Highly Elevated Serum Hepcidin in Patients with Acute Myeloid Leukemia prior to and after Allogeneic Hematopoietic Cell Transplantation : Does This Protect from Excessive Parenchymal Iron Loading?

Abstract EN

Hepcidin is upregulated by inflammation and iron.

Inherited (HFE genotype) and treatment-related factors (blood units (BU), Iron overload) affecting hepcidin (measured by C-ELISA) were studied in 42 consecutive patients with AML prior to and after allogeneic hematopoietic cell transplantation (HCT).

Results.

Elevated serum ferritin pre- and post-HCT was present in all patients.

Median hepcidin pre- and post-HCT of 358 and 398 ng/mL, respectively, were elevated compared to controls (median 52 ng/mL) (P<.0001).

Liver and renal function, prior chemotherapies, and conditioning had no impact on hepcidin.

Despite higher total BU after HCT compared to pretransplantation (P<.0005), pre- and posttransplant ferritin and hepcidin were similar.

BU influenced ferritin (P=.001) and hepcidin (P=.001).

No correlation of pre- or posttransplant hepcidin with pretransplant ferritin was found.

HFE genotype did not influence hepcidin.

Conclusions.

Hepcidin is elevated in AML patients pre- and post-HCT due to transfusional iron-loading suggesting that hepcidin synthesis remains intact despite chemotherapy and HCT.