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izvor podataka: crosbi

Systemic inflammation up-regulates serum hepcidin in exacerbations and stabile chronic obstructive pulmonary disease (CROSBI ID 224442)

Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija

Tandara, Leida ; Žanić Grubišić, Tihana ; Gudelj, Ivan ; Jurišić, Zrinka ; Tandara, Marijana ; Gugo, Katarina ; Mladinov, Suzana ; Salamunić, Ilza Systemic inflammation up-regulates serum hepcidin in exacerbations and stabile chronic obstructive pulmonary disease // Clinical biochemistry, 48 (2015), 8; 1252-1257. doi: 10.1016/j.clinbiochem.2015.07.010

Podaci o odgovornosti

Tandara, Leida ; Žanić Grubišić, Tihana ; Gudelj, Ivan ; Jurišić, Zrinka ; Tandara, Marijana ; Gugo, Katarina ; Mladinov, Suzana ; Salamunić, Ilza

engleski

Systemic inflammation up-regulates serum hepcidin in exacerbations and stabile chronic obstructive pulmonary disease

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.

COPD ; Hepcidin ; Interleukin-6 ; Iron metabolism ; Systemic inflammation

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Podaci o izdanju

48 (8)

2015.

1252-1257

objavljeno

0009-9120

1873-2933

10.1016/j.clinbiochem.2015.07.010

Povezanost rada

Farmacija, Kliničke medicinske znanosti

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