Hypereosinophilic syndrome: diagnosis and treatment

Peroš-Golubičić, Tatjana; Smojver-Ježek, Silvana

doi:10.1097/mcp.0b013e3281eb8eb8

Cited by 10 publications

(4 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Immunophenotype, T-cell clonal and cytogenetic studies, and molecular analyses to detect Fip1-like 1 (FIP1L1)-platelet-derived growth factor receptor-a (PDGFRA) gene fusion should therefore probably be performed for every patient suspected of having CSS, at least those who are ANCA-negative and/or without histologically proven vasculitis, to detect myeloid neoplasms associated with eosinophilia and abnormalities of PDGFRA, platelet-derived growth factor receptor b (PDGFRB) or fibroblast growth factor receptor 1 (FGFR1) [65][66][67][68][69][70]. Analysis of cytokine profiles of T-cell subsets, including eosinophilopoietic (IL-3 and granulocyte-macrophage colony-stimulating factor) and/ or Th2 type cytokines (IL-4, IL-5, IL-13), measurement of serum tryptase, and cytogenetic analysis focusing on imatinib targeted tyrosine kinases can be done in some specialized centers to identify lymphocytic-HES, characterized by chronic reactive polyclonal hypereosinophilia secondary to IL-5 overproduction by T cells [71].…”

Section: Potential Clinical Overlap With Hypereosinophilic Syndromesmentioning

confidence: 99%

Churg–Strauss syndrome: evidence for disease subtypes?

Pagnoux

Guillevin

2010

Current Opinion in Rheumatology

115

View full text Add to dashboard Cite

Because of its practical and therapeutic repercussions, the priority remains the prompt, relatively easy identification of the most severely affected patients at CSS diagnosis, before searching for and trying to classify subsets. Large, collaborative studies are needed to determine whether other subgroups might be associated with outcomes and warrant different, and possibly new, therapeutic strategies.

show abstract

Section: Potential Clinical Overlap With Hypereosinophilic Syndromesmentioning

confidence: 99%

Churg–Strauss syndrome: evidence for disease subtypes?

Pagnoux

Guillevin

2010

Current Opinion in Rheumatology

115

View full text Add to dashboard Cite

show abstract

“…Hyper‐eosinophilic syndrome : HES is a continuum of heterogeneous diseases in which end‐organ tissue damage coexists with prolonged, elevated blood eosinophil counts (>1.5 × 10 9 cells/L), and for which other eosinophilic disorders have been ruled out .…”

Section: Interleukin‐5 As Mediator Of Homeostasis and Diseasementioning

confidence: 99%

Molecular and clinical rationale for therapeutic targeting of interleukin‐5 and its receptor

Molfino¹,

Gossage²,

Kolbeck³

et al. 2011

Clin Experimental Allergy

190

138

View full text Add to dashboard Cite

Interleukin-5 is a Th2 homodimeric cytokine involved in the differentiation, maturation, migration, development, survival, trafficking and effector function of blood and local tissue eosinophils, in addition to basophils and mast cells. The IL-5 receptor (IL-5R) consists of an IL-5-specific α subunit that interacts in conformationally dynamic ways with the receptor's βc subunit, an aggregate of domains it shares with binding sites of IL-3 and granulocyte-macrophage colony-stimulating factor. IL-5 and IL-5R drive allergic and inflammatory immune responses characterizing numerous diseases, such as asthma, atopic dermatitis, chronic obstructive pulmonary disease, eosinophilic gastrointestinal diseases, hyper-eosinophilic syndrome, Churg-Strauss syndrome and eosinophilic nasal polyposis. Although corticosteroid therapy is the primary treatment for these diseases, a substantial number of patients exhibit incomplete responses and suffer side-effects. Two monoclonal antibodies have been designed to neutralize IL-5 (mepolizumab and reslizumab). Both antibodies have demonstrated the ability to reduce blood and tissue eosinophil counts. One additional monoclonal antibody, benralizumab (MEDI-563), has been developed to target IL-5R and attenuate eosinophilia through antibody-dependent cellular cytotoxicity. All three monoclonal antibodies are being clinically evaluated. Antisense oligonucleotide technology targeting the common βc IL-5R subunit is also being used therapeutically to inhibit IL-5-mediated effects (TPI ASM8). Small interfering RNA technology has also been used therapeutically to inhibit the expression of IL-5 in animal models. This review summarizes the structural interactions between IL-5 and IL-5R and the functional consequences of such interactions, and describes the pre-clinical and clinical evidence supporting IL-5R as a therapeutic target.

show abstract

“…More detailed examination allowed them to diagnose a T-cell pleomorphic lymphoma. Sometimes peripheral eosinophilia is present in patients with benign clonal T-cell population that produce high levels of IL-5 (15,16). Our patient did not present clonality of circulating lymphocytes.…”

Section: Discussionmentioning

confidence: 68%

Pachydermatous eosinophilic dermatitis

Salomon

Białynicki‐Birula²,

Woźniak³

et al. 2017

Journal of the American Academy of Dermatology

View full text Add to dashboard Cite

SUMMARY A case is presented of a female Caucasian patient with chronic peripheral blood eosinophilia and unusual skin manifestations. Within a couple of years, the patient developed multiple hyperkeratotic and hyperpigmented papules and plaques all over the body, palmoplantar keratoderma, pachydermia of acral parts of the body, and generalized pruritus. Generalized lymphadenopathy appeared. Other relevant symptoms were persistent peripheral blood hypereosinophilia and increased level of total IgE. The patient was diagnosed with a very rare condition, pachydermatous eosinophilic dermatitis, and was administered combined therapy with dapsone, oral methylprednisolone and fexophenadine. After one month of treatment, the skin changes markedly improved.

show abstract

Hypereosinophilic syndrome: diagnosis and treatment

Cited by 10 publications

References 42 publications

Churg–Strauss syndrome: evidence for disease subtypes?

Churg–Strauss syndrome: evidence for disease subtypes?

Molecular and clinical rationale for therapeutic targeting of interleukin‐5 and its receptor

Pachydermatous eosinophilic dermatitis

Contact Info

Product

Resources

About