Introduction: Molecular biomarkers for fibrotic sarcoidosis are limited, and telomere biology may reflect systemic ageing, fatigue, inflammation, and symptom burden.

Objectives: To assess whether peripheral blood leukocyte telomere length (LTL) and telomere-related genes (TERT, TINF2, TRF2) are associated with pulmonary fibrosis and patient-reported outcomes, particularly fatigue.

Materials and Methods: Cross-sectional study of 41 sarcoidosis patients, including 22 with radiographic fibrosis. Relative LTL and gene expression were quantified by qPCR (ΔΔCT/fold change). Groups were compared using age- and sex-adjusted analyses. Associations were assessed with Spearman’s correlation. Linear regression was used to explore factors associated with fatigue (FAS). Fibrosis prediction was explored using logistic regression models.

Results: LTL and telomere-related gene expression did not differ between patients with and without fibrosis (all p>0.05). Fibrosis was associated with worse lung function, including lower FEV1% (66 vs 82, p=0.006) and lower FEV1/FVC (59.5 vs 85, p=0.024), with a trend toward lower FVC% (80 vs 95, p=0.093). Fatigue was significantly associated with shorter telomeres (fold change: ρ=−0.658, p=0.002; ΔΔCT: ρ=+0.658, p=0.002). Exploratory multivariable analyses suggested that this relationship persisted after adjustment for selected clinical covariates, including lung function, sex, age, and dyspnoea. Telomere-based models did not improve fibrosis prediction beyond clinical variables.

Conclusions: qPCR-based leukocyte telomere measures were not associated with pulmonary fibrosis in sarcoidosis and did not improve fibrosis prediction, but shorter telomeres were associated with greater fatigue, including in exploratory multivariable analyses. These findings support further validation in larger cohort.