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Increased serum hepcidin levels in patients with porphyria cutanea tarda
Author(s) -
Darwich E.,
ToFigueras J.,
MolinaLópez R.A.,
Deulofeu R.,
Olbina G.,
Westerman M.,
SánchezTápias J.M.,
MuñozSantos C.,
Herrero C.
Publication year - 2013
Publication title -
journal of the european academy of dermatology and venereology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.655
H-Index - 107
eISSN - 1468-3083
pISSN - 0926-9959
DOI - 10.1111/j.1468-3083.2012.04511.x
Subject(s) - hepcidin , medicine , porphyria cutanea tarda , homeostasis , ferritin , endocrinology , oxidative stress , inflammation , porphyria , immunology
Background Increased iron stores‐ are common in porphyria cutanea tarda (PCT) patients, but the pathophysiological pathways remain unknown. Down‐regulation of hepcidin, a peptide which regulates systemic iron homeostasis, has been demonstrated in different conditions associated with PCT, such as haemochromatosis, chronic hepatitis C (CHC) and excessive alcohol intake. However, serum hepcidin levels have not yet been studied in PCT patients. Objective To measure the serum hepcidin levels in patients with PCT, CHC and control patients, and to assess the association of hepcidin with serum markers of inflammation, iron overload and oxidative stress. Methods Hepcidin levels were measured by a competitive enzyme‐linked immunosorbent assay in serum samples of patients presenting PCT ( n = 30), CHC ( n = 31) and healthy volunteers ( n = 52). Results The mean of serum hepcidin levels was significantly higher in the PCT group (129.6 ng/mL) in comparison with the mean values in the CHC (41.3 ng/mL) and control (70.8 ng/mL) groups. The serum concentration of ferritin and interleukin‐6 (IL‐6) was also significantly higher in the PCT group, and correlated strongly with the hepcidin levels. The PCT patients with hepatitis C virus (HCV) infection showed significantly higher hepcidin levels than the group of CHC patients without porphyria. Conclusion Serum hepcidin levels are increased in patients with PCT suggesting that the mechanisms regulating iron homeostasis in PCT differ from those involved in other related disorders, such as haemochromatosis, HCV infection or alcohol abuse.