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.
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http://dx.doi.org/10.1111/j.1468-3083.2012.04511.x | DOI Listing |
Obes Rev
January 2025
Advanced Centre for Evidence Based Child Health, Advanced Pediatrics Centre, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Introduction: Obesity is a potential risk factor for anemia in children. This systematic review (SR) was undertaken to estimate the association of obesity with iron deficiency (ID) and ID anemia (IDA), in children.
Methods: A systematic literature search for observational studies was done in PubMed, EMBASE, Scopus, and the Cochrane library, with additional hand-searching.
Sci Rep
January 2025
Institute of Comparative Molecular Endocrinology, Ulm University, 89081, Ulm, Germany.
Hepatocellular carcinoma (HCC) remains the most prevalent type of primary liver cancer worldwide. p53 is one of the most frequently mutated tumor-suppressor genes in HCC and its deficiency in hepatocytes triggers tumor formation in mice. To investigate iron metabolism during liver carcinogenesis, we employed a model of chronic carbon tetrachloride injections in liver-specific p53-deficient mice to induce liver fibrosis, cirrhosis and subsequent carcinogenesis.
View Article and Find Full Text PDFEur J Prev Cardiol
January 2025
Brigham and Women's Hospital, Boston, MA.
Aims: Hepcidin regulates plasma and tissue iron levels. We studied the association of hepcidin levels with the risk of incident heart failure (HF) and cardiac dysfunction in older adults.
Methods: We included adults from the ongoing, longitudinal Atherosclerosis Risk in Communities (ARIC) study who were free from prevalent anemia and HF at Visit 5 (2011-2013) and had available hepcidin and covariate data.
J Trace Elem Med Biol
January 2025
Biochemistry Laboratory, Department of Zoology, Dr. Harisingh Gour Vishwavidyalaya (A Central University), Sagar, Madhya Pradesh 470003, India. Electronic address:
One of the most common diseases worldwide is anemia, which is characterized by insufficient erythrocyte production. Numerous complex factors, such as chronic diseases, genetic mutations, and nutritional inadequacies, contribute to this widespread syndrome. This review focuses specifically on anemias caused by defective hepcidin production.
View Article and Find Full Text PDFOur knowledge of which bone marrow cells affect red cell production is still incomplete. To explore the role of osteocytes in the process we performed bulk RNAseq of osteocytes isolated from control and phlebotomized mice. The top-upregulated gene following phlebotomy was , erythroferrone ( ).
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