Objectives: Hepcidin is a biomarker produced by hepatocytes in chronic disease anemia and is known to increase during chronic inflammation. This study compares the hepcidin levels in idiopathic pulmonary fibrosis (IPF) patients and controls, evaluating its relationship with anemia and systemic inflammation in IPF patients. Methods: This study included 82 IPF patients and 31 controls. Hepcidin levels were compared between the two groups. In the IPF group, the hepcidin and anemia parameters were compared between anemic and non-anemic patients. The significance between the hepcidin and systemic inflammation parameters such as Erythrocyte Sedimentation Rate, CRP (C-reactive protein) levels, ferritin levels, and the Systemic Immune–Inflammation Index (SII) was investigated. Erythrocyte Sedimentation Rate, C-reactive protein (CRP) levels, and ferritin levels were measured using automated analyzers. Hepcidin and erythropoietin (EPO) levels were determined using ELISA kits. Results: A significant difference in hepcidin levels was found between the IPF and control groups (37.13 ± 14.92 vs. 25.77 ± 11.25, p < 0.001). No significant difference in hepcidin levels was found between anemic and non-anemic IPF patients (38.25 ± 16.2 vs. 36.7 ± 14.6, p = 0.719). No significant correlation was found between hepcidin levels and anemia parameters (serum iron, ferritin, vitamin B12, serum transferrin, transferrin saturation, total iron-binding capacity, hemoglobin, folate, and erythropoietin) in IPF patients. Despite significant differences in the systemic inflammation parameters (ferritin and CRP) between patients and controls, no significant correlation was found between their hepcidin and systemic inflammation parameters. Conclusions: Our study demonstrates that the hepcidin levels in IPF patients are elevated independently of anemia and systemic inflammation. We propose that hepcidin could be a potential biomarker to be investigated in IPF patients.

The effects of chronic intermittent hypoxia associated with obstructive sleep apnea (OSA) on iron metabolism remain incompletely understood. This study aimed to evaluate whether serum hepcidin levels are associated with OSA severity independently of obesity and systemic inflammation. A total of 136 patients who underwent polysomnography for suspected OSA between April and December 2025 were included in the study. Participants were classified into control and OSA groups according to the Apnea–Hypopnea Index (AHI), and the OSA group was further categorized as mild, moderate, or severe. Demographic and anthropometric characteristics and Epworth Sleepiness Scale scores were recorded. Serum hepcidin levels were measured using an ELISA method and compared between groups, and their associations with clinical and polysomnographic parameters were analyzed. Serum hepcidin levels were significantly higher in patients with OSA than in the control group (48.83 ± 11.92 vs. 41.53 ± 12.43 ng/mL; p < 0.001) and increased progressively with disease severity. Hepcidin levels were not significantly correlated with conventional iron parameters but showed a strong positive association with the Oxygen Desaturation Index (ODI). In multivariable regression analysis, the positive relationship between AHI and serum hepcidin levels remained significant after adjustment for body mass index and C-reactive protein levels (p < 0.001). These findings suggest that elevated serum hepcidin levels in OSA are linked to hypoxic stress independently of obesity and systemic inflammation, indicating that hepcidin may represent a potential biomarker reflecting disease severity in OSA.

Hepcidin centrally regulates iron homeostasis and responds to inflammation, iron status, hypoxia, and erythropoietic signaling, yet circulating hepcidin in stable bronchiectasis is poorly characterized. We compared serum hepcidin between 61 patients with stable bronchiectasis and 39 controls without bronchiectasis and assessed associations with anemia, iron metabolism, systemic inflammation, severity, and phenotype. Hepcidin was lower in bronchiectasis (20.34 ± 7.85 vs. 28.34 ± 9.82 ng/mL; median, 20.31 [15.07–25.35] vs. 25.03 [21.00–34.66] ng/mL; p < 0.001). It showed no significant associations with anemia status or hematologic, iron metabolism, erythropoietic, or inflammatory indices. Exploratory analyses identified phenotype differences (p = 0.002); levels were lowest in chronic obstructive pulmonary disease–bronchiectasis (15.98 ± 6.52 ng/mL), compared with bronchiectasis alone (21.57 ± 6.71) and asthma–bronchiectasis (24.81 ± 9.00). Low hepcidin discriminated bronchiectasis from controls (AUC = 0.729; 95% bootstrap CI: 0.628–0.822); the ≤20.85 ng/mL cutoff yielded 59.0% sensitivity and 79.5% specificity. To our knowledge, this is the first human case–control evidence of reduced circulating hepcidin in stable bronchiectasis. The absence of significant associations with systemic inflammation or anemia/iron status, alongside phenotype differences, suggests that hepcidin may be a candidate biomarker of biological heterogeneity in bronchiectasis not reflected by routine markers.

Background/Objectives: Idiopathic pulmonary fibrosis (IPF) may progress despite antifibrotic therapy, highlighting the need for biomarkers of early treatment-associated biological changes. This study aimed to assess the potential role of hepcidin in monitoring treatment response by evaluating pre- and post-treatment serum hepcidin levels in patients with IPF receiving antifibrotic therapy. Methods: This prospective observational cohort study included 38 clinically stable patients diagnosed with IPF according to the 2022 American Thoracic Society/European Respiratory Society (ATS/ERS)criteria between January and July 2025. Serum hepcidin was measured by ELISA at antifibrotic therapy initiation and month 3. Demographic data, pulmonary function tests, diffusing capacity for carbon monoxide (DLCO), and 6 min walk test results were recorded. Analyses were performed using SPSS 25.0. Results: Mean serum hepcidin decreased from 33.00 ± 16.74 to 24.41 ± 12.42 ng/mL (p < 0.001), with reductions observed in 30 of 38 patients (78.9%). Mean forced vital capacity (FVC) increased from 73.83 ± 18.10% predicted to 77.74 ± 15.70% predicted (p < 0.001). Median DLCO increased from 68.50 (51.00–80.50)% predicted to 72.50 (60.00–83.75)% predicted (p < 0.001). Six-minute walk distance did not change significantly (p = 0.078), nor did hemoglobin, C-reactive protein, or erythrocyte sedimentation rate. The change in hepcidin did not differ between the pirfenidone and nintedanib groups (p = 0.817). Although FVC and DLCO increased over three months, these short-term functional changes should be interpreted cautiously, as test familiarization, measurement variability, and regression to the mean cannot be excluded; therefore, they should not be considered evidence of fibrosis reversal or a direct treatment effect. Conclusions: Our study provides the first real-world data demonstrating a significant decrease in serum hepcidin following antifibrotic treatment in patients with IPF. These findings suggest that serum hepcidin may have potential clinical utility as a biomarker for assessing response to antifibrotic therapy in IPF.