Elevated Serum Hepcidin in Patients with AML Prior to and After Allogeneic Hematopoietic Cell Transplantation Does Not Correlate with Transfusional Body Iron, HFE Genotype or Graft Versus Host Disease and May Protect From Excessive Parenchymal Iron Loadin

Ann-Kathrin Eisfeld*,1, Mark Westerman, PhD*,2, Rainer Krahl*,3, Sabine Leiblein, PhD*,4, Uwe Gerd Liebert*,5, Marianne Hehme*,6, Dietger Niederwieser, MD7 and Haifa Kathrin Al-Ali, MD*,1

Author address: 

1 Hematology/Oncology, University of Leipzig, Leipzig, Germany, 2 Intrinsic LifeSciences, LLC, La Jolla, CA, USA, 3 Department of Hematology/Oncology, University of Leipzig, Leipzig, Germany, 4 University of Leipzig, 5 Institute of Virology,


Poster Board III-982 Hepcidin (hep), a 25-amino-acid peptide, is the central regulator of iron homeostasis. Its transcription is upregulated by inflammatory cytokines and iron and is downregulated by iron deficiency, ineffective erythropoiesis, and hypoxia. Also HFE gene mutations are associated with less liver hepcidin messenger RNA. Both inherited (HFE genotype) and treatment-related factors influencing hep expression in patients (pts) with AML prior to and after allogeneic hematopoietic cell transplantation (HCT) as blood transfusions (BT), body iron and anemia were studied. The impact of chemotherapy, conditioning regimen, and Graft versus Host Disease (GvHD) on serum hep was analysed. Patients and methods: 42 consecutive pts (23 male/19 female, median age 57 [range:18-70] years) with AML who underwent allogeneic HCT from February, 2008 - February, 2009 at the University of Leipzig were included. Each patient was assessed 10 days prior to and at a median of 3 (range: 3-5) months after HCT. Donors were matched related in 8 (19%) and matched unrelated (MUD) in 34 (81%) pts. Preparative regimen consisted of 12 Gy TBI/cyclophosphamid 120 mg/kg (ATG was included for unrelated HCT) in 13 (31%) and fludarabin 30 mg/m2/day for 3 days/2 Gy TBI) in 29 (69%) pts. Acute GvHD > grade II was present in 13 (31%) and chronic GvHD in 17 (40%) pts. HFE genotype prior to and after HCT was assessed by PCR technique. Body iron was assessed by serum ferritin (sf) (normal values

abstract No: 


Full conference title: 

51st American Society of Haematologists Annual Meeting
    • ASH 51st (2009)