GM-CSF and Eosinophil Chemotactic Factors in an Acute Lymphoblastic Leukemia Patient with Eosinophilia

Kita, Ruka; Enokihara, H; Nagashima, Shigeki; Tsunogake, Satoshi; Yamato, Hajime; Saito, Kenji; Furusawa, Shinpei; Shishido, Hideo; Fukushima, Yasutsugu; Fukuda, Takeshi

doi:10.1159/000204396

Cited by 5 publications

(2 citation statements)

References 7 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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“…Several interesting cytogenetic changes have been associated with a subset of this disease [1,4,5] although in some cases, no cytogenetic abnormalities were detected [2,6]. It is possible that some of these cases represent reactive eosinophilia due to an as yet unidentified foreign antigen on leukemic cells.…”

Section: Introductionmentioning

confidence: 99%

Intense eosinophilia with abnormal ultrastructure as presenting manifestation of acute lymphoblastic leukemia

Ghosh¹,

Hiwase²,

Muirhead³

2000

Haematologia

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A patient with acute lymphoblastic leukemia presented with intense eosinophilia. Under the light microscope these eosinophils showed smaller eosinophilic granules and were detected as neutrophils by Coulter Gen-S cell counter. This counter identifies cell morphology by size and forward and right angle light scatter of cells. Under electron microscopy these eosinophils had smaller and fewer granules and very few crystalloid structures, thereby explaining the inability of the cell counter to identify them as eosinophils. Eosinophilia subsided at 6 months of treatment, i.e. 5 months after the patient went into morphological remission; cytogenetic and bone marrow analyses revealed no abnormality.

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Treatment of neoplastic meningeal xenografts by intraventricular administration of an antiganglioside monoclonal antibody, 3F8

et al. 1999

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GM-CSF and Eosinophil Chemotactic Factors in an Acute Lymphoblastic Leukemia Patient with Eosinophilia

Cited by 5 publications

References 7 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

Intense eosinophilia with abnormal ultrastructure as presenting manifestation of acute lymphoblastic leukemia

Treatment of neoplastic meningeal xenografts by intraventricular administration of an antiganglioside monoclonal antibody, 3F8

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