Emotional stress [ 79 ], fasting [ 75 ], or dehydration [ 80 ] caused by physical activity can also increase the concentration of SUA. Although occasionally an acute gout flare may be linked with the medication(s) or condition(s), the enhanced SUA should be only temporarily sustained and a gout flare is considered unlikely to occur if a longer duration and higher dose treatment are avoided [ 81 ]. This may match with the fact that most gout patients do not know the trigger(s) of their gout flares [ 82 ].…”

Section: The Causes Of Hyperuricemia Irrelevant To Goutmentioning

confidence: 99%

Why Does Hyperuricemia Not Necessarily Induce Gout?

Zhang

2021

Biomolecules

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Hyperuricemia is a risk factor for gout. It has been well observed that a large proportion of individuals with hyperuricemia have never had a gout flare(s), while some patients with gout can have a normuricemia. This raises a puzzle of the real role of serum uric acid (SUA) in the occurrence of gout flares. As the molecule of uric acid has its dual effects in vivo with antioxidant properties as well as being an inflammatory promoter, it has been placed in a delicate position in balancing metabolisms. Gout seems to be a multifactorial metabolic disease and its pathogenesis should not rely solely on hyperuricemia or monosodium urate (MSU) crystals. This critical review aims to unfold the mechanisms of the SUA role participating in gout development. It also discusses some key elements which are prerequisites for the formation of gout in association with the current therapeutic regime. The compilation should be helpful in precisely fighting for a cure of gout clinically and pharmaceutically.

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Section: The Causes Of Hyperuricemia Irrelevant To Goutmentioning

confidence: 99%

Why Does Hyperuricemia Not Necessarily Induce Gout?

Zhang

2021

Biomolecules

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“…Elevation of serum UA levels has also been reported in several clinical trials of FVP against COVID-19 (Doi et al, 2020, Udwadia et al, 2021, Zhao et al, 2021. Furthermore, a COVID-19 patient with history of hyperuricemia developed acute gouty arthritis upon receiving FVP (Hase et al, 2020). We previously conducted a randomized, multi-center open-label clinical trial of FVP against COVID-19.…”

Section: Introductionmentioning

confidence: 99%

Baseline uric acid levels and steady-state favipiravir concentrations are associated with occurrence of hyperuricemia among COVID-19 patients

Koseki

Nakajima

Iwasaki

et al. 2022

International Journal of Infectious Diseases

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Objectives Favipiravir is an antiviral which is being evaluated for the treatment of COVID-19. Use of favipiravir is associated with elevation of serum uric acid levels. Risk factors for the occurrence of hyperuricemia are unclear. Methods Specimens from patients who received 10 days of favipiravir in a previous clinical trial (jRCTs041190120) were used. Serum favipiravir concentrations were measured by LC-MS. Factors associated with development of hyperuricemia were investigated by the logistic regression analysis. Optimal cut-off values for the baseline serum uric acid levels and steady-state serum favipiravir concentrations in predicting the occurrence of hyperuricemia were determined by ROC curve analysis. Results Among 66 COVID-19 patients who were treated with favipiravir for 10 days, the steady-state serum favipiravir concentrations were significantly correlated with serum uric acid levels. High baseline serum uric acid levels and steady-state serum favipiravir concentrations during therapy were factors associated with the development of hyperuricemia. The cut‑off baseline serum uric acid level and steady-state serum favipiravir concentration during favipiravir administration to predict hyperuricemia were 3.7 mg/dL and 46.14 μg/mL, respectively. Conclusions Patients who have high baseline serum uric acid levels or achieve high steady-state serum favipiravir concentrations during therapy are susceptible to hyperuricemia.

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“…A case of increased uric acid levels and acute gouty arthritis after commencement of favipiravir treatment was reported in a patient with SARS-CoV-2 infection. The mechanism behind hyperuricemia could be inhibitory action on urate excretion transporters like organic anion transporter (OAT1) and OAT3, by favipiravir and favipiravir hydroxide, that prompted reduced uric acid secretion from tubules, as well as the increased reabsorption of uric acid via urate transporter by favipiravir hydroxide, altogether leading to a fall in the excretion of uric acid [36]. Similar results were observed in a randomized, comparative, open-label, multicenter, phase 3 clinical trial assessing the efficacy and safety of favipiravir in patients with mild to moderate COVID-19 illness.…”

Section: Favipiravirmentioning

confidence: 99%

Safety profile of COVID-19 drugs in a real clinical setting

Chiu

Bhardwaj

Sah

2022

Eur J Clin Pharmacol

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Purpose The coronavirus disease 2019 caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus has affected millions all over the world and has been declared pandemic, as of 11 March 2020. In addition to the ongoing research and development of vaccines, there is still a dire need for safe and effective drugs for the control and treatment against the SARS-CoV-2 virus infection. Numerous repurposed drugs are under clinical investigations whose reported adverse events can raise worries about their safety. The aim of this review is to illuminate the associated adverse events related to the drugs used in a real COVID-19 setting along with their relevant mechanism(s). Method Through a literature search conducted on PubMed and Google Scholar database, various adverse events suspected to be induced by eight drugs, including dexamethasone, hydroxychloroquine, chloroquine, remdesivir, favipiravir, lopinavir/ ritonavir, ivermectin, and tocilizumab, administered in COVID-19 patients in clinical practice and studies were identified in 30 case reports, 3 case series, and 10 randomized clinical trials. Results Mild, moderate, or severe adverse events of numerous repurposed and investigational drugs caused by various factors and mechanisms were observed. Gastrointestinal side effects such as nausea, abdominal cramps, diarrhea, and vomiting were the most frequently followed by cardiovascular, cutaneous, and hepatic adverse events. Few other rare adverse drug reactions were also observed. ConclusionIn light of their ineffectiveness against COVID-19 as evident in large clinical studies, drugs including hydroxychloroquine, lopinavir/ritonavir, and ivermectin should neither be used routinely nor in clinical studies. While lack of sufficient data, it creates doubt regarding the reliability of chloroquine and favipiravir use in COVID-19 patients. Hence, these two drugs can only be used in clinical studies. In contrast, ample well-conducted studies have approved the use of remdesivir, tocilizumab, and dexamethasone under certain conditions in COVID-19 patients. Consequently, it is significant to establish a strong surveillance system in order to monitor the proper safety and toxicity profile of the potential anti-COVID-19 drugs with good clinical outcomes.

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Acute Gouty Arthritis During Favipiravir Treatment for Coronavirus Disease 2019

Cited by 17 publications

References 6 publications

Why Does Hyperuricemia Not Necessarily Induce Gout?

Why Does Hyperuricemia Not Necessarily Induce Gout?

Baseline uric acid levels and steady-state favipiravir concentrations are associated with occurrence of hyperuricemia among COVID-19 patients

Safety profile of COVID-19 drugs in a real clinical setting

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