A Multidisciplinary Approach to Eosinophilic Myocarditis

McDermott, Jaime; Thompson, Shelley L.; Landa, Rio

doi:10.1016/s0735-1097(21)03222-8

Cited by 1 publication

(1 citation statement)

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“…Importantly, cases reported by Eger et al [77] highlight the importance of considering the blood eosinophil count in asthmatics who switch from an anti-IL-5/5Ra agent to an anti-IL-4/13 agent. Hypereosinophilia with systemic clinical manifestations may develop if treatment does not focus on appropriate control of blood eosinophil levels, as anti-IL-5/5Ra agents and corticosteroids do [77][78][79]. These observations support the indication for dual therapy with anti-IL-5 agents and dupilumab in this clinical scenario, as suggested by Eger et al and supported by Descamps et al [74].…”

Section: Symptomatic Hypereosinophilia Induced By Dupilumab: Case Rep...mentioning

confidence: 65%

Eosinophilia Induced by Blocking the IL-4/IL-13 Pathway: Potential Mechanisms and Clinical Outcomes

Olaguíbel¹,

Sastre²,

Rodríguez³

et al. 2022

J Investig Allergol Clin Immunol

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Currently, five biological drugs for uncontrolled severe asthma treatment are marketed. They all block type 2 inflammatory pathways, either by targeting IgE (omalizumab), the IL-5 pathway (mepolizumab, reslizumab, benralizumab), or the IL-4/13 pathway (dupilumab). Hypereosinophilia has been observed in between 4% and 25% of patients treated with dupilumab, being transient in most cases, but persistent cases of symptomatic hypereosinophilia consistent with eosinophil granulomatosis with polyangiitis (EGPA), eosinophilic pneumonia, eosinophilic vasculitis or sudden worsening of asthma symptoms have been described. Cases of EGPA have been described with all biologics, including anti-IL-5, and with leukotriene receptors antagonists in publications or in the Eudravigilance database. In many cases of EGPA, it appears during systemic steroids tapering or after switching from an anti-IL-5 biologic to Dupilumab, suggesting that systemic steroids or the anti IL-5 were masking the vasculitis. This review aims to substantiate the plausible mechanisms of dupilumab-induced hypereosinophilia and review symptomatic hypereosinophilia cases associated with dupilumab therapy. Blockade of the IL-4/IL-13 pathway cause a reduction of eosinophil migration and blood accumulation by inhibiting eotaxin-3, VCAM-1, and TARC without simultaneously inhibiting eosinophilopoiesis in the bone marrow. When choosing the optimal biologic, it seems necessary to consider the presence of hypereosinophilia (>1,500/mL), where an anti-IL-5/IL-5R is preferable. Also, when changing from an anti-IL-5/5R to an anti-IL-4/13R. Close monitoring of blood eosinophils and clinical evolution seems justified in these situations. Nevertheless, dual therapy with anti-IL-5/5R and anti-IL4/IL-13R may be needed for optimal control since both IL-5, and IL-4/13 pathways can simultaneously contribute to airway inflammation.

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