Myeloid Neoplasm with t(8;22)(p11;q11): A Mimicker of Chronic Myeloid Leukaemia in Blast Crisis

Kapatia, Gargi; Remani, K. N.; Naseem, Shano; Parihar, Mayur; Sreedharanunni, Sreejesh

doi:10.1007/s12288-020-01343-3

Cited by 2 publications

(2 citation statements)

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“…To identify the cause and recognize any organ damage À Symptoms related to allergic disorders and family history of allergy HES secondary to allergy À Poor socioeconomic situation, poor nutrition and hygiene À Recent travel to tropical or endemic areas, exposure to pets, intake of undercooked meat or exotic dishes À Accidental ingestion/exposure to excreta of pets/insects À Drug intake (including indigenous drugs) with excess blasts need exclusion of myeloid and lymphoid neoplasms with rearrangement of PDGFRA, PDGFRB, FGFR1, JAK2, or other tyrosine kinase domain fusions. 6,31,32 Patients with B lineage ALL also need exclusion of IL3::IGH translocation, where reactive HE occurs as a secondary phenomenon. 33 Other findings which support the diagnosis of neoplastic HE/HES includes spindle shaped mast cell more than 25% (systemic mastocytosis with HE), loose (PDGFRA associated HE) or tight clusters of mast cells (systemic mastocytosis with HE), myelofibrosis and myeloid or megakaryocytic dysplasia 34 (►Fig.…”

Section: Medical Historymentioning

confidence: 99%

“…30 Patients with excess blasts need exclusion of myeloid and lymphoid neoplasms with rearrangement of PDGFRA, PDGFRB, FGFR1, JAK2, or other tyrosine kinase domain fusions. 6 31 32 Patients with B lineage ALL also need exclusion of IL3::IGH translocation, where reactive HE occurs as a secondary phenomenon. 33…”

Section: Diagnostic Approach To Eosinophilic Disorders 7 22 2...mentioning

confidence: 99%

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Laboratory Workup of Hypereosinophilia

Sundaresan

Sreedharanunni

2023

Indian J Med Paediatr Oncol

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Hypereosinophilia (HE) can be caused by a wide variety of non-hematologic (secondary or reactive) and hematologic (primary, clonal) disorders. Diagnosing hypereosinophilia/hypereosinophilic syndrome (HE/HES) is challenging due to the complex nature of disease manifestations and numerous underlying etiologies. Knowing that only rare cases are clonal, it is wise to rule out reactive conditions and proceed with molecular and other advanced tools. The exclusion of secondary causes needs a detailed clinical evaluation followed by a wide range of serological and imaging investigations. Once reactive eosinophilia has been ruled out, the diagnosis of primary HE/HES is made using a combination of morphologic examination of the blood and bone marrow, conventional cytogenetics, fluorescent in situ hybridization, flow-cytometry, and T-cell clonality evaluation to look for histopathologic or clonal evidence of an underlying hematological disorder. The accurate diagnosis of clonal eosinophilia-causing myeloid and lymphoid neoplasms and the identification of numerous gene rearrangements significantly enhance patient outcomes, because a proportion of these patients (such as PDGFRA and PDGFRB rearrangements) responds well to tyrosine kinase inhibitors. Considering the complex etiopathologies, the cost of testing, and the time involved, the workup needs to be tailored according to the urgency of the situation and the resources available. In urgent situations with organ damage, it is crucial to initiate appropriate management without waiting for the results of investigations. In contrast, in a resource-limited situation, it is acceptable to employ step-by-step rather than comprehensive testing to rule out the most common causes first. Here, we discuss various laboratory investigations employed in diagnosing HE/HES, highlighting their importance in different situations.

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