病例:阿扎胞苷有效治疗1例再生障碍性贫血转骨髓增生异常综合征

2019-12-07 佚名 肿瘤资讯

骨髓增生异常综合征(MDS)是一组临床表现、自然病程和预后差异性很大的疾病。诊断需依赖血细胞计数、形态学、细胞遗传学等相关信息,部分患者存在诊断及和再生障碍性贫血等疾病鉴别诊断困难,临床中需仔细分析,详细排查,密切随访。一旦考虑诊断成立,应按照预后分组同时结合患者年龄、体能状况、合并疾病、治疗依从性等进行综合分析,选择治疗方案。

骨髓增生异常综合征(MDS)是一组临床表现、自然病程和预后差异性很大的疾病。诊断需依赖血细胞计数、形态学、细胞遗传学等相关信息,部分患者存在诊断及和再生障碍性贫血等疾病鉴别诊断困难,临床中需仔细分析,详细排查,密切随访。一旦考虑诊断成立,应按照预后分组同时结合患者年龄、体能状况、合并疾病、治疗依从性等进行综合分析,选择治疗方案。

赵鹏,血液学博士,硕士生导师,贵州医科大学附属医院血液科副主任医师,第十届中华血液学分会青委会委员,中国老年医学学会血液学分会第一届委员会老年血液综合评估诊疗学术工作委员会委员,中国抗癌协会第五届血液肿瘤专业委员会髓系肿瘤学组委员,中国康复医学会第一届血液病康复专委会青委,贵州省预防接种异常反应调查诊断专家组成员,贵州省医学会血液学分会青年委员  。

临床资料

基本情况

患者男性,62岁,因 “乏力、气促3月余” 于2018年3月就诊我院。既往史、个人史、家族史均无特殊。入院查体:贫血貌,周身浅表淋巴结及肝脾未触及。

初诊资料及治疗情况

入院实验室检验:血常规WBC 1.39×109/L,HGB 67g/L,PLT 19×109/L。网织红细胞、叶酸及维生素B12、肿瘤标记物、免疫自身抗体、病毒标记物、Coombs试验、PNH克隆未见异常。骨髓涂片:三系增生低下,未见巨核细胞。FCM、FISH未见异常。骨髓活检:送检少量骨髓组织,主要为皮质下低增生区,造血细胞缺乏,MF-0级。

该患者诊断全血细胞减少,不除外再生障碍性贫血、MDS、免疫相关性血细胞减少?

患者自2018-03-01至04-20接受叶酸、维生素B12正规治疗1个月,后加泼尼松1mg/kg试验性治疗,该患者血象无明显提高。

第二阶段资料及治疗情况

2018年4月患者就诊于中国医学科学院血液学研究所,完善相关检查:

集落形成试验:CFU-E、BFU-E及CFU-GM降低。PNH克隆阴性。

骨髓涂片:粒、巨两系减低,红系增生伴红系形态异常骨髓象。

FCM:髓系原始细胞0.4%,粒系比例较低,红系比例增高,各系表型未见明显异常。

二代测序:ATG2B Exon 9、IDH2 Exon11 突变阳性。染色体:46,XY [20] 。WT1 0.66%。

骨髓活检:骨髓增生极度低下(<10%=,脂肪细胞增多,造血细胞缺乏,MF-0级。

综合上述检验结果,该患者诊断为血细胞减少,考虑再生障碍性贫血。

2018-04-20至2019-03-21患者接受司坦唑醇、环孢素、左旋咪唑、云芝菌、再造生血片、甲泼尼龙片等治疗,间断使用G-CSF。血象曾一度恢复正常,患者病情稳定,定期复查。

第三阶段资料及治疗情况

2018-12月复查T细胞亚群:淋巴细胞比例增高63.5%,余细胞比例无异常。PNH克隆阴性,WTI 0.05%。骨髓涂片:粒红巨三系增生,红系比例增高骨髓象。CD41巨核酶标:全片巨核细胞214个,正常巨核细胞187个,双核巨核细胞15个,多核巨核细胞3个,大单元核小巨核细胞9个。FCM:粒系比例减低,核左移,CD13/CD11b分化抗原表达异常,红系比例增高,CD36表达缺失。染色体:45,XY,-7 [19]/46, XY [1] 。当时发现染色体出现-7异常,提示病情有变化,鉴于此患者血象稳定,故继续目前治疗。2019-04-08血象提示WBC、PLT均下降,复查骨髓活检:骨髓增生大致正常,粒红巨三系造血细胞增生伴幼稚阶段细胞略增多及巨核细胞形态异常。

染色体:45,XY,-7 [20]。二代测序:PTPN11 Exon3 突变,ASXL1 Exon12、TAL1 Exon5、ATG2B Exon9、IDH2 Exon11突变。

两次染色体均提示-7异常,此次骨髓考虑MDS诊断。

考虑该患者诊断为MDS-U(IPSS 中危-2组,IPSS-R 高危组)。2019-04-17和2019-05-22患者分别接受阿扎胞苷 (维达莎?  )75mg/m2×7天治疗,血红蛋白上升至80g/L左右,血小板上升至100×109/L左右。

专家点评

肖志坚,医学博士,主任医师,教授,博士生导师,中国医学科学院血液病医院(血液学研究所)副院所长,骨髓增生异常综合征诊疗中心主任,中华医学会血液学分会秘书长,中国医药生物技术协会精准医疗分会副主任委员,海峡两岸医药卫生交流协会血液病学专业委员会副主任委员,中国病生学会实验血液学专业委员会委员,中国抗癌协会血液肿瘤分会委员,《中华血液学杂志》、《国际输血及血液学杂志》和《白血病·淋巴瘤》杂志副主编,《Blood Review》、《Gene,Chromosomes and Canner》等杂志编委。

1. AA、MDS的诊断及二者的鉴别诊断

AA是一种骨髓造血衰竭(BMF)性疾病,其诊断目前仍参照国际粒细胞减少与AA研究组1987年标准[1],必须除外先天性和其他获得性、继发性BMF,主要包括PNH相关,低增生MDS/AML,自身抗体介导的全血细胞减少等。尽管目前有免疫学、细胞遗传学和分子生物学相关检查,但这些检查结果均未纳入AA的诊断标准,仅用于排除诊断。MDS是一组起源于造血干细胞的异质性髓系克隆性疾病,2016年国际共识小组的工作会议更新了MDS最低诊断标准(表1),其中血细胞减少的标准为:中性粒细胞绝对值<1.8×109/L,血红蛋白<100 g/L,血小板计数<100×109/L。MDS的诊断依赖骨髓细胞分析中细胞发育异常的形态学表现、原始细胞比例升高和细胞遗传学异常。约20%的MDS患者骨髓增生程度低,细胞少,因此难以对细胞发育异常情况进行充分评价,存在诊断困难并与AA鉴别困难。且红系病态造血在AA中非常常见,不能据此鉴别MDS和AA。骨髓活检标本中,网状纤维、CD34+细胞增加以及较多的残存造血面积提示为低增生性MDS而非AA。若存在前体细胞异常定位则更加提示MDS。其他克隆性证据如细胞遗传学、分子生物学指标对于鉴别低增生MDS和AA也非常重要。少部分AA患者在诊断时存在细胞遗传学克隆异常[2],常见有+8、+6、13号染色体异常。一般异常克隆仅占总分裂象的小部分,可能为一过性,可自行消失。有异常核型的AA患者应该每隔3~6个月行1次骨髓细胞遗传学分析,异常分裂象增多提示疾病转化。40% ~60%的MDS患者具有非随机的染色体异常[3],其中以+8、-7/del (7q)、del (20q)、-5/del (5q) 和-Y 最为多见。MDS患者常见的染色体异常中,部分具有诊断价值,而+8、de (20q)和-Y亦可见于AA及其他血细胞减少疾病。

2. AA的克隆演变及G-CSF是否可促进AA克隆演变

AA具有克隆演变为MDS/AML的潜在风险。有体外实验结果示高浓度G-CSF支持-7克隆的扩增。一项回顾性研究分析显示G-CSF的使用和-7克隆的出现具有相关性[4]。一项前瞻性研究对AA患者接受免疫抑制治疗(IST)是否联合G-CSF进行比较,研究结果并不支持克隆演变和G-CSF的使用存在相关性[5],并提出之前观测到的G-CSF的使用和克隆演变间相关性可能和使用G-CSF的AA患者疾病病情较重、克隆演变风险更高有关。2011年,一项中国单中心的研究纳入802例AA患者,研究结果示AA患者5年进展为MDS/AML和PNH的发生率分别为1.7%和2.1%。多因素分析示年龄、疾病严重程度和CSF的使用天数是AA进展为MDS/AML的危险因素[6]。限于大部分研究为回顾性研究且样本量较小,目前AA患者接受G-CSF治疗是否会增加IST治疗转为MDS/AML尚不完全明确。2019年MDS中国诊断与治疗指南[6]仅推荐造血生长因子G-CSF/GM-CSF用于中性粒细胞缺乏且伴有反复或持续性感染的MDS患者。

3. MDS的治疗策略

MDS患者的自然病程和预后的差异性很大。目前MDS的治疗主要根据预后分组进行治疗。MDS可按预后积分系统分组两组,较低危组【IPSS-低危组、中危-1组,IPSS- R-极低危组、低危组和中危组(≤3.5分),WPSS-极低危组、低危组和中危组】和较高危组【IPSS-中危-2、高危组,IPSS-R-中危组(>3.5分)、高危组、极高危组,WPSS-高危组和极高危组】。较高危组患者的总体治疗目标为延长生存,达到治愈。较高危组患者非移植治疗里去甲基化药物是首选药物,与支持治疗组相比,去甲基化药物治疗组可降低患者向AML进展的风险、改善生存。常用的去甲基化药物包括阿扎胞苷(AZA)和地西他滨。较低危组MDS患者如出现严重粒细胞减少和(或)血小板减少,也可应用去甲基化药物治疗,以改善血细胞减少。

本例患者以全血细胞减少就诊,完善检查排除非血液系统疾病导致的血细胞减少、PNH、MF、AML等疾病,考虑诊断为全血细胞减少,不除外AA、MDS、免疫相关性血细胞减少。经叶酸、维生素B12规律治疗及泼尼松治疗,血象无明显升高,提示该患者非免疫相关性血细胞减少,考虑患者诊断不除外AA和MDS。其后,患者接受环孢素、雄激素、左旋咪唑及促造血等治疗,血象恢复,治疗有效,考虑AA。后监测中发现染色体两次MDS中具有诊断价值的克隆性-7异常,提示病情转换。按照WHO 2016分型标准:形态学未达到标准(一系或多系细胞发育异常比例<10%)、但同时伴有持续性血细胞减少的患者,如检出具有MDS诊断价值的细胞遗传学异常,应诊断为MDS未分类型(MDS-U)。该患者诊断为MDS-U,根据预后积分系统进行预后分组为较高危组,目前接受2个疗程的AZA治疗,血红蛋白和血小板较前有所升高,长期疗效和生存有待进一步观察。

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