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Chronic lung allograft dysfunction in 2022, past and updates
被引:2
|作者:
Halitim, P.
[1
,2
]
Tissot, A.
[2
]
机构:
[1] Hop Europeen Georges Pompidou, AP HP, Serv Pneumol & Soins Intens, F-75015 Paris, France
[2] Nantes Univ, CHU Nantes, Inserm, UMR 1064,Serv Pneumol,Inst Thorax,Ctr Res Transpla, F-44093 Nantes, France
关键词:
Lung transplantation;
Graft rejection;
Chronic lung lesion;
Biomarkers;
BRONCHIOLITIS-OBLITERANS-SYNDROME;
RANDOMIZED CONTROLLED-TRIAL;
CELL-FREE DNA;
GASTROESOPHAGEAL-REFLUX DISEASE;
T-REGULATORY-CELLS;
TRANSPLANT RECIPIENTS;
EXTRACORPOREAL PHOTOPHERESIS;
AZITHROMYCIN THERAPY;
CHRONIC REJECTION;
PERIPHERAL-BLOOD;
D O I:
10.1016/j.rmr.2023.01.025
中图分类号:
R56 [呼吸系及胸部疾病];
学科分类号:
摘要:
Introduction. - While short-term results of lung transplantation have improved considerably, long-term survival remains below that achieved for other solid organ transplants.Current knowledge. - The main cause of late mortality is chronic lung allograft dysfunction (CLAD), which affects nearly half of the recipients 5 years after transplantation. Immunologi-cal and non-immune risk factors have been identified. These factors activate the innate and adaptive immune system, leading to lesional and altered wound-healing processes, which result in fibrosis affecting the small airways or interstitial tissue. Several phenotypes of CLAD have been identified based on respiratory function and imaging pattern. Aside from retransplanta-tion, which is possible for only small number of patients, no treatment can reverse the CLAD process.Perspectives. - Current therapeutic research is focused on anti-fibrotic treatments and photo-pheresis. Basic research has identified numerous biomarkers that could prove to be relevant as therapeutic targets.Conclusion. - While the pathophysiological mechanisms of CLAD are better understood than before, a major therapeutic challenge remains.(c) 2023 SPLF. Published by Elsevier Masson SAS. All rights reserved.
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页码:324 / 334
页数:11
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