The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2025
CD26/DPP-IV inhibitors and associations with chronic lung allograft dysfunction in a multicenter cohort.
СтатьяМногоцентровое исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Graham Alexander R, Grau-Sepulveda Maria V, Bush Buckley Erika J, Dilling Daniel F, Faro Albert, Hays Steven R, Kirchner Jerry L, Lehr Carli J, Moneke Isabelle, Passarelli Samuel, Tallarico Erin, Thaxton Abigail, Turner Grant A, Yen Bo Young H, Neely Megan L, Snyder Laurie D
Аннотация
BACKGROUND: CD26/dipeptidyl peptidase 4 inhibitors (gliptins) target proinflammatory pathways that contribute to the development of chronic lung allograft dysfunction (CLAD). We analyzed longitudinal clinical data from 6 North American lung transplant centers to elucidate the effect of gliptin exposure on CLAD development after lung transplantation.
METHODS: This cohort included 6 North American lung transplant centers, 4 sites from the Clinical Trials in Organ Transplantation-20 study and 2 additional sites. First lung transplant recipients between December 2015 and August 2018 were eligible with follow-up through June 2021. Gliptin exposures before CLAD onset, in addition to CLAD risk factors, were included in the models. The primary end-point was a composite of probable CLAD, CLAD-related deaths, and CLAD-related retransplant. Cox regression models were used to assess the association between gliptin use and the CLAD composite end-point.
RESULTS: Seven hundred and seventy-nine patients met inclusion criteria, with 126 (16.2%) having any gliptin exposure. Two hundred and thirty-three (29.9%) patients experienced probable CLAD composite outcome. Across all centers, gliptin exposure at any point was not associated with probable CLAD or definite CLAD across the study period. In a posthoc analysis of centers with median gliptin exposures >6 months, exposure within the first 90 days post-transplant was associated with a decreased risk of definite CLAD composite across the study period (hazard ratio [HR] 0.25; 95% confidence interval [CI], 0.07, 0.83; p < 0.05).
CONCLUSIONS: The association of gliptins and CLAD is complex, but early gliptin use may help protect against CLAD if started within 90 days post-transplant and used for a prolonged period.
METHODS: This cohort included 6 North American lung transplant centers, 4 sites from the Clinical Trials in Organ Transplantation-20 study and 2 additional sites. First lung transplant recipients between December 2015 and August 2018 were eligible with follow-up through June 2021. Gliptin exposures before CLAD onset, in addition to CLAD risk factors, were included in the models. The primary end-point was a composite of probable CLAD, CLAD-related deaths, and CLAD-related retransplant. Cox regression models were used to assess the association between gliptin use and the CLAD composite end-point.
RESULTS: Seven hundred and seventy-nine patients met inclusion criteria, with 126 (16.2%) having any gliptin exposure. Two hundred and thirty-three (29.9%) patients experienced probable CLAD composite outcome. Across all centers, gliptin exposure at any point was not associated with probable CLAD or definite CLAD across the study period. In a posthoc analysis of centers with median gliptin exposures >6 months, exposure within the first 90 days post-transplant was associated with a decreased risk of definite CLAD composite across the study period (hazard ratio [HR] 0.25; 95% confidence interval [CI], 0.07, 0.83; p < 0.05).
CONCLUSIONS: The association of gliptins and CLAD is complex, but early gliptin use may help protect against CLAD if started within 90 days post-transplant and used for a prolonged period.