| 代华平:几乎只累及女性的肺淋巴管平滑肌瘤病,哪些是诊断金标准?-MedSci.cn - 风湿免疫
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罕见病解读系列(4)| 代华平:几乎只累及女性的肺淋巴管平滑肌瘤病,哪些是诊断金标准?

2018-07-07 代华平、王诗尧 呼吸界

近日,国家卫生健康委员会、科技部、工业和信息化部、国家药品监督管理局、国家中医药管理局等五部门联合发布了《第一批罕见病目录》,共收录121种疾病,其中多种为呼吸疾病,为此我们特约专家对此逐一进行分析解读,敬请关注。

近日,国家卫生健康委员会、科技部、工业和信息化部、国家药品监督管理局、国家中医药管理局等五部门联合发布了《第一批罕见病目录》,共收录121种疾病,其中多种为呼吸疾病,为此我们特约专家对此逐一进行分析解读,敬请关注。

肺淋巴管平滑肌瘤病(Lymphangioleiomyomatosis,LAM)是一种罕见的以双肺多发囊泡影为主要表现的疾病,其可分为散发性LAM以及家族性结节性硬化(Tuberous sclerosis complex,TSC)-LAM。

流行病学与危险因素

散发性LAM的准确发病率目前仍不知晓,据LAM基金会估计,女性中LAM的患病率为3~5/100万 。而罹患TSC的患者中LAM的患病率更高,约有30%的TSC女性会出现LAM样的肺部表现 。LAM几乎只累及女性,由以育龄期女性为多见,妊娠期间、月经周期时以及应用外源性雌激素时有疾病进展加速的报道,考虑雌激素在LAM的发病中占据重要地位,而女性患者绝经后肺功能下降速度则变缓。

LAM的发病机制

LAM发病机制的核心是非典型平滑肌样细胞(LAM细胞)在肺组织中过度增殖并出现多发囊腔结构,这种特殊的肺脏表现可能与增生的LAM细胞堵塞远端小气道及破坏肺泡结构有关。LAM细胞增殖的原因在有遗传背景和没有遗传背景的患者中并不相同,在有遗传背景的患者中,TSC基因(尤其是TSC2基因)突变导致mTOR通路激活是导致LAM细胞过度增殖的原因;而在散发性LAM患者中,雌激素的作用及其他生长因子的异常刺激可能是导致LAM细胞过度增殖的原因。同时过度增殖的LAM细胞会累及淋巴管导致淋巴管畸形,该表现与VEGF等生长因子参与疾病发生有关。

病理改变

组织学诊断是LAM诊断的金标准。与发病机制对应,LAM的两个标志性组织病理学特征是肺囊性病变和LAM细胞。大体病理标本可见双肺多发囊性病变,壁较肺气肿稍厚,质地较蜂窝柔软。镜下可见到囊性病变周围及淋巴管、静脉中形成LAM细胞结节, LAM细胞常为梭形,与平滑肌细胞相比通常具有更淡或有空泡的细胞质。含铁血黄素沉着也是常见表现。免疫组化方面,可有黑素细胞的标记(human melanoma black [HMB]-45, Melan-A, tyrosinase, microphthalmia transcription factor, NKI/C3)和/或肌细胞标记(smooth muscle actin, pan-muscle actin, muscle myosin, calponin)表达。另有许多LAM细胞表达雌激素及孕激素受体(estrogen receptor [ER], progesterone receptor [PR]),印证了性激素在LAM发病机制中的作用。



【图1】 典型肺LAM组织学表现(HE染色),于囊壁可见结节增生样LAM细胞(箭头)
 

临床表现

最经典的散发型LAM表现为育龄期女性出现反复自发性气胸(36%)和/或乳糜胸水(21%)、乳糜痰(7%),其他非特异的呼吸系统表现包括乏力(70%)、进行性呼吸困难(70%)、胸痛(<10~15%)、咳嗽(<10~15%)、肺动脉高压(<7%)、咯血(<5%)等。30%的散发型LAM患者可合并肾血管平滑肌脂肪瘤(angiomyolipomas, AML),存在AML的患者可有腹痛、腹块和血尿。

需要注意的是,临床表现提示LAM的患者,一定要系统筛查全身表现,以区别为散发型LAM还是TSC-LAM。TSC-LAM的系统表现还包括:

◆ 皮肤:色素减退斑,亦称叶状白斑(ash-leaf spot),血管纤维瘤,鲨鱼皮样斑;

◆ 中枢神经系统:癫痫、胶质神经元错构瘤(皮质结节)、室管膜下结节、室管膜下巨细胞瘤(subependymal giant cell tumor, SGCT)、白质易位;

◆ 心脏:心脏横纹肌瘤;

◆ 肺:除LAM外,还有多灶性微结节性肺细胞增生(multifocal micronodular pneumocyte hyperplasia, MMPH)和肺透明细胞瘤(clear cell tumor of the lung, CCTL);

◆ 肾脏:肾囊肿,肾血管平滑肌脂肪瘤(TSC-LAM患者中的发病率高于散发型LAM);

◆ 其他:口腔纤维瘤、视网膜错构瘤、恶性肿瘤等。

辅助检查

HRCT:特征性表现为双肺实质内弥漫分布的多发囊泡影,一般直径<2cm,呈圆形或类圆形,壁薄。可合并气胸或胸腔积液(乳糜胸)。



【图2】肺LAM的典型HRCT表现

肺功能:以阻塞性通气障碍及弥撒功能障碍为主要特征,通气障碍早期可表现为小气道病变或可逆的阻塞性通气障碍,进展期表现为不可逆的阻塞性通气障碍、限制性通气障碍及弥散功能减低。

血管内皮生长因子-D(vascular endothelial growth factor-D,VEGF-D):VEGF-D是一种淋巴管生成相关的生长因子,近年来发现LAM患者血清VEGF-D水平异常升高,这可以解释LAM患者存在淋巴管异常。诊断界值为800而且VEGF-D水平与疾病严重程度相对应,更高水平的VEGF-D常提示更加严重的肺部囊性病变及肺功能受损。

诊断与鉴别诊断

诊断流程


LAM:淋巴管平滑肌瘤病;TSC:结节性硬化;TSC-LAM:结节性硬化-淋巴管平滑肌瘤病;AML:血管平滑肌脂肪瘤;VEGF-D:血管内皮生长因子-D;VATS:电视辅助胸腔镜手术。

鉴别诊断

1、肺气肿:多有吸烟史,无吸烟史的青年起病严重肺气肿患者需警惕α-1抗胰蛋白酶缺乏。多发弥漫的肺气肿需与LAM相鉴别。典型肺气肿以上肺分布为著(α-1抗胰蛋白酶缺乏可能出现下肺分布为著),囊性病变无壁,且气肿中可见血管及结缔组织组成的「点状」或「树枝状」凸起结构。

2、肺朗格汉斯细胞组织细胞增多症(pulmonary langerhans cell histiocytosis, pLCH):可为吸烟相关单纯累及肺部的pLCH,亦可为系统性LCH累及肺。pLCH的囊性病变的壁较LAM的囊性病变更厚,上肺为著分布,肋膈角不受累。囊性病变早期可为小结节,后期可相互融合形成不规则囊腔。组织学可见朗格汉斯细胞(CD-1α染色阳性)。

3、Birt-Hogg-Dubé综合征(BHD):同样表现为双肺囊性病变,但分布不均匀,多沿支气管血管束走形,分布较LAM稀疏,大小不等且差异较明显,薄壁且伴有血管束附于一侧。与LAM类似的是,BHD患者同样可出现自发性气胸或肾脏肿瘤,但肾脏肿瘤非AML而多见肾癌。该病本质为FLCN基因突变所致。

治疗及预后

 肺功能正常或轻度受损患者(FEV1≥70%预测值):

◆ 支持治疗为主:戒烟,接种流感及肺炎疫苗,适度运动。散发型LAM患者避免外源性雌激素或妊娠。

◆ 可逆性气道阻塞患者可吸入支气管扩张剂(β2受体激动剂或抗胆碱能药可能均有用),可部分缓解症状,但不影响预后。

 肺功能中重度受损患者(FEV1<70%预测值):

◆ mTOR抑制剂:可抑制TSC基因功能丧失或其他原因导致的mTOR复合物异常激活,从而抑制LAM细胞的异常增殖。一线治疗为西罗莫司,常以小剂量开始给药,检测血药浓度调整剂量,目标谷浓度为小于等于10ng/mL 。西罗莫司是一种抑制性治疗而非治愈性治疗,其可减缓LAM患者肺功能下降速度,因此如患者可耐受则应持续用药,停药后病情进展将恢复原有速度。但是,并非所有LAM患者对西罗莫司的反应均良好,研究发现VEGF-D水平较高的患者对药物反应更佳。不耐受西罗莫司副作用的患者可换用更短效的mTOR抑制剂依维莫司(二线治疗),其疗效可能与西罗莫司相似。

◆ 多西环素:可抑制基质金属蛋白酶(matrix metalloproteinases, MMPs),后者是参与LAM发病的因子之一。有关多西环素的疗效目前均为小样本研究,一些肺功能轻度受损的患者可能从治疗中获益,但整体而言多西环素对于LAM的疗效并不满意,ATS/JRS 2016版指南不推荐使用。

难治或终末期患者:

肺移植:对于足量长程应用mTOR抑制剂仍存在肺功能进行性加重的患者,肺移植是唯一有效治疗手段。在最大型的病例系列研究中(45例双侧移植,34例单侧移植),30日死亡率为5%,1年时存活率为86%,3年时为76%,5年时为65%。

LAM的自然预后

未经治疗者FEV1每年大约下降40~150mL,随着时间的延长病情进展可能加速。LAM患者的中位生存时间各大研究差异较大,西方发达国家的中位生存时间为10~20年,我国尚无大型研究给出明确预后数据。

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    2018-07-09 syscxl
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    2018-07-09 amyloid
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Chest:西罗莫司治疗肺淋巴管平滑肌瘤病是否安全有效?

2017年7月,发表在《Chest》的一项由美国科学家进行的I期临床试验的结果,表明西罗莫司联合羟化氯喹治疗肺淋巴管平滑肌瘤病(LAM)耐受性好。

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