Chinese Journal of Tissue Engineering Research ›› 2015, Vol. 19 ›› Issue (10): 1630-1634.doi: 10.3969/j.issn.2095-4344.2015.10.028
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Luo Hong, Zhang Hong-bin
Online:
2015-03-05
Published:
2015-03-05
Contact:
Zhang Hong-bin, Associate chief physician, Department of Hematology, First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China
About author:
Luo Hong, Master, Department of Hematology, First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China
CLC Number:
Luo Hong, Zhang Hong-bin. Noninfectious pulmonary complications following hematopoietic stem cell transplantation[J]. Chinese Journal of Tissue Engineering Research, 2015, 19(10): 1630-1634.
2.1 植入综合征(engraftment syndrome,ES) 植入综合征是造血干细胞移植后中性粒细胞恢复初期发生的一种临床综合征,又称移植相关性呼吸窘迫综合征。植入综合征发病机制不详,可能与移植过程中血管内皮损伤,肿瘤坏死因子α、白细胞介素1B和白细胞介素8的产生,导致肺泡毛细血管渗漏和中性粒细胞聚集有关。其发生在移植后11 d(4-25 d)[4],发生率7%-59%,主要表现为非感染性发热、皮疹、毛细血管渗漏综合征(CLS)、肺实质浸润,严重者可以出现多器官功能衰竭。胸部高分辨率CT(HRCT)无特异性,表现为小叶间隔增厚,双肺毛玻璃样浑浊、肺门及支气管周围的实变和胸腔积液。植入综合征诊断需要3个主要标准或2个主要标准加1个或更多的次要标准。在异体移植中,还需排除急性移植物抗宿主病。植入综合征一般为自限性,症状较轻者可予以对症支持治疗;较重者需停用重组人粒细胞集落刺激因子(G-CSF),给予糖皮质激素治疗有效。该病总体预后良好,但是需机械通气,继发感染的患者死亡率高。 2.2 弥漫性肺泡出血(diffuse alveolar hemorrhage,DAH) 弥漫性肺泡出血发生率低但却是较严重的并发症。多发生在移植早期,中位发病时间为异基因移植后19 d (5-34 d),自体移植后12 d(0-40 d)[7];其发病率在在异基因移植中为2%-17%,自体移植中为1%-21%[8]。弥漫性肺泡出血的病因及机制不详,可能与非特异性的肺泡毛细血管内皮细胞损伤和细胞因子导致的肺泡炎有关,其发病的危险因素包括年龄、移植前化疗、环磷酰胺累积剂量、全身照射、肾功能不全、中性粒细胞植入及干细胞保存剂二甲基亚砜[9-10]。弥漫性肺泡出血多以进行性的呼吸困难、咳嗽、低氧血症、呼吸衰竭、痰血为表现,其诊断标准[8]:①胸部影像学示弥漫性的多肺叶浸润。②排除感染。③≥3个不同支气管亚段的支气管肺泡灌洗液(bronchoalveolar lavagefluid,BALF)为逐渐增多的血性液体或支气管肺泡灌洗液中含铁血黄素巨噬细胞≥20%,或肺活检至少30%的肺泡表面可见到血液成分存在。造血干细胞移植早期可见不同程度的磨玻璃样浑浊和实变,后期可见小叶和小叶间隔增厚,铺路石样改变[5],可采用糖皮质激素、新鲜冰冻血浆和血浆置换治疗;重组Ⅶa,抗纤维蛋白溶解物等也有报道,疗效亦不确切[7]。弥漫性肺泡出血预后差,最终多因多器官功能衰竭而死亡。 2.3 特发性肺炎综合征(idiopathic pneumonia syndrome,IPS) 特发性肺炎综合征是造血干细胞移植后排除感染、心功能损害、肾功能损害、液体负荷过重等因素的广泛性肺损伤[4-5]。特发性肺炎综合征发生的中位时间为造血干细胞移植后19 d(4-106 d),120 d内发病率是3%-15%,异基因移植患者常见。特发性肺炎综合征死亡率为60%-80%,接受机械通气的患者死亡率增高为95%[5-6,8]。特发性肺炎综合征的病因及机制不清,可能与肿瘤坏死因子、脂多糖、活化T淋巴细胞等有关。其高危因素有清髓移植方案中全身照射、急性移植物抗宿主病、移植患者年龄偏大、ACE D/D基因型、CCL-2/MCP-1血浆水平[11-12]。诊断标准为[8]:①弥漫性肺泡损伤的表现。②排除下呼吸道感染。③排除心功能不全、急性肾功损害、医源性液体负荷过重所致肺功能损害。特发性肺炎综合征的治疗主要是大剂量激素、机械通气及预防感染。有报道依那普利对特发性肺炎综合征有不错的疗效,其对特发性肺炎综合征患者长期生存的影响仍不明。特发性肺炎综合征患者与ACE D/D基因型有关,在实验模型中血管紧张素转换酶抑制剂(ACEI)成功阻滞肺纤维化,但目前没有随机临床研究证实ACEI和AT1受体拮抗剂与干细胞移植后肺部非感染并发症有关[11]。 2.4 肺水肿(pulmonary edema,PE) 肺水肿是移植后早期较常见的一种并发症,常发生在造血干细胞移植后2至3周,临床表现为突发的呼吸困难、体质量增加,双肺湿啰音及低氧血症。肺水肿主要与预处理、液体负荷过大、心肾功能不全等有关。胸片可见Kerley A和B线,严重者可见两肺蝶形片状模糊阴影;胸部高分辨率CT可见小叶间隔增高,肺血管扩张,支气管壁增厚、毛玻璃样浑浊,心脏增大和胸腔积液等。治疗以限水和利尿为主,严重者可进行机械通气。 2.5 急性嗜酸性肺炎(acute eosinophilic pneumonia,AEP) 急性嗜酸性肺炎是造血干细胞移植后少见的肺部并发症。有个案报道其发病时间为移植后65 d、5个月、8个月[13]。急性嗜酸性肺炎诊断标准:①急性发作性发热,呼吸道症状(咳嗽、呼吸困难等)持续时间< 1个月。②肺部X射线片提示双肺浸润性改变。③低氧血症。④纤支镜肺泡灌洗液细胞分类嗜酸性粒细胞 > 25%。⑤排除其他原因的嗜酸性粒细胞增多。糖皮质激素治疗可以获得很好的疗效[13]。 2.6 肺血管内细胞溶解性栓子形成(pulmonary cytolytic thrombi,PCT) 肺血管内细胞溶解性栓子形成是一种只发生在异基因移植后患者的罕见并发症,多见于儿童,可能为移植物抗宿主病的一种形式。临床症状包括发热、呼吸困难和胸痛,无特异性。肺血管内细胞溶解性栓子形成的中位发病时间为造血干细胞移植后72 d。组织病理学显示:细胞坏死的成分形成嗜碱性血栓物质阻塞肺血管,使得血管损害及出血性梗死,无细菌、真菌、病毒等感染征象。免疫组化显示嗜碱性细胞溶解栓子由CD45+的白细胞组成,并致使血管内皮损伤,导致血管病变。胸部高分辨率CT表现为双肺外周多发的结节灶和梗死灶。糖皮质激素治疗有效,因肺血管内细胞溶解性栓子形成导致血管内皮损伤可能继发血管病变,故诊断明确需尽快抗凝治疗[5],但长期预后不详。 2.7 放射性肺炎(radiation pneumonitis)及放射性肺纤维化(radiation fibrosis) 接受全身照射预处理的移植患者约7%发生有症状的放射性肺炎,而大部分的患者虽有胸部影像学的改变但无明显临床症状。放射性肺炎可发生在放疗结束后6周到6个月。临床表现包括发热、白细胞增多和胸部X射片肺实质浸润。胸部高分辨率CT可见双肺对称的毛玻璃样浑浊影和实变。放射性肺炎可进展为不可逆的局部肺纤维化,也可同时产生。目前尚无特异性的治疗手段,多采用激素及对症支持。抗原激活细胞分泌和释放的肿瘤坏死因子α与引起细胞外基质积聚的急性炎症有关[14-15],吡非尼酮可明显抑制细胞相关的肿瘤坏死因子α和γ干扰素的分泌。吡非尼酮( pirfenidone)是一种广谱的抗纤维化、抗炎、抗氧化药物[16-17],是目前惟一一个能显著延长无进展生存期和降低死亡率的特发性肺纤维化治疗药物,动物实验证实吡非尼酮对放射性肺损伤有防护作用,可改善肺纤维化[18]。 2.8 肺动脉高压(pulmonary arterial hypertension,PAH) 肺高压发生在移植后70 d(0-365 d)[19]。组织病理学上以血管增殖和重塑为特点,涉及内皮、血管平滑肌细胞和纤维母细胞在内的3级血管壁增殖和阻塞性的变化。疾病早期可无任何症状或仅表现为非特异性的症状如进行性加重的劳力性呼吸困难、疲劳,主要通过经胸壁超声心动图、右心室导管直接测压诊断。未经治疗,肺动脉高压可导致右心衰和死亡。目前没有统一的治疗方案,皮质激素、吸入性一氧化氮、去纤维蛋白多核苷酸、5型磷酸二酯酶抑制剂(西地那非)可用于治疗肺动脉高压[19]。 2.9 肺静脉闭塞性疾病(pulmonary veno-occlusive disease,PVOD) 肺静脉闭塞性疾病为肺静脉阻塞性疾病,发生率为(0.1-0.2)/百万。临床表现和肺动脉高压相似,多出现在移植后2-6个月。组织病理学特征是广泛的肺静脉血管闭塞,纤维组织增生导致血管硬化,无血栓形成,可发现骨形态蛋白受体Ⅱ型基因缺陷。胸部高分辨率CT可有效识别肺静脉闭塞性疾病[5,19],表现为肺间质性水肿、小叶中心性分布的弥漫性毛玻璃样浑浊、淋巴结肿大和小叶间隔线。肺活检确定肺损伤是诊断的惟一标准。肺静脉闭塞性疾病1年死亡率高达70%[19]。 2.10 闭塞性细支气管炎综合征(bronchiolitis obliterans syndrome,BOS) 闭塞性细支气管炎综合征又称限制性细支气管炎,是移植后期最常见的一种不可逆的气流受阻的肺部非感染性并发症,发病率为2%-30%。闭塞性细支气管炎综合征多发生在移植后的6-12个月[5,20],临床症状和体征非特异性,主要表现为干咳、气促、喘息,30%可无症状,肺部的啰音及哮鸣音是常见的体征,支气管扩张剂无效。一些闭塞性细支气管炎综合征患者也可表现为特发性胸部漏气综合征,如自发性纵隔积气、气胸和间质性肺气肿。危险因素包括移植前肺功能减低、年龄偏大、急性移植物抗宿主病、外周血移植、肺部并发症、预处理、女性供者、移植后100 d内病毒感染。但是包含抗胸腺球蛋白的预处理方案是减低闭塞性细支气管炎综合征的因素[21-23]。胸部高分辨率CT可见支气管壁增厚、外周血管影稀少、空气潴留征、马赛克样灌注征、支气管柱状扩张等[5];胸部高分辨率CT扫描后气道重建,以支气管扩张为主要表现,气道扩张的程度与肺功能损伤有重要联系[24]。诊断闭塞性支气管炎的金标准是肺活检,典型表现是终末细支气管及其相连的肺泡结构内腔的阻塞,阻塞的管腔内被包含有炎症细胞的纤维组织浸润[25]。肺活检在临床上难以实现,临床诊断标准[26]:①合并慢性移植物抗宿主病。②肺功能检测FEV1/FVC< 0.7及FEV1< 75%、RV > 120%的预计值。③胸部高分辨率CT示呼气相空气潴留征、支气管扩张、支气管壁增厚、双肺过度充气。④排除可致阻塞性肺部疾病的其他原因同时还需排除移植物抗宿主引起的肺部其他并发症。糖皮质激素为一线用药,其他免疫抑制剂如环孢素、他克莫司、雷帕霉素、依维莫司、吗替麦考酚酯、白三烯受体拮抗剂等均是闭塞性细支气管炎综合征的有效治疗方案;阿奇霉素、体外光分离血浆法可用于治疗难治性闭塞性细支气管炎综合征患者;另有报道酪氨酸激酶抑制剂、抗CD20单克隆抗体、吸入性环孢素、抗肿瘤坏死因子、硼替佐米治疗闭塞性细支气管炎综合征有效;药物治疗失败患者可采取肺移植[27-28]。闭塞性细支气管炎综合征患者的预后差,5年生存率为12%-27%,淋巴细胞性细支气管炎类型的闭塞性细支气管炎综合征患者较狭窄性支气管炎类型的预后好[29];多数患者死于叠加的肺部感染[5]。 2.11 闭塞性支气管炎伴机化性肺炎(bronchiolitis obliterans organizing pneumonia,BOOP) 闭塞性支气管炎伴机化性肺炎是一个涉及细支气管、肺泡管、肺泡功能失调的疾病[6],其发生率低(0.9%-10.3%),多发生于移植后的108 d(5-2 800 d),发病时间稍早于闭塞性细支气管炎,临床表现为急性或亚急性发热、干咳和呼吸困难;查体可闻及啰音和吸气相爆裂音。其组织病理学特征为细支气管腔内、肺泡管和肺泡内出现机化性渗出物,细支气管内肉芽组织增生,肺泡周围单核细胞浸润。危险因素有高龄、慢性移植物抗宿主病、含马利兰的预处理方案、HLA配型不合等。肺功能表现为轻至中度限制性通气障碍及弥散功能障碍。影像学常见有弥漫性斑块状影、毛玻璃影及结节影,纤维支气管镜和肺活检对其诊断有重要价值,支气管肺泡灌洗液中淋巴细胞增多。目前以肾上腺皮质激素治疗为主,持续6-12个月,治愈率可达65%以上。闭塞性支气管炎伴机化性肺炎患者直接致死原因是呼吸衰竭,移植后并发闭塞性支气管炎伴机化性肺炎的死亡率约19%,主要发生于病情严重、激素治疗较晚者[30]。 2.12 移植后淋巴细胞增生性疾病(post-transplant lymphoproliferative disease,PTLD) 为移植后发病率1%的罕见肺部非感染并发症,主要发生在移植后30 d到6个月,其中肺部浸润约占20%。其发生与免疫抑制直接相关,故异基因移植患者发生移植后淋巴细胞增生性疾病的风险相对较高,其发生可能与移植供者来源的EB病毒使受者淋巴细胞异质性增生有关[5]。肺部移植后淋巴细胞增生性疾病临床可表现为发热和进行性的呼吸困难。确诊依赖活检或EB病毒DNA的定量。治疗主要是减弱免疫抑制,同时可使用抗B细胞的单克隆抗体、抗病毒药、抗肿瘤坏死因子、供者淋巴细胞输注、放化疗等。 2.13 肺泡蛋白沉积症(pulmonary alveolar proteinosis,PAP) 肺泡蛋白沉积症也是造血干细胞移植后罕见的非感染性肺部并发症,以过量的蛋白质沉积于肺泡腔为特征。临床表现为急性可逆的呼吸衰竭和双肺浸润,确诊依赖于电镜下在纤支镜灌洗液中见到过碘酸雪夫染色阳性的蛋白质超微结构。胸部高分辨率CT诊断价值高,表现为:双肺弥漫性斑片状阴影,形成典型的“地图样分布”“碎石路表现”“肺水肿样表现”。全肺灌洗和粒细胞集落刺激因子是主要的治疗方法。移植后继发性肺泡蛋白沉积症预后差。 "
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