Pulmonary tumor embolism
Pulmonary tumor embolism
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DOI：
10.1164/ajrccm.155.6.9196119
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发表时间：
1997-06-01
影响因子：
24.7
通讯作者：
Rizk, NW
中科院分区：
文献类型：
--
作者：
Bassiri, AG;Haghighi, B;Rizk, NW
在癌症患者发病和死亡的各种原因中，也许描述得最少的是肿瘤栓塞。 Schmidt 于 1897 年首次记录了这种情况 (1)，但从那时起，有关此主题的大多数信息都是以病例报告或尸检系列的形式出现。信息匮乏的部分原因是未能认识到这种生前状况。相当一部分此类患者被诊断患有肺血栓栓塞并接受抗凝治疗。尽管最近的研究试图诊断和区分恶性栓塞和血栓栓塞，但肺活检仍然是首选程序。这些研究以及肿瘤栓塞的临床表现是本报告的重点。尽管肿瘤栓塞的具体细胞和分子机制尚不清楚，但我们对这一现象的理解在过去十年中已经有了很大的提高。肿瘤细胞通过主动侵入小静脉、小静脉或肿瘤自身的微脉管系统进入体循环 (2)。肺血管床接收全部心输出量并过滤任何直径为 10 µm 或更大的细胞 (3)。循环中的大多数肿瘤细胞被微循环的机械力和剪切力或免疫系统的各种效应细胞破坏。事实上，进入循环系统的肿瘤细胞只有不到 1% 在通过肺部时存活下来 (4-6)。存活的肿瘤细胞具有广泛的生物学命运和临床表现：（1）肿瘤细胞可能保持无症状。事实上，尸检审查研究表明，18% 至 68% 的肿瘤栓子是偶然发现的 (7, 8)。(2) 肿瘤细胞可能呈现与血栓栓塞性疾病类似的临床表现 (9-12)。(3) 最后，到达毛细血管的肿瘤细胞可能穿过内皮并形成潜在的转移灶 (4, 13)。目前的证据表明，细胞在肺血管系统中的简单截留不足以实现转移。肿瘤细胞必须（1）粘附于肺特异性粘附分子，例如位于血管内皮和基底膜上的层粘连蛋白和纤连蛋白，（2）产生降解弹性蛋白（一种优先位于肺细胞外基质中的分子）的酶，以及（3）能够与肺特异性生长因子结合生长。转移形成的主题超出了本报告的范围，但已在其他地方进行了综述 (14)。
Among the various causes of morbidity and mortality in patients with cancer, perhaps the least well described is tumor embolism. This condition was first documented in 1897 by Schmidt (1), but since then most information on this topic has been in the form of case reports or autopsy series. The paucity of information is due in part to the failure to recognize this condition antemortem. A significant proportion of such patients are diagnosed as having pulmonary thromboembolism and are treated with anticoagulation. Although recent studies have attempted to diagnose and differentiate malignant embolism from thromboembolism, lung biopsy remains the procedure of choice. These studies as well as the clinical manifestations of tumor embolism are the focus of this report. Although the specific cellular and molecular mechanisms of tumor embolism are not yet well understood, our onderstanding of the phenomenon has improved substantially in the last decade. Tumor cells access the systemic circulation via active invasion of small veins, venules, or the tumor's own microvasculature (2). The pulmonary vascular bed receives the entire cardiac output and filters any cell with a diameter of 10 µm or greater (3). Most tumor cells in the circulation are destroyed either by mechanical and shear forces of the microcirculation or by the various effector cells of the immune system. In fact, less than 1% of tumor cells that enter the circulation survive the passage through the lungs (4-6). The surviving tumor cells have a wide spectrum of biological fates and clinical manifestations:(1) Tumor cells may remain asymptomatic. In fact, autopsy review studies have shown that 18% to 68% of tumor emboli are discovered as incidental findings (7, 8).(2) Tumor cells may present a clinical picture similar to thromboembolic disease (9-12).(3) Finally, neoplastic cells that reach the capillaries may traverse the endothelium and form a potential focus of metastasis (4, 13). Current evidence has shown that the simple entrapment of cells in the pulmonary vasculature is insufficient for metastasis. Tumor cells must (1) adhere to lung-specific adhesion molecules such as laminin and fibronectin located on the vascular endothelium and basement membrane,(2) produce enzymes that degrade elastin, a molecule which is preferentially located in the lung extracellular matrix, and (3) be able to grow in association with lung-specific growth factors. The subject of metastasis formation is beyond the scope of this report but has been reviewed elsewhere (14).