Thrombomodulin and syndecan-1 and association with lung function in liver transplant recipients

Liver transplant recipients have an increased risk of pulmonary complications, yet the pathogenesis remains poorly elucidated. The pulmonary endothelium is central in maintaining lung function, and endothelial dysfunction may contribute to airflow obstruction. Soluble thrombomodulin (TM) and syndecan-1 (SDC-1) are markers of endothelial damage, but whether TM and SDC-1 are related to lung function in liver transplant recipients remain unknown. This study investigated whether TM and SDC-1 are associated with forced expiratory volume in one second (FEV₁), forced vital capacity (FVC), and airflow obstruction in liver transplant recipients.

We included liver transplant recipients from The Danish Comorbidity in Liver Transplant Recipients (DACOLT) study. Airflow obstruction was defined as FEV₁/FVC <0.7. TM and SDC-1 were dichotomized, and an elevated concentration was defined as above the 3^rd quartile. Outcomes were analyzed using linear and logistic regression.

340 liver transplant recipients were included. Liver transplant recipients with elevated TM had 39.5 mL lower FEV₁ than liver transplant recipients with low TM (95% CI: -173.7;94.7, p=0.564), and 72.2 mL lower FVC (95% CI: -227.2;82.8, p=0.362), adjusted for confounders. The odds ratio (OR) for airflow obstruction was 1.01 (95% CI: 0.43;2.38, p=0.984). Liver transplant recipients with elevated SDC-1 had 93.4 mL lower FEV₁ than liver transplant recipients with low SDC-1 (95% CI: -223.1;36.3, p=0.159) and 31.2 mL lower FVC (95% CI: -181.6;119.2, p=0.684), adjusted for confounders. The OR for airflow obstruction was 0.97 (95% CI: 0.42;2.27, p=0.950).

In this study, we found no significant associations between TM or SDC-1 and FEV₁, FVC, and airflow obstruction in liver transplant recipients. Further research is warranted to elucidate the mechanisms underlying pulmonary complications in liver transplant recipients.