Löffler’s Endomyocardial Fibrosis With Eosinophilia in Association With Acute Lymphoblastic Leukemia

Blatt, Philip M.; Rothstein, Gerald; Miller, H; Cathey, William J.

doi:10.1182/blood.v44.4.489.489

Cited by 42 publications

(5 citation statements)

References 13 publications

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“…Cases of HE secondary to ALL are very rare. In addition to this child, only 61 patients <25 years (mean age 11 years) with HE and ALL have been described since 1973 to December 2017 ( Table 1 ) [ 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 ].…”

Section: Discussionmentioning

confidence: 99%

Acute Lymphoblastic Leukemia with Hypereosinophilia in a Child: Case Report and Literature Review

Ferruzzi

Santi

Gurdo

et al. 2018

IJERPH

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Background: Hypereosinophilia in children can be primary or secondary. Numerous malignant diseases can cause hypereosinophilia, but it is seldom caused by acute lymphoblastic leukemia (ALL). In the event of protracted hypereosinophilia, it is extremely important to make a correct differential diagnosis. Case presentation: We present the case of an 11-year-old boy of Moroccan origin with ALL with hypereosinophilic onset (eosinophils in peripheral blood, 10,000/µL) in the absence of other signs of neoplastic disease, and compare this case with 61 similar cases in the literature. Following hospital admission, the patient initially presented with headache-caused nocturnal awakenings, evening fever, and cough, and he also lost approximately 7 kg in weight in a month not associated with sweating or itching. We first performed bone marrow aspiration, which showed an increase in eosinophils without cellular morphological abnormalities, and bone marrow immunophenotyping showed that 4.5% of cells had a phenotype compatible with lymphoid blasts. A lumbar puncture was negative. Given the poor marrow involvement, it was necessary to repeat a new bone marrow aspiration two days later, which showed an increase in blasts to 14%. A concomitant bone marrow biopsy showed an infiltration of blasts typical of B-cell ALL equal to 20–30% with associated hypereosinophilia. Cytogenetic analysis showed an hyperdiploid karyotype: 53–55, XY, +X, add(1)(q21q25), +4, +9, +10, +14, +2, +1, +21/46, XY. Conclusions: ALL is one of the possible causes of persistent hypereosinophilia. In patients with ALL and hypereosinophilia, peripheral hypereosinophilia can precede the appearance of blasts. Due to the negative prognosis and the increased risk of complications in these patients, bone marrow aspiration and biopsy are recommended if common causes of secondary hypereosinophilia are excluded.

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Section: Discussionmentioning

confidence: 99%

Acute Lymphoblastic Leukemia with Hypereosinophilia in a Child: Case Report and Literature Review

Ferruzzi

Santi

Gurdo

et al. 2018

IJERPH

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“…The diagnosis of clonal eosinophilia requires the demonstration of either a cytogenetic/molecular marker of clonality or bone marrow histological features that are consistent with an otherwise classified myeloid malignancy. Examples of myeloid disorders that might be accompanied by clonal eosinophilia include both acute myeloid (AML) (Sanada et al , 1989) and lymphoblastic (ALL) (Blatt et al , 1974) leukaemias, chronic myeloid leukaemia (CML) (Keung et al , 2002), myelodysplastic syndrome (MDS) (Kuroda et al , 2000) and MPD (Bain, 2003).…”

Section: Clonal Eosinophiliamentioning

confidence: 99%

Eosinophilia: secondary, clonal and idiopathic

2006

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SummaryBlood eosinophilia signifies either a cytokine-mediated reactive phenomenon (secondary) or an integral phenotype of an underlying haematological neoplasm (primary). Secondary eosinophilia is usually associated with parasitosis in Third World countries and allergic conditions in the West. Primary eosinophilia is operationally classified as being clonal or idiopathic, depending on the respective presence or absence of a molecular, cytogenetic or histological evidence for a myeloid malignancy. The current communication features a comprehensive clinical summary of both secondary and primary eosinophilic disorders with emphasis on recent developments in molecular pathogenesis and treatment.

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“…The underlying pathogenesis of the hypereosinophilia associated with ALL is not clear, perhaps because no single mechanism is common to all cases. Whilst likely a reactive phenomenon, the consequences of the hypereosinophilia may be clinically significant with a risk of hypercoagulability and deposition of major basic protein causing tissue damage, classically resulting in Loeffler endocarditis . Identifying the underlying cause and understanding the mechanisms driving the secondary hypereosinophilia is therefore important, both in terms of managing the causation and limiting the sequelae.…”

Section: Introductionmentioning

confidence: 99%

Cutaneous B‐lymphoblastic lymphoma with IL3/IgH translocation presenting with hypereosinophilia and acute endocarditis

Bomken

Haigh

Bown

et al. 2014

Pediatric Blood & Cancer

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Hypereosinophilia is a rare phenomenon associated with childhood malignancy, predominantly acute lymphoblastic leukaemia. Causation is unclear and likely to have multiple mechanisms. We report a six year old boy presenting with hypereosinophilia and associated Loeffler endocarditis. Three months following his initial hypereosinophilia he developed cutaneous B-lymphoblastic lymphoma. Re-analysis of apparently uninvolved bone marrow, taken at initial presentation, revealed a single, previously unidentified, t(5;14)(q31;q32) positive cell. Using fluorescent in situ hybridisation, we demonstrate IL3/IgH@ fusion in cutaneous lymphoma cells. Our case confirms the association of hypereosinophilia and B-lymphoblastic lymphoma and strengthens the association between IL3 hypersecretion and hypereosinophilia.

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Löffler’s Endomyocardial Fibrosis With Eosinophilia in Association With Acute Lymphoblastic Leukemia

Cited by 42 publications

References 13 publications

Acute Lymphoblastic Leukemia with Hypereosinophilia in a Child: Case Report and Literature Review

Acute Lymphoblastic Leukemia with Hypereosinophilia in a Child: Case Report and Literature Review

Eosinophilia: secondary, clonal and idiopathic

Cutaneous B‐lymphoblastic lymphoma with IL3/IgH translocation presenting with hypereosinophilia and acute endocarditis

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