Extract
Lung transplantation is an established treatment option for well-selected patients with end-stage pulmonary disease, when other therapeutic options are no longer available. Although post-transplant survival has much improved in recent years, the development of chronic lung allograft dysfunction (CLAD), which affects 40–50% of all patients by 5 years post-transplant, remains the major cause of morbidity and mortality [1]. CLAD is defined by a progressive and persistent decline in the forced expiratory volume in the first second (FEV1) of at least 20% compared to the postoperative best value. Several different phenotypes of CLAD have been identified, based on the physiology of the lung function decline, such as obstructive (bronchiolitis obliterans syndrome; BOS), restrictive (restrictive allograft syndrome) or a combination (mixed phenotype), along with the presence or absence of persistent opacities on chest imaging [2, 3]. One of the problems that may arise when interpreting post-transplant lung function decline is that the natural decline in FEV1 after lung transplantation is unknown at present.
Abstract
After bilateral lung transplantation, the natural decline in FEV1 is only slightly increased compared to normal physiological ageing decline in FEV1 in healthy subjects https://bit.ly/3pwkrqq
Footnotes
Conflict of interest: G.M. Verleden reports participation on advisory boards for Zambon, CLAD and cGVHD, outside the submitted work. All other authors have nothing to disclose.
Support statement: R. Vos is supported by a Senior Clinical Research Fellowship of the Research Foundation Flanders (1803521N). G.M. Verleden and D.E. Van Raemdonck are supported by the Broere Charitable Foundation. Funding information for this article has been deposited with the Crossref Funder Registry.
- Received March 25, 2022.
- Accepted August 11, 2022.
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