Fibrosis biomarkers, including MMP-9, YKL-40, and KL-6, show potential for the early detection and phenotyping of chronic lung allograft dysfunction, though larger validation studies are required.
Can fibrosis biomarkers aid in the early detection and differentiation of chronic lung allograft dysfunction phenotypes in lung transplant recipients?
Fibrosis biomarkers may offer a non-invasive method for the early detection and phenotypic differentiation of chronic lung allograft dysfunction following lung transplantation.
Chronic lung allograft dysfunction (CLAD) is the major long-term cause of morbidity and mortality after lung transplantation. Both bronchiolitis obliterans syndrome and restrictive lung allograft syndrome, two main types of CLAD, lead to fibrosis in either the small airways or alveoli and pleura. Pathological pathways in CLAD and other types of fibrosis, for example idiopathic pulmonary fibrosis, are assumed to overlap and therefore fibrosis biomarkers could aid in the early detection of CLAD. These biomarkers could help to differentiate between different phenotypes of CLAD and could, in comparison to biomarkers of inflammation, possibly distinguish an infectious event from CLAD when a decline in lung function is present. This review gives an overview of known CLAD specific biomarkers, describes new promising fibrosis biomarkers currently investigated in other types of fibrosis, and discusses the possible use of these fibrosis biomarkers for CLAD.
Ploeg et al. (Mon,) conducted a review in Chronic lung allograft dysfunction (CLAD). Fibrosis biomarkers was evaluated. Fibrosis biomarkers, including MMP-9, YKL-40, and KL-6, show potential for the early detection and phenotyping of chronic lung allograft dysfunction, though larger validation studies are required.