Hepcidin Isoforms in Chronic Obstructive Pulmonary Disease Compared with the General Population

Hepcidin (Hep), a major regulator of iron metabolism, has several isoforms whose biological functions remain unknown. In chronic obstructive pulmonary disease (COPD) several factors, such as inflammation and hypoxemia, stimulate or inhibit Hep production. Our aims were to assess the isoform concentrations in COPD, explore the associations between the isoforms and pathophysiological variables, and assess the effect of initiation of long-term oxygen treatment (LTOT) on Hep concentrations.

The study population constituted 84 patients with COPD and 59 non-COPD participants. Hep isoforms, parameters of inflammation and iron status, and partial pressures of arterial oxygen (pO2) were measured at baseline and at 6-months follow-up in COPD patients. Associations between isoforms and clinical and biochemical characteristics were examined by multivariable tobit regression, while tobit regression with random effects was used to assess whether initiation of LTOT influenced the isoforms.

At least one isoform was detected in 96% of the participants, of which Hep25 was the most and Hep22 the least common. All isoforms were associated with C-reactive protein and ferritin. Hep25 and Hep24 were also associated with transferrin saturation, and Hep24 was associated with urine albumin-creatinine ratio. None of the isoforms were associated with hemoglobin, pO2, smoking, or COPD. There was a significant reduction of Hep25 and Hep24 from baseline to follow-up.

All isoforms were associated with inflammation, while Hep25 and Hep24 were associated with circulating iron and Hep24 with kidney disease. The concentrations of Hep isoforms were not associated with COPD, nor did initiation of LTOT result in significant changes of isoform concentrations.