<b>Conclusions:</b> This study suggests that serum hepcidin is superior to hemoglobin, serum iron, serum ferritin, TS, and TIBC as an indicator of IDA in pregnant women.
Children and women with iron deficiency anemia had higher zinc-protoporphyrin/heme ratios (children=151 μmol/mol heme and women=155 μmol/mol heme) and lower hepcidin levels (children=1.2ng/mL and women=0.6ng/mL).
Evaluation of a competitive hepcidin ELISA assay in the differential diagnosis of iron deficiency anaemia with concurrent inflammation and anaemia of inflammation in elderly patients.
Given that hepcidin decrease may improve intestinal iron absorption, these results warrant further investigation in a larger cohort and especially in patients with IDA.
In conclusion, we identify the extract of CS as a novel, potent HAMP expression inhibitor, which may be further modified and optimized to become a dietary supplement or a therapeutic option for the amelioration of hepcidin-overexpression-related diseases, including iron deficiency anemia.
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.
In ROC analysis, serum hepcidin and ferritin had similar moderate utility in differentiating iron deficiency anemia from anemia of chronic disorders (AUC 0.63 95% CI 0.47-0.79 and 0.76 95% CI 0.61-0.90, respectively).
In this study, mild acute inflammation did not increase serum hepcidin in women with IDA, suggesting low iron status and erythropoietic drive offset the inflammatory stimulus on hepcidin expression.
Magnetic resonance imaging showed that iron overload was absent in nine patients, mild in one patient with metabolic syndrome, and high (180 μmol/g) in one patient with hereditary spherocytosis discovered after LT. At the end of follow-up, serum hepcidin was normal in 10 patients (11.12 ± 7.6 nmol/L; P<0.05) and low in one patient with iron deficiency anemia.
Recent research regarding hepcidin as a central regulator of iron homeostasis is promising, but it has not been used yet for the routine diagnosis of iron deficiency anemia.
The research showed that the concentration of hepcidin is statistically lower in children (4.4 ng/mL) and adolescents (4.1 ng/mL) who suffer from iron deficiency anemia in comparison with the control group (14 ng/mL, 10 ng/mL, respectively).
The results obtained suggest that in obese children with sufficient iron intake, the altered ferroportin-hepcidin axis may occur without signs of iron deficiency or iron deficiency anemia.
The significant positive correlation between ghrelin and iron and hepcidin levels in the plasma of children with iron deficiency anemia prompted us to hypothesize that ghrelin may affect iron metabolism.
The studies in the patients with iron deficiency anemia (IDA) implied the existence of the association of ghrelin with iron or hepcidin levels in the plasma under the pathophysiological conditions.
The study aims were to evaluate 1) the contribution of AI and iron deficiency anemia (IDA) to newborn iron endowment, 2) hepcidin as a biomarker to distinguish AI from IDA among pregnant women, and 3) risk factors for specific etiologies of maternal anemia.
This study suggests a protective role of HFE in IDA CD patients and confirms the role of TMPRSS6 in predicting oral iron response modulating hepcidin action on iron absorption.