Alfa‐interferon in a Case of Hypereosinophilic Syndrome

Murphy, Philip; Fennelly, David; Stuart, M J; O’Donnell, J. R.

doi:10.1111/j.1365-2141.1990.tb07811.x

Cited by 52 publications

(12 citation statements)

References 6 publications

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“…However, most patients relapse during the steroid taper and often require additional drug therapy. In this regard, interferon-α is currently considered the second-line treatment of choice based on numerous reports of well-documented long-lasting remissions in the majority of treated patients [91,92,93,94,95,96,97,98,99,100,101,102,103,104]. A starting dose of interferon-α between 1 and 3 million units given subcutaneously 3 times per week is recommended and the dose can be increased or decreased depending on drug side effects as well as response [94, 100, 105].…”

Section: Hypereosinophilic Syndromementioning

confidence: 99%

Modern Diagnosis and Treatment of Primary Eosinophilia

Tefferi

2005

Acta Haematol

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The recent discovery of an eosinophilia-specific, imatinib-sensitive, karyotypically occult but fluorescence in situ hybridization-apparent molecular lesion in a subset of patients with blood eosinophilia has transformed the diagnostic as well as treatment approach to eosinophilic disorders. Primary (i.e. nonreactive) eosinophilia is considered either ‘clonal’ or ‘idiopathic’ based on the presence or absence, respectively, of either a molecular or bone marrow histological evidence for a myeloid neoplasm. Clonal eosinophilia might accompany a spectrum of clinicopathological entities, the minority of whom are molecularly characterized; Fip1-like-1-platelet-derived growth factor receptor α (FIP1L1-PDGFRA⁺) systemic mastocytosis, platelet-derived growth factor receptor β (PDGFRB)-rearranged atypical myeloproliferative disorder, chronic myeloid leukemia, and the 8p11 syndrome that is associated with fibroblast growth factor receptor 1 (FGFR1) rearrangement. Hypereosinophilic syndrome (HES) is a subcategory of idiopathic eosinophilia and is characterized by an absolute eosinophil count of ≧1.5 × 10⁹/l for at least 6 months as well as eosinophil-mediated tissue damage. At present, a working diagnosis of primary eosinophilia mandates a bone marrow examination, karyotype analysis, and additional molecular studies in order to provide the patient with accurate prognostic information as well as select appropriate therapy. For example, the presence of either PDGFRA or PDGFRB mutations warrants the use of imatinib in clonal eosinophilia. In HES, prednisone, hydroxyurea, and interferon-α constitute first-line therapy, whereas imatinib, cladribine, and monoclonal antibodies to either interleukin-5 (mepolizumab) or CD52 (alemtuzumab) are considered investigational. Allogeneic transplantation offers a viable treatment option for drug-refractory cases.

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Section: Hypereosinophilic Syndromementioning

confidence: 99%

Modern Diagnosis and Treatment of Primary Eosinophilia

Tefferi

2005

Acta Haematol

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“…Recent studies indicate that some hypereosinophilic syndromes may be due to a clonal proliferation of abnormal cells [6]. IFN alpha has been found effective in patients with hypereosinophilic syndromes who were resistant to glucocorticoids and hydroxyurea [4,5,7,12,16]. Some beneficial activity of IFN has been reported in patients with myeloproliferative variants of the hypereosinophilic syndrome [8,10].…”

Section: Discussionmentioning

confidence: 99%

Complete haematological and cytogenetic response to interferon alpha-2a of a myeloproliferative disorder with eosinophilia associated with a unique t(4;7) aberration

Schöffski¹,

Ganser²,

Pascheberg

et al. 2000

Annals of Hematology

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A female patient with eosinophilia and cardiac symptoms was found to have a unique chromosomal aberration [t(4;7)(q11;p13)] of bone-marrow precursors. The disorder was classified as a chronic myeloproliferative syndrome with eosinophilia. Due to a significant increase in the white blood cell and eosinophil count during initial treatment with prednisone and hydroxyurea, Interferon alpha-2a was administered at a dose of 3-5 x 10(6) I.U. s.c., five times per week, and induced a long-term complete haematological and cytogenetic response. The clinical features of this case are presented and discussed in the context of the current literature.

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“…IFN-α , administered at a starting dose 3 million units three times weekly, has proved very effective for patients exhibiting resistance to corticosteroid therapy as well as for those who develop deleterious side effects resulting from prolonged steroid administration [24][25][26][27] . IFN-α has been associated with prolonged hematologic and cytogenetic remissions, and significant improvement in symptoms and organomegaly, in patients refractory to corticosteroids and hydroxycarbamide [24,28,29] .…”

Section: Interferon-alphamentioning

confidence: 99%

Therapeutic options for patients with clonal and idiopathic hypereosinophia

Quintás‐Cardama

Cortés

2008

Expert Opinion on Investigational Drugs

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Background : The hypereosinophilic syndrome (HES) comprises a heterogeneous group of disorders characterized by chronic, unexplained hypereosinophilia with organ involvement. The discovery of novel molecular targets has changed the therapeutic paradigm in HES. Objective : This article reviews the current medical management of patients with clonal and idiopathic hypereosinophilia with a particular emphasis on emerging new targeted therapies. Methods : The information contained in this review was obtained from public sources such as journals and scientific meeting abstracts. The opinions expressed in this review are solely those of the authors. Results/Conclusion : The development of imatinib-resistant mutations in the FIP1L1-PDGFR-α kinase domain has spurred the development of an array of new tyrosine kinase inhibitors. Moreover, the elucidation of the role of interleukin-5 in the pathogenesis of the lymphocytic variant of HES and the fact that CD52 is expressed on the surface of eosinophils and T cells have led to the clinical use of monoclonal antibodies such as mepolizumab, reslizumumab, and alemtuzumab for the treatment of different forms of hypereosinophilia.

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Alfa‐interferon in a Case of Hypereosinophilic Syndrome

Cited by 52 publications

References 6 publications

Modern Diagnosis and Treatment of Primary Eosinophilia

Modern Diagnosis and Treatment of Primary Eosinophilia

Complete haematological and cytogenetic response to interferon alpha-2a of a myeloproliferative disorder with eosinophilia associated with a unique t(4;7) aberration

Therapeutic options for patients with clonal and idiopathic hypereosinophia

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