Hepcidin and iron species distribution inside the first-trimester human gestational sac

Evans, Patricia; Cindrová‐Davies, Tereza; Muttukrishna, Shanthi; Burton, Graham J.; Porter, John B.; Jauniaux, Eric

doi:10.1093/molehr/gaq101

Cited by 38 publications

(25 citation statements)

References 31 publications

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“…3 Because of liver failure, the deficiency of fetal hepcidin synthesis could be involved in this iron metabolism dysregulation. 12 Interestingly, in several cases of GALD manifesting by fetal death, severe acute fetal liver failure was observed without siderosis, 4 suggesting that early death did not allow progressive iron overload to occur in the second and third trimesters of pregnancy. Our case shows that the mildest forms of GALD, manifesting probably later in pregnancy and without failure of the liver synthesis functions, are not associated with antenatal perturbation of the iron metabolism to the degree that iron overload occurs.…”

Section: Discussionmentioning

confidence: 99%

Neonatal Liver Cirrhosis Without Iron Overload Caused by Gestational Alloimmune Liver Disease

et al. 2012

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Gestational alloimmune liver disease has emerged as the major cause of antenatal liver injury and failure. It usually manifests as neonatal liver failure with hepatic and extrahepatic iron overload, a clinical presentation called neonatal hemochromatosis. We report on a newborn in whom fetal hepatomegaly was detected during pregnancy and who presented at birth with liver cirrhosis and mild liver dysfunction. Liver biopsy showed the absence of iron overload but strong immunostaining of hepatocytes for the C5b-9 complex, the terminal complement cascade neoantigen occurring specifically during complement activation by the immunoglobulin G-mediated classic pathway, which established the alloimmune nature of the hepatocyte injury. The infant survived with no specific therapy, and follow-up until 36 months showed progressive normalization of all liver parameters. This case report expands the recognized clinical spectrum of congenital alloimmune liver disease to include neonatal liver disease and cirrhosis, even in the absence of siderosis. Such a diagnosis is of utmost importance regarding the necessity for immunotherapy in further pregnancies to avoid recurrence of alloimmune injury.

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Section: Discussionmentioning

confidence: 99%

Neonatal Liver Cirrhosis Without Iron Overload Caused by Gestational Alloimmune Liver Disease

et al. 2012

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“…Other than the liver, hepcidin is also found in tissues with no recognized role in systemic iron homeostasis, including the heart (Merle et al, 2007), the brain (McCarthy and Kosman, 2014), the kidney (Kulaksiz, 2005) and the placenta (Evans et al, 2011). The function of this extra-hepatic hepcidin remains unknown, but one hypothesis is that it is involved in local iron control.…”

Section: Introductionmentioning

confidence: 99%

An essential cell-autonomous role for hepcidin in cardiac iron homeostasis

Lakhal‐Littleton

Wolna

Chung

et al. 2016

eLife

156

192

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Hepcidin is the master regulator of systemic iron homeostasis. Derived primarily from the liver, it inhibits the iron exporter ferroportin in the gut and spleen, the sites of iron absorption and recycling respectively. Recently, we demonstrated that ferroportin is also found in cardiomyocytes, and that its cardiac-specific deletion leads to fatal cardiac iron overload. Hepcidin is also expressed in cardiomyocytes, where its function remains unknown. To define the function of cardiomyocyte hepcidin, we generated mice with cardiomyocyte-specific deletion of hepcidin, or knock-in of hepcidin-resistant ferroportin. We find that while both models maintain normal systemic iron homeostasis, they nonetheless develop fatal contractile and metabolic dysfunction as a consequence of cardiomyocyte iron deficiency. These findings are the first demonstration of a cell-autonomous role for hepcidin in iron homeostasis. They raise the possibility that such function may also be important in other tissues that express both hepcidin and ferroportin, such as the kidney and the brain.DOI: http://dx.doi.org/10.7554/eLife.19804.001

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“…The fetus may be able to regulate placental iron trafficking via production of fetal hepcidin that is produced by the fetal liver early in gestation (8). Hepcidin is the master regulator of iron homeostasis, and the production of this hormone is known to be regulated by iron stores, inflammation, hypoxia, and erythropoietic activity (9).…”

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confidence: 99%

Prevalence of anemia and associations between neonatal iron status, hepcidin, and maternal iron status among neonates born to pregnant adolescents

et al. 2015

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ArticlesBackground: Little is known about anemia and iron status in US newborns because screening for anemia is typically not undertaken until 1 y of age. This study was undertaken to characterize and identify determinants of iron status in newborns born to pregnant adolescents. Methods: Pregnant adolescents (≤ 18 y, n = 193) were followed from ≥ 12 wk gestation until delivery. Hemoglobin, ferritin, soluble transferrin receptor, serum iron, hepcidin, erythropoietin (EPO), IL-6, and C-reactive protein were assessed in maternal and cord blood. results: At birth, 21% of the neonates were anemic (Hb < 13.0 g/dl) and 25% had low iron stores (ferritin < 76 µg/l). Cord serum ferritin concentrations were not significantly associated with gestational age (GA) at birth across the range of 37-42 wk. Neonates born to mothers with ferritin < 12 µg/l had significantly lower ferritin (P = 0.003) compared to their counterparts. Hepcidin and IL-6 were significantly (P < 0.05) higher in neonates born to mothers with longer durations of active labor. conclusion: Given the importance of the iron stores at birth on maintenance of iron homeostasis over early infancy, additional screening of iron status at birth is warranted among those born to this high risk obstetric population.

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Hepcidin and iron species distribution inside the first-trimester human gestational sac

Cited by 38 publications

References 31 publications

Neonatal Liver Cirrhosis Without Iron Overload Caused by Gestational Alloimmune Liver Disease

Neonatal Liver Cirrhosis Without Iron Overload Caused by Gestational Alloimmune Liver Disease

An essential cell-autonomous role for hepcidin in cardiac iron homeostasis

Prevalence of anemia and associations between neonatal iron status, hepcidin, and maternal iron status among neonates born to pregnant adolescents

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