Revue des maladies respiratoires · 2023
[Chronic lung allograft dysfunction in 2022, past and updates].
Аннотация на английскомСтатьяОбзорНазвание и аннотация: Перевод пока не подготовлен
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Halitim P, Tissot A
Аннотация
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. Immunological 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 retransplantation, 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 photopheresis. 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.
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. Immunological 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 retransplantation, 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 photopheresis. 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.