Severe hepatotoxicity as a rare side effect of anakinra in a patient with systemic JIA

Murray, Grainne M; Ng, S. K.; Johansen, Lauren; Ramanan, Athimalaipet V

doi:10.1093/rheumatology/keab202

Cited by 6 publications

(2 citation statements)

References 7 publications

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“…The mechanism of liver injury caused by ANK is unknown. A possible starting point for future research could be related to the IL-1 receptor antagonist (IL-1RN) and IL-1β polymorphism, which has already been associated with antiretroviral hepatotoxicity [ 32 , 33 ].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Drug-Induced Liver Injury in Hospitalized Patients with SARS-CoV-2 Infection

et al. 2022

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Elevated liver enzymes are frequently reported in SARS-CoV-2-infected patients. Several mechanisms of liver injury have been proposed, but no clear conclusions were drawn. We aimed to evaluate hepatocellular and cholestatic injury in relation to the administration of potentially hepatotoxic drugs included in the current COVID-19 therapeutic guidelines in a retrospective cohort of 396 hospitalized COVID-19 patients. The main findings of our study are: (1) Significant increase in aminotransferases level was observed during hospitalization, suggesting drug-related hepatotoxicity. (2) Tocilizumab was correlated with hepatocellular injury, including ALT values greater than five times the upper limit of normal. (3) Anakinra was correlated with ALT values greater than three times the upper limit of normal. (4) Younger patients receiving tocilizumab or anakinra had a higher risk of hepatocellular injury. (5) The combination of favipiravir with tocilizumab was associated with AST values greater than three times the upper limit of normal and with an increase in direct bilirubin. (6) The administration of at least three potentially hepatotoxic drugs was correlated with hepatocellular injury, including ALT values greater than five times the upper limit of normal, and with the increase in indirect bilirubin. (7) Remdesivir and favipiravir by themselves did not correlate with hepatocellular or cholestatic injury in our study cohort.

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Section: Discussionmentioning

confidence: 99%

Evaluation of Drug-Induced Liver Injury in Hospitalized Patients with SARS-CoV-2 Infection

et al. 2022

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“…Murray G.M. et al [ 14 ] reported a case of a 13-year-old boy with sJIA who was treated with pulsed intravenous MPDN and anakinra 3 mg/kg afterwards with prompt clinical improvement and laboratorial value normalization, with IL-1RA discontinuation after 10 days of treatment. Posteriorly, MAS led to reintroduction of anakinra, with severe elevation of hepatic enzymes 1 month later, with suspension of therapy leading to steadfast cessation of liver injury.…”

Section: Discussionmentioning

confidence: 99%

Anakinra and hepatotoxicity in pediatric rheumatology: a case series

Martins,

Azevedo,

Ganhão

et al. 2023

Pediatr Rheumatol

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Background Anakinra is a recombinant interleukin-1 (IL-1) receptor antagonist used in systemic juvenile idiopathic arthritis (sJIA), refractory Kawasaki disease (KD) and cryopyrin-associated autoinflammatory syndrome (CAPS). Anakinra associated hepatotoxicity, while rare, has been described in several cases in daily practice. In this case series the authors describe three pediatric patients with this side effect in the setting of severe macrophage activation syndrome (MAS) in KD and sJIA. Case presentation The first patient was a 12-year-old boy who presented with fever, maculo-papular exanthema and polyarthralgia. Tonsillitis, distal limb induration and tender cervical lymph nodes were observed. Erythrocyte-sedimentation rate (ESR), C-reactive protein (CRP), ferritin (11,975 ng/mL), D-dimers (5,98 mg/L FEU) and soluble CD25 (3645 pg/mL) levels were elevated. Exclusion of sepsis / toxic shock syndrome warranted introduction of IV methylprednisolone and immunoglobulin (IG IV), with partial response. A MAS secondary to KD was assumed, and anakinra 2 mg/kg/day was introduced. Twenty days later he developed new-onset nausea and severe cyto-cholestasis, normalizing after 2 months of drug discontinuation. Posterior onset of polyarthritis and evanescent lead to a final diagnosis of sJIA. The second patient was a 2-year-old boy with a 10-day history of fevers, generalized rash, hepatosplenomegaly and strawberry tongue. Leucocytosis with neutrophilia and elevated CRP were observed. Initial treatment with IVIG in the setting of incomplete KD was ineffective. Mild anaemia, leukopenia and very high serum ferritin (maximum 26,128 ng/mL) ensued. Presumptive sJIA associated MAS was treated with IV methylprednisolone and anakinra 2 mg/kg/day, with prompt response. Four weeks later transaminitis was detected, and temporary anakinra suspension led to normalisation of laboratorial values. The third case related to a 4-year-old boy presenting with fever, maculopapular rash and cervical lymphadenopathy. CRP and ESR were elevated, and KD was diagnosed. IVIG and methylprednisolone were initiated with clinical worsening, warranting for anakinra introduction at 2 mg/kg/day. After three weeks, liver enzymes progressively elevated, resolving on 2 weeks of anakinra discontinuation. Conclusions To the best of our knowledge, this is the first case series describing anakinra associated hepatotoxicity in pediatric patients with rheumatic diseases other than sJIA, bringing additional insight to therapeutic monitoring in patients undergoing this treatment.

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Anakinra

2021

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Severe hepatotoxicity as a rare side effect of anakinra in a patient with systemic JIA

Cited by 6 publications

References 7 publications

Evaluation of Drug-Induced Liver Injury in Hospitalized Patients with SARS-CoV-2 Infection

Evaluation of Drug-Induced Liver Injury in Hospitalized Patients with SARS-CoV-2 Infection

Anakinra and hepatotoxicity in pediatric rheumatology: a case series

Anakinra

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