High pretransplant hepcidin levels are associated with poor overall survival and delayed platelet engraftment after allogeneic hematopoietic stem cell transplantation

Abstract

Iron overload is considered a risk factor for mortality in patients with hematopoietic malignancies. Hepcidin is a key regulator of systemic iron balance. We previously reported dynamic changes of serum hepcidin‐25 levels in patients with hematologic malignancies after allogeneic hematopoietic stem cell transplantation (allo‐HSCT). In this study, we retrospectively analyzed the association of pretransplant hepcidin‐25 levels with overall survival (OS), engraftment, and other clinical outcomes of allo‐HSCT in patients with hematologic malignancies. A total of 166 patients were divided into two groups depending on their pretransplant serum hepcidin‐25 levels; their median age was 49.5 years, and the median follow‐up time was 46.8 months. At 3 years, the patients in the high‐hepcidin group had a significantly lower OS than those in the low‐hepcidin group (49.2 vs. 69.0%, respectively; P = 0.006). Multivariate analysis revealed that pretransplant serum hepcidin‐25 level, sex, and disease status were independently associated with OS. The incidence of platelet engraftment was significantly lower in the high‐hepcidin group than in the low‐hepcidin group, whereas no significant differences were observed in neutrophil and reticulocyte engraftments between these groups. Hence, pretransplant serum hepcidin levels can be a marker for predicting delayed platelet recovery after allo‐HSCT.

Erythroferrone and hepcidin as mediators between erythropoiesis and iron metabolism during allogeneic hematopoietic stem cell transplant

“…Few studies have examined the significance of serum hepcidin in the context of allogeneic HCT 53 , 54 , 55 , 56 , 57 and none has analyzed in detail the interplay between iron metabolism and erythropoietic activity in this setting. In 2014, Kautz identified erythroferrone (ERFE), an erythropoietic regulator of iron mobilization and absorption through hepcidin suppression.…”

Pulmonary Infection Within 100 Days After Transplantation Impaired Platelet Recovery in Patients with Hematologic Malignancies: A Propensity-Score-Matched Analysis

“…Infection, iron overload, aGvHD, CMV infection, the use of ganciclovir or valganciclovir, and in vivo T cell depletion are significantly associated with increased risk of SFPR [10,23,24,31,33]. Thrombopoiesis, which occurs within a specialized bone marrow microenvironment, is a complex biological process that is initiated with the differentiation of hematopoietic stem cells (HSCs) to megakaryocytic progenitors and eventually results in the maturation of megakaryocytes to produce functional platelets [18,34].…”

Recent Advancements in Poor Graft Function Following Hematopoietic Stem Cell Transplantation

“…Hepcidin expressed by the liver, it modulates iron absorption and release and is overexpressed when IO decreases these processes, and the erythropoiesis demands can eventually not be met ( 119 ). The rates of OS and PLT engraftment were significantly lower in the high hepcidin group than in the low hepcidin group ( 120 ). Hepcidin may be an alternative marker of IO to predict delayed PLT engraftment after allo-HSCT; however, there is currently no accepted validated method for evaluating hepcidin.…”