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BMJ Case Rep. 2021 May 27;14(5):e242096. doi: 10.1136/bcr-2021-242096.
2
CHIC2 deletion, a surrogate for FIP1L1-PDGFRA fusion, occurs in systemic mastocytosis associated with eosinophilia and predicts response to imatinib mesylate therapy.CHIC2缺失作为FIP1L1-PDGFRA融合的替代指标，见于伴有嗜酸性粒细胞增多的系统性肥大细胞增多症，并可预测对甲磺酸伊马替尼治疗的反应。
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3
Detection of FIP1L1-PDGFRA fusion by FISH.通过荧光原位杂交检测FIP1L1-PDGFRA融合基因。
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4
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FIP1L1-PDGFRA positive chronic eosinophilic leukaemia and associated central nervous system involvement.FIP1L1-PDGFRA阳性慢性嗜酸性粒细胞白血病及相关中枢神经系统受累
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The hypereosinophilic syndrome: fluorescence in situ hybridization detects the del(4)(q12)-FIP1L1/PDGFRA but not genomic rearrangements of other tyrosine kinases.高嗜酸性粒细胞综合征：荧光原位杂交检测到del(4)(q12)-FIP1L1/PDGFRA，但未检测到其他酪氨酸激酶的基因组重排。
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Response to imatinib mesylate in patients with hypereosinophilic syndrome.甲磺酸伊马替尼治疗高嗜酸性粒细胞综合征患者的疗效。
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[Durable efficacity and remission after treatment with imatinib mesylate for FIP1L1-PDGFRA transcript negative associated eosinophilic cardiomyopathy].甲磺酸伊马替尼治疗FIP1L1-PDGFRA转录本阴性相关嗜酸性粒细胞性心肌病后的持久疗效与缓解
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本文引用的文献

1
Hypereosinophilic Syndrome, Multiorgan Involvement and Response to Imatinib.高嗜酸性粒细胞综合征、多器官受累及对伊马替尼的反应
Cureus. 2020 Jun 7;12(6):e8493. doi: 10.7759/cureus.8493.
2
World Health Organization-defined eosinophilic disorders: 2019 update on diagnosis, risk stratification, and management.世界卫生组织定义的嗜酸性粒细胞疾病：2019 年诊断、风险分层和管理更新。
Am J Hematol. 2019 Oct;94(10):1149-1167. doi: 10.1002/ajh.25617.
3
Hypereosinophilia: a diagnostic challenge.嗜酸性粒细胞增多症：一项诊断挑战。
Neth J Med. 2018 Dec;76(10):431-436.
4
Hypereosinophilic syndrome: a multicenter, retrospective analysis of clinical characteristics and response to therapy.嗜酸性粒细胞增多综合征：一项多中心回顾性分析临床特征和治疗反应。
J Allergy Clin Immunol. 2009 Dec;124(6):1319-25.e3. doi: 10.1016/j.jaci.2009.09.022.
5
Elevated serum levels of soluble interleukin-2 receptor in chronic eosinophilic leukemia/hypereosinophilic syndrome with FIP1L1-PDGFR alpha fusion gene.伴有FIP1L1-PDGFRα融合基因的慢性嗜酸性粒细胞白血病/高嗜酸性粒细胞综合征患者血清可溶性白细胞介素-2受体水平升高。
Int J Hematol. 2008 May;87(4):440-441. doi: 10.1007/s12185-008-0064-9.
6
Cough and hypereosinophilia due to FIP1L1-PDGFRA fusion gene with tyrosine kinase activity.具有酪氨酸激酶活性的FIP1L1-PDGFRA融合基因导致的咳嗽和嗜酸性粒细胞增多症。
Eur Respir J. 2006 Jan;27(1):230-2. doi: 10.1183/09031936.06.00089405.
7
A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome.一种由血小板衍生生长因子受体A（PDGFRA）基因与FIP1L1基因融合产生的酪氨酸激酶，作为伊马替尼治疗特发性嗜酸性粒细胞增多综合征的靶点。
N Engl J Med. 2003 Mar 27;348(13):1201-14. doi: 10.1056/NEJMoa025217.
8
Response of idiopathic hypereosinophilic syndrome to treatment with imatinib mesylate.甲磺酸伊马替尼治疗特发性高嗜酸性粒细胞综合征的疗效
Leuk Res. 2002 Sep;26(9):881-4. doi: 10.1016/s0145-2126(02)00046-2.
9
Treatment of hypereosinophilic syndrome with imatinib mesilate.甲磺酸伊马替尼治疗高嗜酸性粒细胞综合征
Lancet. 2002 May 4;359(9317):1577-8. doi: 10.1016/S0140-6736(02)08505-7.

哮喘和鼻炎患者的融合基因。

fusion gene in a patient with asthma and rhinitis.

机构信息

Department of Medicine, Nippon Life Hospital, Osaka, Osaka, Japan.

Department of Pathology, Nippon Life Hospital, Osaka, Osaka, Japan.

出版信息

BMJ Case Rep. 2021 May 27;14(5):e242096. doi: 10.1136/bcr-2021-242096.

DOI:10.1136/bcr-2021-242096
PMID:34045202
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8162092/
Abstract

Eosinophilia in asthma or rhinitis is usually considered to be reactive to the allergic diseases. We report a 33-year-old man with asthma and rhinitis, and progressive hypereosinophilia. Fluorescence in situ hybridization analysis detected interstitial chromosomal deletion at 4q12 in cells of the bone marrow. The patient was diagnosed as myeloproliferative neoplasm with a fusion gene, and successfully treated with the tyrosine kinase inhibitor, imatinib. Clonal expansion of eosinophils due to the fusion gene could underlie refractory mechanisms in patients with bronchial asthma or allergic rhinitis.

摘要

哮喘或鼻炎中的嗜酸性粒细胞增多通常被认为是对过敏性疾病的反应。我们报告了一例 33 岁的男性哮喘和鼻炎患者，伴有进行性嗜酸性粒细胞增多。荧光原位杂交分析检测到骨髓细胞中 4q12 染色体的染色质缺失。该患者被诊断为伴有 融合基因的骨髓增殖性肿瘤，酪氨酸激酶抑制剂伊马替尼治疗有效。融合基因导致的嗜酸性粒细胞克隆性扩增可能是支气管哮喘或过敏性鼻炎患者难治机制的基础。