Increased levels of ERFE-encoding FAM132B in patients with congenital dyserythropoietic anemia type II

Russo, Roberta; Andolfo, Immacolata; Manna, Francesco; Rosa, Gianluca De; Falco, Luigia De; Gambale, Antonella; Bruno, Mariasole; Ricchi, Paolo; Girelli, Domenico; Franceschi, Lucia De; Iolascon, Achille

doi:10.1182/blood-2016-06-724328

Cited by 27 publications

(43 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This study raises questions about this new erythroid hormone and its role in hepcidin suppression in different types of anemia. [10][11][12][13] As there have been no previous reports on the relation between human serum erythroferrone and iron status parameters levels in cases with iron deficiency anemia; the present study aimed to demonstrate the relation between serum erythroferrone and iron status parameters levels in this widespread type of pediatric anemia.…”

Section: Discussionmentioning

confidence: 92%

See 1 more Smart Citation

Erythroferrone and iron status parameters levels in pediatric patients with iron deficiency anemia

Gendy

El-Hawy

Shehata

et al. 2018

European J of Haematology

View full text Add to dashboard Cite

Serum erythroferrone levels in iron deficiency anemia patients (191.55 ± 83.74 pg/mL) were significantly higher than those in control group (42.22 ± 16.55 pg/mL) (P < .001). In iron deficiency anemia patients, serum erythroferrone concentrations correlated negatively with hemoglobin concentration (r = -.39; P = .01), serum iron (r = -.63; P < .001), transferrin saturation (r = -.66; P < .001), and serum ferritin (r = -.46; P = .004) while positive correlation was observed between serum erythroferrone concentrations and TIBC (r = .62; P < .001) CONCLUSION: The newly identified erythroferrone hormone may act as physiological hepcidin suppressor in cases with iron deficiency anemia, and so it may serve as a specific promising target of therapy in such cases.

show abstract

Section: Discussionmentioning

confidence: 92%

“…Erythroferrone is lately identified by Kautz et al as key regulator of iron homeostasis during stress erythropoiesis by suppressing hepcidin expression. This study raises questions about this new erythroid hormone and its role in hepcidin suppression in different types of anemia …”

Section: Discussionmentioning

confidence: 98%

Erythroferrone and iron status parameters levels in pediatric patients with iron deficiency anemia

Gendy

El-Hawy

Shehata

et al. 2018

European J of Haematology

View full text Add to dashboard Cite

show abstract

“…In murine models, a hormone named erythroferrone (ERFE) has been identified as the hepcidin suppressing agent produced by erythroblasts [9,31]. In humans, the ERFE ortologue encoded by the gene FAM132B seems also involved in hepcidin suppression under conditions of increased erythropoiesis [32,33], although in combination with other factors still poorly characterized [23]. Finally, inflammation strongly stimulates hepcidin synthesis through several interleukins (IL), mainly IL-6 [34] and IL-1β [35].…”

Section: Pathophysiological Advances In Iron Metabolismmentioning

confidence: 99%

Modern iron replacement therapy: clinical and pathophysiological insights

et al. 2017

Self Cite

View full text Add to dashboard Cite

Iron deficiency, with or without anemia, is extremely frequent worldwide, representing a major public health problem. Iron replacement therapy dates back to the seventeenth century, and has progressed relatively slowly until recently. Both oral and intravenous traditional iron formulations are known to be far from ideal, mainly because of tolerability and safety issues, respectively. At the beginning of this century, the discovery of hepcidin/ferroportin axis has represented a turning point in the knowledge of the pathophysiology of iron metabolism disorders, ushering a new era. In the meantime, advances in the pharmaceutical technologies are producing newer iron formulations aimed at minimizing the problems inherent with traditional approaches. The pharmacokinetic of oral and parenteral iron is substantially different, and diversities have become even clearer in light of the hepcidin master role in regulating systemic iron homeostasis. Here we review how iron therapy is changing because of such important advances in both pathophysiology and pharmacology.

show abstract

“…He showed jaundice, gallstones and liver iron overload with high transferrin saturation, low hepcidin/ferritin ratio and increased level of erythroferrone. 10 Consequently to iron loading, he developed diabetes and complained of impotence. Mutations neither in HFE nor in HBA and HBB genes were detected.…”

Section: 8mentioning

confidence: 99%

GATA1 erythroid-specific regulation of SEC23B expression and its implication in the pathogenesis of congenital dyserythropoietic anemia type II

et al. 2017

Self Cite

View full text Add to dashboard Cite

Increased levels of ERFE-encoding FAM132B in patients with congenital dyserythropoietic anemia type II

Cited by 27 publications

References 16 publications

Erythroferrone and iron status parameters levels in pediatric patients with iron deficiency anemia

Erythroferrone and iron status parameters levels in pediatric patients with iron deficiency anemia

Modern iron replacement therapy: clinical and pathophysiological insights

GATA1 erythroid-specific regulation of SEC23B expression and its implication in the pathogenesis of congenital dyserythropoietic anemia type II

Contact Info

Product

Resources

About