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dc.contributor.authorVan Rijnsoever, M.
dc.contributor.authorGalhenage, S.
dc.contributor.authorMollison, L.
dc.contributor.authorGummer, J.
dc.contributor.authorTrengove, R.
dc.contributor.authorOlynyk, John
dc.date.accessioned2017-01-30T11:24:28Z
dc.date.available2017-01-30T11:24:28Z
dc.date.created2016-12-04T19:30:48Z
dc.date.issued2016
dc.identifier.citationVan Rijnsoever, M. and Galhenage, S. and Mollison, L. and Gummer, J. and Trengove, R. and Olynyk, J. 2016. Dysregulated erythropoietin, hepcidin, and bone marrow iron metabolism contribute to interferon-induced anemia in hepatitis C. Journal of Interferon and Cytokine Research. 36 (11): pp. 630-634.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/11393
dc.identifier.doi10.1089/jir.2016.0043
dc.description.abstract

© Mary Ann Liebert, Inc.Anemia is a complication of interferon-containing hepatitis C treatments. We characterized effects of interferon-based therapy on hepcidin and erythropoietin (EPO) production, iron metabolism, hemolysis, and hematopoiesis. Standard hemopoiesis [reticulocyte hemoglobin (Hb), reticulocyte production index (RPI), free Hb, and haptoglobin], iron biochemistry, hepcidin, and EPO levels were measured in 10 subjects over 12 weeks. There was a rapid decline in Hb during treatment, from a mean pretreatment (t = 0 weeks) Hb of 158.6 to 125.2 g/L at week 4 (P = 0.003) and 122.8 g/L at week 12 (P = 0.005). Paradoxically, the RPI (a measure of bone marrow responsiveness to EPO) decreased on initiation of hepatitis C virus treatment from 0.78% to 0.53% (P = 0.04). Despite worsening anemia, there was no significant increase in EPO levels. Hepcidin levels increased to >20nM in 3 subjects from 5.8 to 27.5nM (P = 0.009) compared with 9.6 to 12.3nM (P = 0.5) for the remainder of subjects. Hepcidin levels peaked at week 1 before returning to baseline levels at week 4. Subjects who responded with a rise in serum hepcidin levels to >20nM had a significantly greater drop in Hb (27.2 g/L, P = 0.008) and reticulocyte Hb (-1.4 g/L, P = 0.013) compared with the subjects who did not exhibit any change in hepcidin production. In conclusion, 30% of subjects treated with interferon exhibited significant transient increase in serum hepcidin levels, which was associated with more extreme anemia and decreased iron availability as evidenced by decreased reticulocyte Hb. In addition, there was a failure to upregulate EPO production in response to anemia and hemolysis (https://clinicaltrials.gov trial NCT01726400).

dc.titleDysregulated erythropoietin, hepcidin, and bone marrow iron metabolism contribute to interferon-induced anemia in hepatitis C
dc.typeJournal Article
dcterms.source.volume36
dcterms.source.number11
dcterms.source.startPage630
dcterms.source.endPage634
dcterms.source.issn1079-9907
dcterms.source.titleJournal of Interferon and Cytokine Research
curtin.accessStatusFulltext not available
curtin.facultyFaculty of Health Sciences


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