1例骨髓细胞形态似急性早幼粒细胞白血病的 急性淋巴细胞白血病案例分析

<正>颗粒性急性淋巴细胞白血病(G-ALL)是急性淋巴细胞白血病(ALL)少见的一种亚型,形态上归属于ALL-L2型,个别为ALL-L1型。G-ALL患者骨髓细胞中一般含有大量的嗜苯氨蓝颗粒,与急性早幼粒细胞白血病(AML)细胞中初级颗粒,T淋巴细胞白血病(TLGLL)大颗粒和NK细胞大颗粒性白血病中的嗜天青颗粒及幼稚嗜碱性粒细胞的嗜碱性颗粒难以区分,笔者查阅资料,国内仅有1例将G-ALL误诊为嗜碱性粒细胞白血病的报道~([1])。笔者临床工作中遇到1例骨髓细胞形态极似AML-M3的G-ALL病例,现报道如下。     

颗粒型急性淋巴细胞白血病

目前急性白血病的分类仍主要依靠细胞形态学和细胞化学的评价。原始细胞胞浆中存在嗜天青颗粒常被认为是急性髓细胞白血病(AML)典型的形态学表现,而急性淋巴细胞白血病(ALL)则否,这是鉴别二者的一个重要的和普遍被接受的细胞形态学标准。但是,近年来报道少数ALL患者原始细胞中也可存在嗜天青颗粒。就使这一鉴别标准产生了问题。1983年Stein等将ALL患者5％以上的原始细胞胞浆中存在直径大于0.5μm的一或多个嗜天青颗粒或包涵体者,正式命名为颗粒型急性淋巴细胞白血病(G-ALL),将其视为ALL的一个亚型。现综述如下。     

六种少见伴嗜酸粒细胞增多血液病的嗜酸粒细胞形态学观察及相关分析

目的分析六种少见伴嗜酸粒细胞增多的血液病嗜酸细胞的形态学特征。方法回顾性观察61例伴嗜酸粒细胞增多血液病患者骨髓及外周血涂片嗜酸粒细胞形态,其中急性髓系白血病（AML）伴嗜酸粒细胞增多23例,包括：AML伴inv（16）t（16;16）,（CBFB／MYH11）10例;AML伴t（8;21）（q22;q22）,（AML／ETO）13例;慢性粒细胞白血病慢性期（CML-CP）伴嗜酸粒细胞增多18例;慢性粒．单细胞白血病（CMML）伴嗜酸粒细胞增多6例;骨髓增生异常综合征（MDS）伴嗜酸粒细胞增多8例,急性淋巴细胞白血病（ALL）伴嗜酸粒细胞增多6例。每组计数200个骨髓嗜酸粒细胞,分析各阶段嗜酸粒细胞比例以及形态特征。结果AML伴inv（16）t（16;16）骨髓嗜酸粒细胞,以嗜酸中晚幼粒细胞为主,形态异常特点为颗粒增多而细小,有少量细小的嗜碱颗粒散在嗜酸颗粒上;AML伴t（8;21）（q22;q22）骨髓嗜酸粒细胞以嗜酸晚幼粒细胞为主,形态异常特点为颗粒增多,多数胞核和胞质上覆盖粗大紫红色嗜碱性颗粒;CML—CP骨髓以嗜酸晚幼粒及杆状核粒细胞为主,形态异常为颗粒多、细小、密集,少量金黄色颗粒覆盖在胞核上,少数为灰黑色嗜碱颗粒;CMML骨髓嗜酸细胞以嗜酸分叶核粒细胞为主,形态异常特点为颗粒虽少但颗粒粗大,易见双核畸形;MDS骨髓嗜酸粒细胞以中晚幼粒细胞为主,形态异常特点为颗粒粗大,分布不均匀,折光性强,呈多色性改变;ALL骨髓嗜酸粒细胞以杆状核和分叶核粒细胞为主,形态轻度异常,特点为嗜酸颗粒减少,浆内颗粒分布不均匀,有明显无颗粒间隙。结论六种少见伴嗜酸粒细胞增多血液病,除各自原发病形态特点外,嗜酸粒细胞数量和异常形态特征各不相同,通过形态学初步筛查可为遗传学检查和治疗提供初步依据。     

颗粒性急性B淋巴细胞白血病形态学及流式散点图特点

目的分析颗粒性急性B淋巴细胞白血病(G-ALL)形态学及流式散点图特点,提高对此类疾病的诊断水平。方法对确诊的1例少见G-ALL患者的形态学及流式散点图进行分析,总结其特点。结果 G-ALL在形态学上多数具有髓系白血病细胞的特点,但过氧化物酶染色呈阴性,且此类细胞均高表达CD34。结论在诊断G-ALL方面,形态学具有明显的局限性,如需明确确诊必须依靠免疫学分型。该类原始淋巴细胞既有典型B淋巴细胞的免疫标志又有髓系原始细胞的形态学特点,因此单纯依靠细胞形态学无法或者难以明确诊断,这也是形态学容易误诊的最主要的原因。     

8例急性嗜碱粒细胞白血病的临床、形态学和遗传学研究

作者从455例经电镜检查的急性白血病中选出诊断8例急性嗜碱粒细胞白血病(男5例女3例,年龄9～82岁)。他们的临床表现与其它AML 不能区别,7例经化疗,4例取得CR。存活1～63~+月。实验参数:WBC(2.8～144)×10~9/L,Hb 53～134g/L(7例贫血),8例血小板计数均减少。骨髓标本原始细胞占33～99%,血液和骨髓嗜碱粒细胞增多者各3例,8例中无一见到Auer 氏小体。光镜检查,2例原始细胞中偶见明显的嗜碱颗粒,伴有细胞向成熟嗜碱粒细胞和肥大细胞分化。此2例血和骨髓中也有成熟和幼稚的嗜碱粒细胞增多。3例原始细胞无颗粒,且不存在嗜碱粒细胞分化证据;另3例在原始细胞中罕见或偶见嗜天青或深蓝色颗粒,其中有些颗     

大颗粒淋巴细胞白血病

大颗粒淋巴细胞(LGL)在正常人外周血中占单核细胞总数的10%～15%.其中大部分(85%)来自CD3-NK细胞(NK-LGL),少部分(15%)来自CD3+T细胞(T-LGL).形态学上,LGL为偏心核、胞质丰富,伴粗大嗜苯胺蓝颗粒的中至大细胞.     

颗粒型急性淋巴细胞白血病

急粒白血病(AML)原始细胞胞浆内常有嗜天青颗粒。急淋白血病(ALL)原淋细胞胞浆内出现显著的嗜天青颗粒,形态学上类似于AML,易造成诊断的混淆。为阐述ALL该种特殊的形态学亚型,作者报道5例颗粒型ALL,作了详细的细胞化学、细胞遗传学、免疫学标记和1例电镜观察。作者自66例ALL骨髓涂片检查中,检出5例ALL胞浆内含粉红至红色嗜天青颗粒的原淋细胞>5%。女性3例,男性2例。年龄6-18岁。全部病例按标准方     

以嗜碱早幼粒细胞为主的急性嗜碱粒细胞白血病一例报告

目的 探讨急性嗜碱粒细胞白血病的血液细胞学特点,提高对本病的认识.方法 回顾性分析我院1例急性嗜碱粒细胞白血病的病例资料.结果 患者因头痛7d,发热4d入院,经骨髓象结合细胞化学染色诊断为急性早幼粒细胞白血病,予维A酸、亚砷酸治疗后,骨髓象未见好转.后经专家会诊,结合流式细胞仪检测、染色体核型、融合基因检查等,诊断为急性嗜碱粒细胞白血病.结论 急性嗜碱粒细胞白血病是一种少见类型白血病,对于形态不典型者诊断需结合细胞化学染色、染色体核型分析、融合基因检查及临床疗效等进行综合分析.     

混合表型急性白血病细胞Chediak-Higashi包涵体的观察

急性白血病细胞胞质内常可见大小不一的紫红色嗜苯胺蓝颗粒或Auer小体,而巨大包涵体十分罕见,近年对急性白血病伴Chediak-Higashi(PCH)包涵体有较多病例报道[1-4],这种PCH颗粒在急性髓系白血病(AML)[1-4]、慢性粒细胞白血病(CML)[5]、骨髓增生异常综合征(MDS)[6]中均有描述,主要出现在早期的粒细胞和单核细胞中.我们曾对203例急性白血病患者进行细胞形态学观察,结果表明,在AML细胞中可见到多少不一的PCH颗粒[7].     

慢粒急变嗜碱粒细胞白血病一例

慢粒急变嗜碱粒细胞白血病一例河北医科大学附属第二医院（石家庄０５００００）史敏慢性粒细胞白血病（ＣＭＬ）急性嗜碱细胞白血病变临床已有报道，但嗜碱粒细胞形态特殊者，文献介绍尚少，我们报道一例嗜碱粒细胞颗粒巨大，并伴假Ｃｈｅｄｉａｋ颗粒。病例患者，女，４...     

Therapy-related acute leukemia

Acute leukemias that arise as a result of treatment with DNA-damaging agents exhibit distinctive molecular, genetic, and clinico-pathologic features. In this timely article, the authors dissect the pathogenetic basis of therapy-related leukemias, elucidating important molecular mechanisms through which DNA damage causes these disorders. The authors also discuss how these molecular aberrations translate into specific clinical syndromes, and in addition, point out potential molecular targets for the development of innovative treatment approaches.     

急性髓系白血病与急性淋巴系白血病的蛋白质组比较研究

本研究通过对急性髓系白血病(AML)与急性淋巴系白血病(ALL)细胞比较蛋白质组分析,寻找亚型特异性的蛋白质表达谱。应用双向电泳分别分离AML不同亚型(M1、M2、M3)、ALL患者骨髓白血病细胞蛋白质,利用PDQuest 7.4软件分析双向电泳图谱差异蛋白质点,基质辅助的激光解析飞行时间质谱和生物信息学鉴定差异蛋白质。结果显示:经过电泳图谱分析得到21个差异蛋白质点,质谱鉴定提示15种蛋白有统计学意义。在AML中高表达的蛋白质包括髓过氧化物酶(MPO)、硫氧还蛋白依赖的过氧化物还原酶(PRDX3),钙网蛋白(CALR)、烯酰辅酶A水合酶ECH1等7种,在ALL中高表达的蛋白质包括ARHGDIB、肌动蛋白抑制蛋白1(PFN1)、肌动蛋白(ACTG1)等8种。结论:AML与ALL细胞存在差异蛋白质表达谱,这将有助于发现早期诊断的分子标志物及特异性治疗靶标。     

Adult acute lymphoblastic leukemia

Much progress has been made in understanding the biology of and therapy for acute lymphoblastic leukemia (ALL). This progress has translated into the recognition of several subgroups of ALL and the institution of risk-adapted therapies. New therapies are emerging based on the definition of specific cytogenetic-molecular abnormalities. Changes in the pathologic classification of ALL have led to therapeutic consequences. Adaptation of successful treatment strategies in children with ALL has resulted in similar complete remission rates in adults. Prognosis has Improved especially in mature B-cell ALL and T-cell lineage ALL. However, regardless of ALL subgroup, long-term survival in adults is still inferior to that in children. Development of new drugs and agents tailored to subset-specific cytogenetic-molecular characteristics is vital to the therapeutic success in adult ALL.     

Pneumatosis intestinalis in children with acute lymphoblastic leukemia and acute myeloid leukemia

Purpose  

To describe symptoms, diagnostic features, treatments, and outcomes of pneumatosis intestinalis (PI) in pediatric patients being treated for acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).     

Adult acute nonlymphocytic leukemia

Chemotherapy of adults with acute nonlymphocytic leukemia has improved in recent years, yielding complete remissions in 65 per cent and cure in 10 to 15 per cent of all treated patients. Allogeneic bone marrow transplantation cures approximately one half of eligible young patients who gain an initial remission with chemotherapy. Autologous bone marrow transplantation may ultimately prove to be of value for the large numbers of patients who are over 40 years of age or who lack histocompatible siblings. Current investigative approaches in all these areas, based on insights into the pathophysiology of disease discussed in this article, should enhance the outcome for affected patients in the next decade.     

Adult acute myeloid leukemia

Acute myeloid leukemia (AML) is a group of several different diseases, the treatment and outcome of which depend on several factors, including leukemia karyotype, patient age, and comorbid conditions. Despite advances in understanding the molecular biology of AML, its treatment remains challenging. Standard regimens using cytarabine and anthracyclines for induction followed by some form of postremission therapy produce response rates of 60% to 70%, with less than 20% of all patients achieving long-term disease-free survival. New therapies are emerging based on the definition of specific cytogenetic-molecular abnormalities. Such targeted therapies offer the promise of better antileukemic activity in adult AML.