Annales de biologie clinique · 2022
[Hematological hypereosinophilia].
СтатьяНазвание и аннотация: Перевод в очереди
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Ghariani Ines, Mahmoud Oumaima, Hamzaoui Saloua, Braham Néjia, Bekir Leila
Аннотация
INTRODUCTION: Hematological disorders are the third cause of hypereosinophilia, after allergic and parasitic disease. The objective of our study is to show the epidemiological, clinical, biological and therapeutic characteristics of hematological hypereosinophilia.
PATIENTS AND METHODS: This is a retrospective study over a 4-year period (March 2017-March 2021) concerning 14 patients with hematological hypereosinophilia.
RESULTS: Fourteen patients were included (9 women and 5 men). The median age at diagnosis was 55 years. Hematological hypereosinophilia was mainly of clonal etiology. Clinical manifestations were either specific to hypereosinophilia, such as organ damage, or related to the etiology of hypereosinophilia, such as hepato-splenomegaly and lymphadenopathy. Moderate and severe forms were the most commonly reported. Several other quantitative and qualitative abnormalities of the blood picture were reported. Identification of the FIP1L1-PDGFRA fusion gene by molecular biology (RT-PCR) was positive in two patients. Imatinib was the main treatment for clonal forms.
CONCLUSION: Hematological hypereosinophilia is a rare and complex pathology. Our study has confirmed this epidemiological, clinical, biological and therapeutic heterogeneity and has enabled us to realize the contribution of molecular biology in the diagnosis and the treatment of hypereosinophilia.
PATIENTS AND METHODS: This is a retrospective study over a 4-year period (March 2017-March 2021) concerning 14 patients with hematological hypereosinophilia.
RESULTS: Fourteen patients were included (9 women and 5 men). The median age at diagnosis was 55 years. Hematological hypereosinophilia was mainly of clonal etiology. Clinical manifestations were either specific to hypereosinophilia, such as organ damage, or related to the etiology of hypereosinophilia, such as hepato-splenomegaly and lymphadenopathy. Moderate and severe forms were the most commonly reported. Several other quantitative and qualitative abnormalities of the blood picture were reported. Identification of the FIP1L1-PDGFRA fusion gene by molecular biology (RT-PCR) was positive in two patients. Imatinib was the main treatment for clonal forms.
CONCLUSION: Hematological hypereosinophilia is a rare and complex pathology. Our study has confirmed this epidemiological, clinical, biological and therapeutic heterogeneity and has enabled us to realize the contribution of molecular biology in the diagnosis and the treatment of hypereosinophilia.