Background: Hepcidin, the systemic iron regulator, is induced during inflammation and leads to low circulating and increased intracellular iron levels. Results: (Patho)physiologically relevant H 2 O 2 levels up-regulate hepcidin via STAT3 in cultured liver cells. Conclusion: Intracellular and extracellular H 2 O 2 acts similarly to IL-6 on hepcidin up-regulation and requires a functional STAT3-binding site. Significance: H 2 O 2 is an important link between inflammation and iron metabolism.

SAA combined with CRP might be used as prognostic serological biomarkers in early-stage melanoma patients, helping to discriminate low-risk patients from high-risk patients needing adjuvant treatment.