Infliximab as a Therapy for Idiopathic Hypereosinophilic Syndrome

Taverna, Josephine A.; Lerner, Adam; Goldberg, Lynne J.; Werth, Stephen G.; Demierre, Marie‐France

doi:10.1001/archderm.143.9.1110

Cited by 8 publications

(4 citation statements)

References 18 publications

(21 reference statements)

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“…A recent case report documents the successful treatment of a patient with idiopathic HES with infliximab, a chimeric human‐mouse antibody for tumour necrosis factor. The exact mechanism of action in this context is unknown 14 …”

Section: Discussionmentioning

confidence: 99%

Isolated symptomatic cutaneous disease in hypereosinophilic syndrome

2010

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A 41-year-old Phillipino man presented with a 3-year history of a relapsing and remitting generalized chronic pruritic erythematous papular and plaque-like eruption. Investigations showed a persistently elevated eosinophil count. His disease was limited to cutaneous involvement with an absence of demonstrable internal organ involvement, despite extensive investigations and multidisciplinary review. Other causes of eosinophilia were excluded. A diagnosis of idiopathic hypereosinophilic syndrome was made. Our patient's presentation raises a number of issues related to hypereosinophilic syndrome. In particular, relating to managing hypereosinophilic syndrome and the challenge of minimizing therapy side-effects. Our case highlights the considerable morbidity of untreated isolated cutaneous disease, for which he was hospitalized with suicidal ideations. In a minority of reports, skin involvement is the only manifestation of hypereosinophilic syndrome.

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Section: Discussionmentioning

confidence: 99%

Isolated symptomatic cutaneous disease in hypereosinophilic syndrome

2010

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“…38 Golimumab Uveitis, 39 refractory juvenile idiopathic arthritis-associated uveitis. 40 Infliximab Pityriasis rubra pilaris, 30 idiopathic hypereosinophilic syndrome, 41 cachexia in advanced pancreatic cancer patients, 42 refractory retinal vasculitis due to sarcoidosis, 43 cardiac sarcoidosis, 44 Takayasu arteritis, 45 refractory dermatomyositis, 46 steroid-resistant graft-versus-host disease, 47 complex regional pain syndrome, 48 hidradenitis suppurativa, 49 pyoderma gangrenosum, 50 Behçet's disease, 51 childhood refractory chronic uveitis, 26 refractory neuro-Behçet. 52 Anakinra Colchicine-resistant familial Mediterranean fever, 53 Schnitzler's syndrome, 54 Muckle-Wells syndrome, 55 acute gout, 56 hidradenitis suppurativa.…”

Section: Agentmentioning

confidence: 99%

Informed consent and biological agents in rheumatology and internal medicine

Mandarelli

Iannone

Ferracuti

et al. 2022

Eur J Clin Investigation

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Background:The need for highly effective therapies in rheumatologic diseases has led to the widespread and growing use of a heterogeneous class of molecules called biological agents. The increasing experience with biological agents has raised concerns about safety and efficacy issues that need to be discussed in the informed consent acquisition process. Methods:The authors performed a review of the literature on biological agents focusing on their most important characteristics concerning the informed consent procedures. Results:No studies specifically addressed the issue of informed consent in patients receiving biological agents. Several studies reported data about off-label use of biological agents usually with no obvious attention to informed consent shortcomings. Conclusion:The reported association between biological agents and serious infections or malignancies, including reactivation of latent tuberculosis, needs specific disclosure in informed consent acquisition, together with information about the possible efficacy in clinical contexts often characterized by resistance to previous treatments. Ethical and clinical issues bound to the need for experimenting with new agents with potentially serious adverse effects deserve specific attention. Studies aimed at evaluating mental capacity to consent in subjects receiving biological agents are required.

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“…Other agents employed in the therapy of HES include alemtuzumab, a monoclonal antibody reactive with CD52 (Dearden et al , 2002) and infliximab, a monoclonal antibody reactive with tumour necrosis factor (TNF‐α) (Taverna et al , 2007). Alemtuzumab has been utilized with success in one patient with lymphocytic HES and a CD3 − CD4 + clone (Pitini et al , 2004) and another with HES of Undefined Complex variant (Sefcick et al , 2004).…”

Section: Treatment Of Hesmentioning

confidence: 99%

“…However, in the absence of carefully done clinical trials, its potential remains unknown. One patient with HES in the undefined/complex variant presenting with erythroderma responded to infliximab (Taverna et al , 2007).…”

Section: Treatment Of Hesmentioning

confidence: 99%

The hypereosinophilic syndromes: current concepts and treatments

2009

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SummaryThe hypereosinophilic syndromes (HES) encompass a spectrum of diseases that have increased blood eosinophils and tissue damage in common. The clinical manifestations are protean and may involve any organ system, but especially the skin. Our understanding of these diseases has drastically changed over the past 15 years, along with new classifications that characterize patients with marked eosinophilia. One HES variant, myeloproliferative, is actually chronic eosinophilic leukaemia with a unique genetic marker, FIP1L1-PDGFRA. Such patients are well-controlled by administration of the kinase inhibitor, imatinib, and remissions appear durable with continued imatinib therapy. FIP1L1-PDGFRA is expressed in several cell lineages, thus explaining increases in neutrophils and mast cells in HES. The lymphocytic HES variant is associated with T-cell clones producing interleukin-5 (IL-5) and can evolve into lymphoma. While myeloproliferative and lymphocytic HES are well established and permit elimination of the term, idiopathic, to these varieties, most HES patients do not fall into these categories and are classified as complex (using the 2006 Workshop Report). A recent study showed that a monoclonal antibody to IL-5, mepolizumab, reduced glucocorticoid therapy in HES patients who did not possess the FIP1L1-PDGFRA mutation while controlling eosinophilia and preventing recurrence or progression of tissue damage. These advances augur well for continued progress in the understanding and treatment of HES.

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Infliximab as a Therapy for Idiopathic Hypereosinophilic Syndrome

Cited by 8 publications

References 18 publications

Isolated symptomatic cutaneous disease in hypereosinophilic syndrome

Isolated symptomatic cutaneous disease in hypereosinophilic syndrome

Informed consent and biological agents in rheumatology and internal medicine

The hypereosinophilic syndromes: current concepts and treatments

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