{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T14:51:48Z","timestamp":1779202308116,"version":"3.51.4"},"reference-count":33,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2022,6,1]],"date-time":"2022-06-01T00:00:00Z","timestamp":1654041600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clinical Transplantation"],"published-print":{"date-parts":[[2022,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Introduction<\/jats:title><jats:p>The randomized IronIC trial evaluated the effect of intravenous ferric derisomaltose on physical capacity in iron\u2010deficient, maintenance heart transplant (HTx) recipients. Iron deficiency was defined as in heart failure with high cut\u2010points for ferritin to compensate for inflammation. However, intravenous iron did not improve physical capacity except in patients with ferritin &lt;30\u00a0\u03bcg\/L. We aimed to explore determinants of iron status in the 102 IronIC participants to better define iron deficiency in the HTx population.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We assessed key governors of iron homeostasis, such as hepcidin, soluble transferrin receptor (sTfR), and interleukin\u20106 (IL\u20106). We also measured growth factors and inflammatory markers with relevance for iron metabolism. The results were compared to those of 21 healthy controls.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Hepcidin did not differ between HTx recipients and controls, even though markers of inflammation were modestly elevated. However, HTx recipients with ferritin &lt;30\u00a0\u03bcg\/L or sTfR above the reference range had significantly reduced hepcidin levels suggestive of true iron deficiency. In these patients, intravenous iron improved peak oxygen uptake. Hepcidin correlated positively with ferritin and negatively with sTfR.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>HTx recipients with iron deficiency as defined in heart failure do not have elevated hepcidin levels, although inflammatory markers are modestly increased. The high ferritin cut\u2010offs used in heart failure may not be suitable to define iron deficiency in the HTx population. We suggest that hepcidin and sTfR should be measured to identify patients with true iron deficiency, who might benefit from treatment with intravenous iron.<\/jats:p><\/jats:sec>","DOI":"10.1111\/ctr.14695","type":"journal-article","created":{"date-parts":[[2022,5,9]],"date-time":"2022-05-09T15:09:10Z","timestamp":1652108950000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Iron homeostasis in heart transplant recipients randomized to ferric derisomaltose or placebo"],"prefix":"10.1111","volume":"36","author":[{"given":"Kristine V.","family":"Brautaset Englund","sequence":"first","affiliation":[{"name":"Institute of Clinical Medicine Faculty of Medicine University of Oslo  Oslo Norway"},{"name":"Department of Cardiology Oslo University Hospital, Rikshospitalet  Oslo Norway"},{"name":"K.G. Jebsen Cardiac Research Center and Center for Heart Failure Research Faculty of Medicine University of Oslo  Oslo Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Charlotte M.","family":"\u00d8stby","sequence":"additional","affiliation":[{"name":"Department of Cardiology Oslo University Hospital, Rikshospitalet  Oslo Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kaspar","family":"Broch","sequence":"additional","affiliation":[{"name":"Institute of Clinical Medicine Faculty of Medicine University of Oslo  Oslo Norway"},{"name":"Department of Cardiology Oslo University Hospital, Rikshospitalet  Oslo Norway"},{"name":"K.G. Jebsen Cardiac Research Center and Center for Heart Failure Research Faculty of Medicine University of Oslo  Oslo Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thor","family":"Ueland","sequence":"additional","affiliation":[{"name":"Research Institute of Internal Medicine Oslo University Hospital Rikshospitalet  Oslo Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P\u00e5l","family":"Aukrust","sequence":"additional","affiliation":[{"name":"Institute of Clinical Medicine Faculty of Medicine University of Oslo  Oslo Norway"},{"name":"Research Institute of Internal Medicine Oslo University Hospital Rikshospitalet  Oslo Norway"},{"name":"Department of Rheumatology Dermatology and Infectious Disease Oslo University Hospital  Oslo Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Einar","family":"Gude","sequence":"additional","affiliation":[{"name":"Department of Cardiology Oslo University Hospital, Rikshospitalet  Oslo Norway"},{"name":"K.G. 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