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首页> 外文期刊>Journal of cutaneous pathology >Aleukemic cutaneous myeloid sarcoma
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Aleukemic cutaneous myeloid sarcoma

机译：皮肤无髓性皮肤肉瘤

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Background: Aleukemic cutaneous myeloid sarcoma (CMS) represents an important yet rare entity denoting the presence of a cutaneous myeloid leukemic infiltrate without concurrent peripheral blood or bone marrow disease. The clinicopathologic diagnosis remains elusive due to isolated skin findings and variable immunostaining. Cytogenetic and molecular findings have infrequently been reported. Methods: Twenty-five patients with CMS were identified in the Massachusetts General Hospital pathology database between 2004 and 2012. Patients were excluded if concurrent blood or marrow acute myeloid leukemia (AML), myelodysplastic syndrome or lymphoproliferative disorder were diagnosed. Results: Three patients were identified: a neonate with recurrent CMS and marrow disease that never met diagnostic criteria for AML and two patients relapsing as CMS without concurrent blood or marrow disease following chemotherapy-induced complete remission. Histology showed atypical mononuclear cell interstitial dermal infiltrates. All cases were CD68+, lysozyme+ and CD117-; one of two were CD34+; two of three were myeloperoxidase negative. 11q23 rearrangement, t(1;14), NPM1 (nucleophosmin I), FLT3-ITD (Fms-like tyrosine kinase 3-internal tandem duplication), and novel FLT3-D835 mutations were identified. Conclusion: An isolated atypical cutaneous infiltrate may represent aleukemic CMS and should prompt a search for other extramedullary sites of involvement. Immunohistochemistry, molecular and cytogenetic studies can help differentiate aleukemic CMS from benign and malignant, monocytic and histiocytic mimickers, and may potentially indicate therapy and prognosis.
机译：背景：白血病患者的皮肤髓样肉瘤（CMS）是一种重要而罕见的实体，表明存在皮肤髓样白血病的浸润，而没有并发外周血或骨髓疾病。由于孤立的皮肤发现和可变的免疫染色，临床病理诊断仍然难以捉摸。细胞遗传学和分子发现很少报道。方法：2004年至2012年间，在马萨诸塞州总医院病理数据库中鉴定了25例CMS患者。如果诊断出同时存在血液或骨髓急性髓性白血病（AML），骨髓增生异常综合症或淋巴增生性疾病，则将这些患者排除在外。结果：确定了三例患者：复发性CMS和骨髓疾病的新生儿，从未达到AML的诊断标准;两名患者因化疗导致的完全缓解后复发为CMS，而没有并发血液或骨髓疾病。组织学显示非典型单核细胞间质真皮浸润。所有病例均为CD68 +，溶菌酶+和CD117-。两种之一是CD34 +;三分之二是髓过氧化物酶阴性。确定了11q23重排，t（1; 14），NPM1（核磷脂I），FLT3-ITD（Fms样酪氨酸激酶3内部串联重复）和新的FLT3-D835突变。结论：孤立的非典型皮肤浸润可能代表无创性CMS，应促使寻找其他涉及的髓外部位。免疫组织化学，分子和细胞遗传学研究可以帮助将古生性CMS与良性和恶性，单核细胞和组织细胞性小盲人区分开来，并可能表明治疗和预后。

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