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<p>Temporal arteritis with marked eosinophilic infiltration is uncommon and can present as either a localized arteritis or a manifestation of systemic eosinophilic disease. We report a 48-year-old woman who presented with fatigue, intermittent fever, and bilateral painful cord-like swelling in the frontal region. Laboratory tests showed marked eosinophilia and elevated total IgE with mild inflammation, while anti-neutrophil cytoplasmic antibodies were negative. Biopsies of both superficial temporal arteries demonstrated transmural eosinophilic infiltration with disruption of the internal elastic lamina and intraluminal thrombosis without giant cells or granulomas. During follow-up, the patient developed hepatobiliary enzyme elevation, and biopsies of the esophagus, liver, and a breast mass confirmed eosinophilic infiltration. Bone marrow examination showed eosinophilic hyperplasia without evidence of a myeloproliferative neoplasm and no FIP1L1-PDGFRA fusion was detected. These findings supported a diagnosis of hypereosinophilic syndrome (HES) with temporal artery involvement. Prednisolone improved systemic symptoms, but temporal arteritis relapsed during tapering and was refractory to methotrexate. The addition of mepolizumab achieved sustained remission and enabled further glucocorticoid (GC) reduction. This case highlights that bilateral or GC-dependent eosinophilic temporal arteritis warrants evaluation for systemic eosinophilic disorders, and suggests that IL-5 blockade can be an effective GC-sparing strategy in HES.</p>

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Bilateral temporal arteritis with multiorgan eosinophilic infiltration treated with IL-5 targeted antibody

  • 期刊论文

  • 发表日期：

    2026年5月28日

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  • Kotomi Murata,
  • Tomonori Hishinuma,
  • Hiromitsu Asashima,
  • Haruka Miki,
  • Yuya Kondo,
  • Hiroto Tsuboi,
  • Isao Matsumoto

摘要

Temporal arteritis with marked eosinophilic infiltration is uncommon and can present as either a localized arteritis or a manifestation of systemic eosinophilic disease. We report a 48-year-old woman who presented with fatigue, intermittent fever, and bilateral painful cord-like swelling in the frontal region. Laboratory tests showed marked eosinophilia and elevated total IgE with mild inflammation, while anti-neutrophil cytoplasmic antibodies were negative. Biopsies of both superficial temporal arteries demonstrated transmural eosinophilic infiltration with disruption of the internal elastic lamina and intraluminal thrombosis without giant cells or granulomas. During follow-up, the patient developed hepatobiliary enzyme elevation, and biopsies of the esophagus, liver, and a breast mass confirmed eosinophilic infiltration. Bone marrow examination showed eosinophilic hyperplasia without evidence of a myeloproliferative neoplasm and no FIP1L1-PDGFRA fusion was detected. These findings supported a diagnosis of hypereosinophilic syndrome (HES) with temporal artery involvement. Prednisolone improved systemic symptoms, but temporal arteritis relapsed during tapering and was refractory to methotrexate. The addition of mepolizumab achieved sustained remission and enabled further glucocorticoid (GC) reduction. This case highlights that bilateral or GC-dependent eosinophilic temporal arteritis warrants evaluation for systemic eosinophilic disorders, and suggests that IL-5 blockade can be an effective GC-sparing strategy in HES.