Abstract
Chronic lung allograft rejection remains one of the major causes of morbi-mortality after lung transplantation. The term Chronic Lung Allograft Dysfunction (CLAD) has been proposed to describe the different processes that lead to a significant and persistent deterioration in lung function without identifiable causes. The two main phenotypes of CLAD are Bronchiolitis Obliterans Syndrome (BOS) and Restrictive Allograft Syndrome (RAS), each of them characterized by particular functional and imaging features. These entities can be associated (mixed phenotype) or switched from one to the other. If CLAD remains a clinical diagnosis based on spirometry, computed tomography (CT) scan plays an important role in the diagnosis and follow-up of CLAD patients, to exclude identifiable causes of functional decline when CLAD is first suspected, to detect early abnormalities that can precede the diagnosis of CLAD (particularly RAS), to differentiate between the obstructive and restrictive phenotypes, and to detect exacerbations and evolution from one phenotype to the other. Recognition of early signs of rejection is crucial for better understanding of physiopathologic pathways and optimal management of patients.
Highlights
More than 4500 lung transplantations (LTs) are performed every year worldwide.Despite global improvements in surgical techniques and post-operative management of patients, long-term outcomes after lung transplantation remain poor compared to those of other solid organ transplantation
Different phenotypes have emerged in recent literature, and the division became more apparent when Sato et al defined a restrictive phenotype affecting up to 30% of patients, with evidence of functional decline, named Restrictive Allograft Syndrome (RAS) [2]
If the diagnosis of Chronic Lung Allograft Dysfunction (CLAD) relies on spirometry, computed tomography (CT) has proven to be an important complementary tool in the diagnosis and characterization of the different subtypes [4]
Summary
More than 4500 lung transplantations (LTs) are performed every year worldwide. Despite global improvements in surgical techniques and post-operative management of patients, long-term outcomes after lung transplantation remain poor compared to those of other solid organ transplantation. The first cause of death remains graft failure/chronic rejection [1], clinically presenting as progressive pulmonary function decline. Different phenotypes have emerged in recent literature, and the division became more apparent when Sato et al defined a restrictive phenotype affecting up to 30% of patients, with evidence of functional decline, named Restrictive Allograft Syndrome (RAS) [2]. The term Chronic Lung Allograft Dysfunction (CLAD) has been proposed to encompass the different phenotypes of chronic lung transplant rejection [3]. Evidence of an obstructive and restrictive profile (FEV1/FVC < 0.7 and low TLC) associated with pulmonary opacities defines the mixed phenotype. Known as neutrophilic reversible allograft dysfunction, ARAD is characterized by the presence of neutrophils in bronchoalveolar lavage and a functional obstructive profile mimicking BOS [13]. Two randomized clinical trials have demonstrated that a prophylactic treatment with azithromycin was associated with a significant reduction of the prevalence of BOS [16,17]
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