Hypereosinophilia in acute B‐lineage lymphoblastic leukaemia

Girodon, François; Bergoin, E.; Favre, Bernardine; Martha, Sandrine-Anne; Mugneret, Francine; Couillault, G.; Carli, Paule‐Marie; Maynadié, Marc

doi:10.1111/j.1365-2141.2005.05469.x

Cited by 11 publications

(13 citation statements)

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“…We point out that persistent hypereosinophilia may occur together with ALL also in the absence of anemia, thrombocytopenia and leukocytosis, thus requiring appropriate investigation, including bone marrow aspirate [20]. …”

Section: Discussionmentioning

confidence: 99%

Hypereosinophilia in childhood acute lymphoblastic leukaemia at diagnosis: report of 2 cases and review of the literature

et al. 2014

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Hypereosinophilia as first clinical presentation has rarely been reported in paediatric acute lymphoblastic leukaemia. It is commonly associated with specific cytogenetic abnormalities. Although eosinophilia is considered a reactive, non-neoplastic epiphenomenon, it adversely affects patient outcomes, both in children and adults. We describe herewith two paediatric patients who had marked eosinophilia at onset of acute lymphoblastic leukaemia. We point out the importance of a correct differential diagnosis in persistent, unexplained peripheral hypereosinophilia. Clinicians should keep in mind that eosinophilia can be part of the overall pattern of acute leukaemia and therefore needs to be properly investigated. We also provide some recommendations for an appropriate approach to hypereosinophilia - related morbidities.

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Section: Discussionmentioning

confidence: 99%

Hypereosinophilia in childhood acute lymphoblastic leukaemia at diagnosis: report of 2 cases and review of the literature

et al. 2014

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“…40,41 Eosinophilia in B-Cell and T-Cell Neoplasms.-Eosinophilia may also be associated with a variety of Bcell and T-cell neoplasms. [42][43][44][45][46][47][48][49][50] B-cell lymphoblastic leukemia (BLL) with eosinophilia is one such example. It is often associated with a characteristic cytogenetic abnormality t(5;14), which juxtaposes the IL3 gene on chromosome 5 to the immunoglobulin heavy chain locus (IgH) on chromosome 14.…”

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confidence: 99%

“…It is often associated with a characteristic cytogenetic abnormality t(5;14), which juxtaposes the IL3 gene on chromosome 5 to the immunoglobulin heavy chain locus (IgH) on chromosome 14. [43][44][45] These cases are recognized in the 2008 WHO classification as B lymphoblastic leukemia with t(5;14); IL3-IgH.'' 51 This rearrangement implies a ''reactive'' eosinophilia, in which increased IL-3 expression by malignant, lymphoblastic clones provides a paracrine signal, driving polyclonal expansion of the eosinophils.…”

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confidence: 99%

“…51 This rearrangement implies a ''reactive'' eosinophilia, in which increased IL-3 expression by malignant, lymphoblastic clones provides a paracrine signal, driving polyclonal expansion of the eosinophils. [43][44][45] Case reports have documented other chromosomal aberrations in BLL with eosinophilia. [47][48][49][50] In some cases, the same cytogenetic changes are found in cases of BLL without eosinophilia, making it unclear whether the association is diagnostically or clinically meaningful.…”

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confidence: 99%

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Diagnostic Complexities of Eosinophilia

Montgomery

Dunphy

Mooberry

et al. 2013

Archives of Pathology &Amp; Laboratory Medicine

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Context.— The advent of molecular tools capable of subclassifying eosinophilia has changed the diagnostic and clinical approach to what was classically called hypereosinophilic syndrome. Objectives.— To review the etiologies of eosinophilia and to describe the current diagnostic approach to this abnormality. Data Sources.— Literature review. Conclusions.— Eosinophilia is a common, hematologic abnormality with diverse etiologies. The underlying causes can be broadly divided into reactive, clonal, and idiopathic. Classically, many cases of eosinophilia were grouped together into the umbrella category of hypereosinophilic syndrome, a clinical diagnosis of exclusion. In recent years, an improved mechanistic understanding of many eosinophilias has revolutionized the way these disorders are understood, diagnosed, and treated. As a result, specific diagnoses can now be assigned in many cases that were previously defined as hypereosinophilic syndrome. Most notably, chromosomal rearrangements, such as FIP1L1-PDGFRA fusions caused by internal deletions in chromosome 4, are now known to be associated with many chronic eosinophilic leukemias. When present, these specific molecular abnormalities predict response to directed therapies. Although an improved molecular understanding is revolutionizing the treatment of patients with rare causes of eosinophilia, it has also complicated the approach to evaluating and treating eosinophilia. Here, we review causes of eosinophilia and present a framework by which the practicing pathologist may approach this diagnostic dilemma. Finally, we consider recent cases as clinical examples of eosinophilia from a single institution, demonstrating the diversity of etiologies that must be considered.

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“…Consequently, we screened the database of FRALLE 2000 French ALL treatment study (2000-2010) and launched a call within the GFCH (Groupe Francophone de Cytogénétique Hématologique) for patients with B-ALL presenting with t(5;14)(q31;q32). Four other cases were retrieved including a recently relapsed case previously reported at diagnosis (14) and one published very recently (15). All these 6 patients were diagnosed between 2004 and 2016 and were treated according to national protocols (FRALLE 2000 for the 4 pediatric patients, GRAALL 05 and 14 for the 2 adult patients).…”

Section: Patientsmentioning

confidence: 99%