Systemic inflammation up-regulates serum hepcidin in exacerbations and stabile chronic obstructive pulmonary disease
| Autor: | Katarina Gugo, Marijan Tandara, Ilza Salamunić, Gudelj Ivan, Leida Tandara, Suzana Mladinov, Tihana Zanic Grubisic, Zrinka Jurišić |
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| Rok vydání: | 2015 |
| Předmět: |
Male
medicine.medical_specialty Reticulocytes Iron Clinical Biochemistry Gene Expression Transferrin receptor Inflammation Systemic inflammation Hemoglobins Pulmonary Disease Chronic Obstructive Hepcidins Hepcidin Total iron-binding capacity hemic and lymphatic diseases Internal medicine Receptors Transferrin medicine Humans Hypoxia Erythropoietin Aged COPD Interleukin-6 Iron metabolism Aged 80 and over biology medicine.diagnostic_test Chemistry C-reactive protein Transferrin nutritional and metabolic diseases General Medicine Middle Aged Hypoxia (medical) Oxygen Ferritin C-Reactive Protein Endocrinology Case-Control Studies Immunology Disease Progression biology.protein Female medicine.symptom |
| Zdroj: | Clinical Biochemistry. 48:1252-1257 |
| ISSN: | 0009-9120 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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