Leida Tandara1, Tihana Zanic Grubisic2, Gudelj Ivan3, Zrinka Jurisic4, Marijan Tandara5, Katarina Gugo6, Suzana Mladinov7, Ilza Salamunic8. 1. Department of Medical Laboratory Diagnosis, University Hospital Center Split, 21000 Split, Croatia. Electronic address: leida.tandara@gmail.com. 2. Department of Medical Biochemistry and Hematology, Faculty of Pharmacy and Biochemistry, University of Zagreb, 10000 Zagreb, Croatia. Electronic address: tihana_zanic@yahoo.co.uk. 3. Clinical Department for Pulmonary Diseases, Universiti Hospital Center Split, 21000 Split, Croatia. Electronic address: ivan.gudelj.1956@gmail.com. 4. Department of Cardiology, University Hospital Center Split, 21000 Split, Croatia. Electronic address: zrinkacn@gmail.com. 5. Department of Human Reproduction, Clinic for Women's Diseases and Obstetrics, University Hospital Center Split, 21000 Split, Croatia. Electronic address: marijan.tandara@inet.hr. 6. Department of Medical Laboratory Diagnosis, University Hospital Center Split, 21000 Split, Croatia. Electronic address: katarina.gugo@gmail.com. 7. Clinical Department for Pulmonary Diseases, Universiti Hospital Center Split, 21000 Split, Croatia. Electronic address: suzana.mladinov@gmail.com. 8. Department of Medical Laboratory Diagnosis, University Hospital Center Split, 21000 Split, Croatia. Electronic address: ilza.salamunic@gmail.com.
Abstract
OBJECTIVES: Hepcidin is the main regulator of systemic iron homeostasis and its expression is modulated by iron status, hypoxia, erythroid factors and inflammation. The aim of our study was to examine a relationship between level of hepcidin and iron status, erythropoietic activity, hypoxia and inflammation in exacerbations and stable COPD patients. We hypothesized that hepcidin concentration is changed in COPD patients and is substantially influenced by inflammation and/or hypoxia. DESIGN AND METHODS: The study included 40 COPD patients and 30 healthy subjects. We measured haemoglobin, serum level of hepcidin and parameters indicative for inflammation: interleukin-6 (IL-6) and C reactive protein (CRP); hypoxia: partial oxygen pressure and haemoglobin oxygen saturation; iron status: iron, total iron binding capacity (TIBC), transferring saturation and ferritin; and erythropoietic activity: soluble transferrin receptors, reticulocytes, and erythropoietin. RESULTS: Hepcidin was elevated in exacerbations and in a stable phase compared to the control group and we found positive correlations of hepcidin with inflammatory markers IL-6 and CRP. Hepcidin also correlated positively with ferritin and inversely with TIBC. However, in COPD patients reticulocyte count was significantly reduced and negative correlation with hepcidin was established in exacerbation. No correlations were observed with iron, or indices of hypoxia. In the control group, positive associations were observed only with indices of iron status, positive with ferritin and negative one with TIBC. CONCLUSION: Systemic inflammation and elevated values of IL-6 present in exacerbations and stabile COPD might be responsible for the observed increased hepcidin level.
OBJECTIVES:Hepcidin is the main regulator of systemic iron homeostasis and its expression is modulated by iron status, hypoxia, erythroid factors and inflammation. The aim of our study was to examine a relationship between level of hepcidin and iron status, erythropoietic activity, hypoxia and inflammation in exacerbations and stable COPDpatients. We hypothesized that hepcidin concentration is changed in COPDpatients and is substantially influenced by inflammation and/or hypoxia. DESIGN AND METHODS: The study included 40 COPDpatients and 30 healthy subjects. We measured haemoglobin, serum level of hepcidin and parameters indicative for inflammation: interleukin-6 (IL-6) and C reactive protein (CRP); hypoxia: partial oxygen pressure and haemoglobin oxygen saturation; iron status: iron, total iron binding capacity (TIBC), transferring saturation and ferritin; and erythropoietic activity: soluble transferrin receptors, reticulocytes, and erythropoietin. RESULTS:Hepcidin was elevated in exacerbations and in a stable phase compared to the control group and we found positive correlations of hepcidin with inflammatory markers IL-6 and CRP. Hepcidin also correlated positively with ferritin and inversely with TIBC. However, in COPDpatients reticulocyte count was significantly reduced and negative correlation with hepcidin was established in exacerbation. No correlations were observed with iron, or indices of hypoxia. In the control group, positive associations were observed only with indices of iron status, positive with ferritin and negative one with TIBC. CONCLUSION: Systemic inflammation and elevated values of IL-6 present in exacerbations and stabile COPD might be responsible for the observed increased hepcidin level.
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