Delta Hgb is higher in anemic patients who received IV iron.

<p>Delta Hgb values represent the difference of the hemoglobin value that was measured directly prior to surgery and the baseline hemoglobin level. <b>(A)</b> Baseline Hgb values were higher in non-anemic patients (14.3g/dl [13.48, 14.9], n = 48) than in both anemic patients with (10.8g/dl [10.05, 11.7], n = 79, *p<0.0001) and without (11.3g/dl [10.1, 11.93], n = 64, ^#p<0.0001) IV iron treatment. <b>(B)</b> Delta Hgb values were higher in anemic patients who were administered with IV iron (n = 40) (0.45g/dl [0.05, 1.05] vs. 0.1g/dl [-0.48, 0.73], *p = 0.03) compared to anemic patients without IV iron treatment (n = 26). <b>(C)</b> Patients with an increase in Hgb levels of ≥0.6g/dl were considered responders. Delta Hgb values were higher in the group of responders (1.1g/dl [0.8, 1.45], n = 19 patients) compared to the delta Hgb values in the group of anemic non-responders (0.1g/dl [-0.3, 0.3], n = 21 patients).</p

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<p>Four studies that analyzed hepcidin as a potential biomarker and/or the correlation between hepcidin and ferritin.</p

Comparison of hepcidin levels in the groups of responders and non-responders.

<p>Serum hepcidin levels were lower in anemic patients with a good response to IV iron (2.07ng/ml [0.25, 7.97], n = 19) compared to anemic patients with an impaired response (10.62ng/ml [3.93, 34.77], n = 21; *p = 0.04).</p

Multivariable regression analysis of delta Hgb.

<p>Multivariable regression analysis of delta Hgb.</p

Multivariable regression analysis for potential confounding effects.

<p>Multivariable regression analysis for potential confounding effects.</p

Correlation of serum hepcidin levels with parameters of the iron status.

<p>Serum hepcidin levels of the three patient groups of non-anemic controls, anemic patients treated with IV iron and anemic patients without IV iron treatment, were correlated to the iron parameters. The x- and y-scales are depicted logarithmic (log10). Values of “0” were replaced with 0.01 in order to depict them in the logarithmic graph. Serum hepcidin levels correlated with <b>(A)</b> serum iron levels (n = 146 XY-pairs (n = 9 non-anemics, n = 58 anemics without IV iron, n = 79 anemics plus IV iron); r = 0.19; Spearman *p = 0,02), <b>(B)</b> transferrin protein levels (n = 143 XY-pairs (n = 6 non-anemics, n = 58 anemics without IV iron, n = 79 anemics plus IV iron); r = -0,55; Spearman *p<0.0001), <b>(C)</b> ferritin levels (n = 143 XY-pairs (n = 6 non-anemics, n = 58 anemics without IV iron, n = 79 anemics plus IV iron); r = 0,75 Spearman *p<0.0001) and <b>(D)</b> transferrin saturation (n = 142 XY-pairs (n = 5 non-anemics, n = 58 anemics without IV iron, n = 79 anemics plus IV iron); r = 0.37; Spearman *p<0.0001).</p

Characteristics of responders and non-responders.

<p>Characteristics of responders and non-responders.</p

Intravenous Iron Carboxymaltose as a Potential Therapeutic in Anemia of Inflammation

<div><p>Intravenous iron supplementation is an effective therapy in iron deficiency anemia (IDA), but controversial in anemia of inflammation (AI). Unbound iron can be used by bacteria and viruses for their replication and enhance the inflammatory response. Nowadays available high molecular weight iron complexes for intravenous iron substitution, such as ferric carboxymaltose, might be useful in AI, as these pharmaceuticals deliver low doses of free iron over a prolonged period of time. We tested the effects of intravenous iron carboxymaltose in murine AI: Wild-type mice were exposed to the heat-killed <i>Brucella abortus</i> (BA) model and treated with or without high molecular weight intravenous iron. 4h after BA injection followed by 2h after intravenous iron treatment, inflammatory cytokines were upregulated by BA, but not enhanced by iron treatment. In long term experiments, mice were fed a regular or an iron deficient diet and then treated with intravenous iron or saline 14 days after BA injection. Iron treatment in mice with BA-induced AI was effective 24h after iron administration. In contrast, mice with IDA (on iron deficiency diet) prior to BA-IA required 7d to recover from AI. In these experiments, inflammatory markers were not further induced in iron-treated compared to vehicle-treated BA-injected mice. These results demonstrate that intravenous iron supplementation effectively treated the murine BA-induced AI without further enhancement of the inflammatory response. Studies in humans have to reveal treatment options for AI in patients.</p></div

Hepatic mRNA levels of pSTAT3, MCP-1, SOD2 and activin B in the liver of WT mice after BA and intravenous iron injection.

<p><b>(A)</b> Phosphorylated STAT3 levels compared to α-tubulin in the liver of C57BL/6 mice 4h after intraperitoneal BA or PBS administration followed by intravenous iron or PBS treatment for an additional 2h. <b>(B)</b> Hepatic MCP-1 mRNA levels were determined in WT mice after intraperitoneal BA or PBS administration followed by intravenous iron or PBS injection for an additional 2h (n = 3, 2-way ANOVA P<0,0001; **P = 0.007: PBS/PBS vs BA/PBS; *P = 0.02: PBS/PBS vs BA/iron; **P = 0.007: PBS/iron vs BA/PBS); (*P = 0.02: PBS/iron vs BA/iron; **P = 0.008: BA/PBS vs BA/iron; not shown in the graph). <b>(C)</b> Hepatic SOD2 mRNA levels in WT mice 4h after intraperitoneal BA or PBS administration followed by intravenous iron or PBS treatment for an additional 2h (n = 3, 2-way ANOVA P = 0.0002; **P = 0.004: PBS/PBS vs BA/PBS; **P = 0.004: PBS/PBS vs BA/iron); (**P = 0.006: PBS/iron vs BA/PBS; **P = 0.007: PBS/iron vs BA/iron, not shown in graph). <b>(D)</b> Hepatic activin B mRNA levels in WT mice 4h after intraperitoneal BA or PBS administration followed by intravenous iron or PBS injection for an additional 2h (n = 3, 2-way ANOVA P<0,0001; **P = 0.009: PBS/PBS vs BA/PBS; ***P = 0.0002: PBS/PBS vs BA/iron); (**P = 0.009: PBS/iron vs BA/PBS; ***P = 0.0003: PBS/iron vs BA/iron, not shown in graph).</p

Intravenous iron treated BA-induced anemia in mice.

<p>WT mice were challenged with intraperitoneal BA injection and 14d later treated with intravenous iron. <b>(A)</b> Hemoglobin levels 24h after the iron treatment in mice fed a regular (black bars) or iron deficient (white bars) diet (regular diet: n = 3, 2-way ANOVA P < 0,0001; ***P = 0.0006: PBS/PBS vs BA/PBS; *P = 0.02: BA/PBS vs BA/iron). <b>(B)</b> Hemoglobin levels 7d after the intravenous iron treatment as in (A) (iron deficient diet: n = 4, 2-way ANOVA P = 0.002; ***P = 0.0007: PBS/PBS vs BA/PBS; **P = 0.003: BA/PBS vs BA/iron). <b>(C)</b> Serum iron levels 24h after intravenous iron treatment in mice on a regular or iron deficient diet (iron deficient diet: n = 4, 2-way ANOVA P = 0.007; **P = 0.006: PBS/PBS vs BA/PBS; **P = 0.006: BA/PBS vs BA/iron). <b>(D)</b> Serum iron levels 7d after intravenous iron treatment as in (C).</p