罕见鞍区孤立性梭形细胞肉瘤样癌一例

2019-06-18 周迎 袁涛 刘小海 中国医学科学院学报

患者,女,33岁,因“头痛、多尿、多饮8月,月经紊乱3月,视力下降1周”入院。患者于2015年1月无明显诱因出现多尿、多饮,饮水量10L/d,饮水量与尿量相当,伴双颞侧间断性头部胀痛,就诊于当地医院行头部MRI,提示鞍内占位(大小约12mm×6mm×13mm),垂体柄增粗,未诊治。6月尿量减少至3L/d,同时出现月经紊乱,未予重视。9月出现视力下降(<10 cm),遂至北京协和医院内分泌科门诊就诊

鞍区恶性肿瘤非常罕见,既往报道为转移性疾病,以乳腺癌肺癌转移较为多见,占所有转移癌的1%~5%。20%的患者可出现鞍区病变的症状,其中,中枢性尿崩症占45%,视神经功能障碍占28%,垂体前叶功能减退占24%,第Ⅲ、Ⅳ及Ⅵ颅神经麻痹占22%,头痛占16%。梭形细胞癌(spindle cell carcinoma,SCC)也是一种罕见的疾病,特点为分化差的癌组织包含肉瘤样结构(梭形细胞或巨细胞),但没有特异性的肉瘤成分。既往报道SCC发生于乳腺、口腔、肾脏、肺、肠道及肝胆胰系统,鞍区尚无确凿证据。北京协和医院于2015年9月9日至10月16日收治并经病理科确诊了1例侵袭性较高的孤立性鞍区梭形细胞肉瘤样癌,现报道如下。
 
患者,女,33岁,因“头痛、多尿、多饮8月,月经紊乱3月,视力下降1周”入院。患者于2015年1月无明显诱因出现多尿、多饮,饮水量10L/d,饮水量与尿量相当,伴双颞侧间断性头部胀痛,就诊于当地医院行头部MRI,提示鞍内占位(大小约12mm×6mm×13mm),垂体柄增粗,未诊治。6月尿量减少至3L/d,同时出现月经紊乱,未予重视。9月出现视力下降(<10 cm),遂至北京协和医院内分泌科门诊就诊。查体血压92/59mmHg(1mmHg=0.133kPa),脉搏124次/min。生化结果提示全垂体前叶功能减退及高泌乳素血症。
 
入院后给予氢化可的松100mg静脉每8h滴注1次,血压逐渐升至120/80mmHg,尿量增至10L/d。禁水加压素试验符合中枢性尿崩症,口服弥凝治疗有效(尿量减至3L/d)。脑脊液分析提示轻度淋巴细胞增多,白细胞300/0.5ml(90%淋巴细胞),甲胎蛋白、癌胚抗原及β-人绒毛膜促性腺激素(β-human chorionic gonadotrophin,β-HCG)均正常;细菌、真菌涂片+培养、抗酸染色、墨汁荚膜染色及病毒相关抗体均阴性。头部MRI提示垂体前叶占位(大小约12.1mm×9.0mm×6.7mm),下丘脑占位(大小约7.0mm×9.4mm),T1及T2均等信号,增强后环形强化;视交叉受压。
 
入院次日,患者出现视物重影,眼科医师确诊为右眼外展受限。因考虑MRI疑似脓肿,给予静脉广谱抗生素治疗7d(头孢他啶+甲硝唑),复查头MRI示鞍区占位扩大,侵及右侧海绵窦,伴大量低信号区。检测患者血自身免疫相关抗体、β-HCG及肿瘤标记物、胸腹盆增强CT均阴性。全身18F-FDGPET-CT及18F-FDSPET-CT提示鞍区活动增强(FDGPET/CT SUV最大值4.73,FDSPET/CT SUV最大值1.49)。因考虑视交叉受压,给予甲强龙(500mg/d)冲击治疗3d,视力无改善。
 
2015年9月23日于北京协和医院神经外科行鞍区活检及减压术,切除占位10mm×10mm×10mm。术中可见灰色质韧病灶,血供差。病理结果:显微镜下观察该肿物由分化很差的肉瘤样成分组成(梭形细胞及巨细胞)。肿瘤细胞有梭形细胞核,可见有丝分裂相形成束及旋涡。局部可见垂体细胞、上皮样细胞及巨细胞,包括多核巨细胞及肿瘤巨细胞。未见特异性肉瘤成分。免疫组织化学检测结果提示全细胞角蛋白(AE1/AE3)及上皮细胞膜抗体染色(EMA)阳性(图2B~C);CD3、CD20、CD34、CD38、平滑肌动蛋白(SMA)、肌间线蛋白及S-100蛋白均阴性(图2D~E);Ki-67因子60%。
 
病理诊断为孤立性鞍区梭形细胞肉瘤样癌/未分化癌。鞍区占位革兰染色、细菌及真菌培养均阴性。经北京协和医院多科会诊建议患者进行放化疗,但患者拒绝并要求出院。术后7d复查头MRI提示下丘脑占位继续扩大(大小约21mm×16mm×11mm),右侧海绵窦、双视束及双侧鼻窦均可见异常信号。随访患者出院后5个月死亡。



图1 发病4个月间的头部MRI变化。蓝色、红色及黄色箭头分别表示下丘脑、垂体及海绵窦的病灶改变,绿色箭头表示手术对蝶窦的影响。A.T1增强相冠状位(当地医院,入院前3个月);B.T1增强相矢状位(当地医院,入院前3个月);C.T2相冠状位(入院后首次评估);D.T1增强相冠状位(入院后首次评估);E.T1增强相矢状位(入院后首次评估);F.T2相冠状位(入院后7d评估);G.T1增强相冠状位(入院后7d评估);H.T1增强相矢状位(入院后7d评估);I.T2相冠状位(术后7d评估);J.T1增强相冠状位(术后7d评估);K.T1增强相矢状位(术后7d评估)。



图2 鞍内及鞍上肿物的病理检查结果(×200)显微镜下观察,肿物呈现包含肉瘤样分化的低分化癌组织,肿瘤细胞包括大量的梭形细胞、上皮细胞及巨细胞。A.HE染色;B.细胞角蛋白(AE1/AE3)染色;C.上皮细胞膜抗原染色;D.肌间线蛋白染色;E.平滑肌动蛋白染色;F.Ki-67染色
 
本例患者诊断非常困难。未行活检前,患者临床表现及影像学结果支持鞍区脓肿;脑脊液结果疑似鞍区炎症,但FDG和FDSPET-CT结果无法辨别炎症及恶性肿瘤。既往报道鞍区恶性肿瘤皆为转移性疾病,患者的临床表现与之相似。鞍区转移癌的原发病灶多位于乳腺(50.6%)及肺部(21.6%),发生于皮肤、甲状腺、肠道、前列腺、肾脏及胰腺非常罕见。但本例患者全身CT及PET-CT结果未见其他部位存在明显病灶,且非鞍区转移性恶性肿瘤好发年龄(60~70岁)。从临床角度,患者对广谱抗生素及大剂量糖皮质激素治疗无效,鞍区占位短期内迅速进展,仍提示恶性病变。最终诊断依赖于病理的细胞学及免疫组织化学结果。
 
令人震惊的是,患者的病理支持孤立性的鞍区恶性肿瘤(细胞来源仅见垂体细胞),与PET-CT结果一致。我们回顾既往鞍区恶性肿瘤的来源,尚未见鞍区SCC的报道。此外,由于患者病灶的发生部位及肿瘤的高侵袭性(Ki-67>20%),需考虑垂体癌的可能性。垂体癌非常罕见,为腺垂体上皮细胞来源的肿瘤,并出现脑脊液和/或全身系统性转移,通常源自侵袭性垂体腺瘤。该患者未见转移灶,病理亦不支持垂体腺瘤,且不在目前世界卫生组织定义的垂体肿瘤分类中。最后,患者的病理结果提示肉瘤样细胞,需与鞍区肉瘤鉴别。鞍区肉瘤是罕见肿瘤,免疫组织化学CD34、SMA及肌间线蛋白阳性,通常诱发于垂体腺瘤放疗后。该患者之前未接受放疗,病理细胞学未见特异性肉瘤成分,免疫组织化学检测进一步确证。
 
由于患者同时表达AE1/AE3及EMA,考虑肉瘤样细胞可能为鞍区癌细胞出现肉瘤样变或癌细胞化生。既往报道鞍区恶性肿瘤总体预后差。治疗方面,手术不能改善总体预后,但对于视力受损的患者推荐进行减压术。辅助性放疗可用于全身状况较差的患者,且对鞍区病灶有局部控制效果,减少短期死亡率,但不能保障长期生存。其他部位的原发SCC通常局部有侵袭性、系统性转移,尽管使用多种治疗手段,预后较差。胰腺SCC的术后平均生存期为6个月。对于肺SCC,放疗及化疗可一定程度缓解疾病,但不同的身体状态、肿瘤分期均会导致疗效的差异性。
 
综上,本罕见病例有助于丰富鞍区恶性肿瘤的分类;对于进展较快的鞍区占位,临床医生应考虑鞍区原发恶性肿瘤的可能性,及早准确的病理学诊断对于鞍区恶性肿瘤的诊治具有重要意义。
 
原始出处:

周迎,袁涛,刘小海,肖雨,卢朝辉,有慧,程欣,金自孟,赵维纲,胡明明.罕见鞍区孤立性梭形细胞肉瘤样癌一例[J].中国医学科学院学报,2018,40(03):427-431.

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    2019-06-20 syscxl
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    2019-06-20 jxrzshh
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    2019-06-19 183****7028

    学习

    0

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    2019-06-19 njwbhuang

    非常少见,感谢分享。

    0

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