Delayed Alveolar Epithelialization: A Distinct Pathology in Diffuse Acute Lung Injury.
Delayed Alveolar Epithelialization: A Distinct Pathology in Diffuse Acute Lung Injury.
复制标题
延迟肺泡上皮化：弥漫性急性肺损伤的独特病理学。
DOI：
10.1164/rccm.201706-1094le
复制
发表时间：
2018
影响因子：
24.7
通讯作者：
Kradin,RichardL
中科院分区：
文献类型：
--
作者：
Taylor,MartinS;Chivukula,RaghuR;Myers,LauraC;Jeck,WilliamR;Tata,PurushothamaR;O'Donnell,WalterJ;Farver,CarolF;Thompson,BTaylor;Rajagopal,Jayaraj;Kradin,RichardL
Diffuse alveolar damage (DAD) is the most common histologic finding in acute respiratory distress syndrome (1). DAD proceeds through overlapping phases of acute injury with hyaline membrane formation, proliferation by type 2 alveolar epithelial cells (AEC2s), and fibroplasia (2, 3). Although it has long been appreciated that variable degrees of lung repair can occur after human acute lung injury, the cellular mechanisms underlying this response remain poorly understood. Recently, mouse models have identified nests or “pods” of proliferating peribronchiolar cells that arise after lung injury and may participate in regeneration (4, 5). However, these findings have yet to be corroborated in human patients.Here we report fulminant idiopathic acute lung injury requiring extracorporeal membrane oxygenation (ECMO) in two previously healthy young adults. Both presented with acute syndromes of fever and progressive dyspnea with bilateral airspace opacities on computed tomography (Figures 1A and 1B). Both clinically deteriorated despite treatment for presumptive community-acquired pneumonia and met Berlin criteria for severe acute respiratory distress syndrome (6). Hypoxemia worsened despite maximal medical therapy, including low tidal volume (, 6 ml/kg) ventilation, paralytics, recruitment maneuvers, positive endexpiratory pressure titration, pulmonary vasodilators, and prone positioning. Extensive autoimmune and infectious studies, including PCR and sequencing assays, were unrevealing. The first patient, a 27-year-old man, underwent bilateral lung transplantation after 101 days on ECMO and has recovered and returned to work. The second, a 35-year-old woman, required ECMO support for 85 days and has slowly recovered, although with a restrictive ventilatory deficit and pulmonary fibrosis.
弥漫性肺泡损伤中广泛的鳞状化生伴细胞学异型性，类似鳞状细胞癌：附2例报告。
影响因子：
3.3
作者：
S. Ogino;T. Franks;Mona Yong;M. Koss
通讯作者：
M. Koss
影响因子：
23.9
作者：
Hogan, Brigid L. M.;Barkauskas, Christina E.;Chapman, Harold A.;Epstein, Jonathan A.;Jain, Rajan;Hsia, Connie C. W.;Niklason, Laura;Calle, Elizabeth;Le, Andrew;Randell, Scott H.;Rock, Jason;Snitow, Melinda;Krummel, Matthew;Stripp, Barry R.;Thiennu Vu;White, Eric S.;Whitsett, Jeffrey A.;Morrisey, Edward E.
通讯作者：
Morrisey, Edward E.