Comparison of two ways of iron intake for patients with colorectal cancer and iron deficiency.
Ontology highlight
ABSTRACT:
DISEASE(S): Metastatic Colorectal Cancer,Iron Deficiency Anemia In Patients With Metastatic Or Inoperable Colorectal Cancer,Iron Deficiency Anemia
PROVIDER: 2532903 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
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Project description:Primary objectives: To compare the efficacy of two iron regimens for the treatment of postoperative anemia in patients undergoing colorectal neoplasia surgery.
Primary endpoints: Change in hemoglobin levels from postoperative day 1 to day 30
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Project description:Primary objectives: To evaluate the effect of iron therapy on platelet counts in patients with colorectal cancer and iron deficiency
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Project description:Iron plays the central role in the oxygen transport by the erythrocyte as a constituent of heme and hemoglobin. The importance of iron and heme also resides in their regulatory roles during erythroblast maturation. The transcription factor Bach1 may be involved in their regulatory roles since it is inactivated by direct binding of heme. To address whether Bach1 is involved in the responses of erythroblasts to iron status, low iron conditions that induced severe iron deficiency in mice were established. Under iron deficiency, extensive gene expression changes and mitophagy disorder were induced during maturation of erythroblasts. Bach1 mice showed more severe iron deficiency anemia in the developmental phase of mice and a retarded recovery once iron was replenished when compared with wild-type mice. In the absence of Bach1, the expression of globin genes and Hmox1 (encoding heme oxygenase-1) was de-repressed in erythroblasts under iron deficiency, suggesting that Bach1 represses these genes in erythroblasts under iron deficiency to balance the levels of heme and globin. Moreover, an increase in genome-wide DNA methylation was observed in erythroblasts of Bach1–/– mice under iron deficiency. These findings reveal the principle role of iron as a regulator of gene expression in erythroblast maturation and suggest that the iron-heme-Bach1 axis is important for a proper adaptation of erythroblast to iron deficiency to avoid toxic aggregates of non-heme globin.
2016-12-14 | GSE78955 | GEO
Project description:Iron (Fe) deficiency can represent a serious constraint on crop growth and productivity. A number of members of the bHLH transcription factor family are known to be involved in the plant Fe deficiency response. Plants have evolved two distinct uptake strategies when challenged by Fe deficiency: dicotyledonous and non-graminaceous species rely mostly on a reduction strategy regulated by bHLH transcription factors, whereas rice relies on a chelation strategy, also regulated by bHLH transcription factors. CmbHLH1, a bHLH transcription factor which is localized within the nucleus, was isolated from chrysanthemum. Its transcription was up-regulated both by Fe deficiency and by the exogenous application of abscisic acid. The roots of transgenic chrysanthemum plants in which CmbHLH1 was up-regulated were better able than those of the wild type chrysanthemum cultivar to acidify their immediate external environment by enhancing the transcription of the H(+)-ATPase encoding gene CmHA. However, there was no effect of the transgene on the efficiency of uptake of either manganese or zinc. Here, Chrysanthemum CmbHLH1 contributed to Fe uptake via H(+)-ATPase mediated acidification of the rhizosphere. ABA may be positively involved in the process.
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Project description:Interventions: Two groups:Iron Isomaltoside 1000 Inj. (100mg/ml and 500mg/5mls), Intravenous infusion 20mg/kg (<50kg BW) or 1000mg (>50kg BW) single +/- second dose 2 weeks later (in time frame of 3-10 weeks before operation) versus Standard care(control) - no iron supplement
Primary outcome(s): Preoperative change in hemoglobin concentration;Preoperative change in serum ferritin
Study Design: Parallel
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Project description:Iron deficiency in the human body is a global issue with an impact on more than two billion individuals worldwide. The most important functions ensured by adequate amounts of iron in the body are related to transport and storage of oxygen, electron transfer, mediation of oxidation-reduction reactions, synthesis of hormones, the replication of DNA, cell cycle restoration and control, fixation of nitrogen, and antioxidant effects. In the case of iron deficiency, even marginal insufficiencies may impair the proper functionality of the human body. On the other hand, an excess in iron concentration has a major impact on the gut microbiota composition. There are several non-genetic causes that lead to iron deficiencies, and thus, several approaches in their treatment. The most common methods are related to food fortifications and supplements. In this review, following a summary of iron metabolism and its health implications, we analyzed the scientific literature for the influence of iron fortification and supplementation on the gut microbiome and the effect of probiotics, prebiotics, and/or synbiotics in iron absorption and availability for the organism.
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Project description:Background and objectivesFew randomized controlled trials have compared intravenous iron products head to head in CKD patients with iron deficiency anemia. This study compared the efficacy and safety of two intravenous iron products (ferumoxytol [Feraheme injection] and iron sucrose [Venofer]) in patients with CKD and iron deficiency anemia.Design, setting, participants, & measurementsIn this phase II, randomized, open-label, active-controlled, multicenter clinical trial, patients were randomized 1:1 to either 1.02 g ferumoxytol (2 × 510-mg injections) or 1.0 g iron sucrose administered as either a slow injection or infusion (10 doses for dialysis patients and 5 doses for nondialysis patients). Inclusion criteria included hemoglobin<11.0 g/dl, transferrin saturation<30%, and eGFR<60 ml/min per 1.73 m(2) or a diagnosis of underlying CKD (e.g., nephropathy or nephritis). The primary end point was change in hemoglobin from baseline to week 5.ResultsIn total, 162 patients were randomized. Demographics were balanced between the treatment groups. Adverse event profiles of the two regimens were fairly similar: overall adverse events, 48% ferumoxytol versus 65% iron sucrose; related adverse events, 10% ferumoxytol versus 16% iron sucrose; and adverse events leading to study discontinuation, 1% ferumoxytol versus 5% iron sucrose. Rates of serious adverse events and related serious adverse events were similar between the ferumoxytol and iron sucrose groups: serious adverse events, 9% versus 7%, respectively and related serious adverse events, 1% versus 1%, respectively. Overall, increases in hemoglobin were similar between treatment groups. Based on an ANOVA model adjusted for baseline hemoglobin level and dialysis status, the least squares mean change from baseline to week 5 was 0.8 ± 0.1 g/dl in the ferumoxytol-treated group and 0.7 ± 0.1 g/dl in the iron sucrose group. The difference in the mean change from baseline between the two treatment groups was 0.1 g/dl (95% confidence interval, -0.2 to 0.4).ConclusionIn this randomized, controlled trial, ferumoxytol and iron sucrose showed comparable efficacy and adverse events rates.
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Project description:Iron refractory iron deficiency anemia is a hereditary recessive anemia due to a defect in the TMPRSS6 gene encoding Matriptase-2. This protein is a transmembrane serine protease that plays an essential role in down-regulating hepcidin, the key regulator of iron homeostasis. Hallmarks of this disease are microcytic hypochromic anemia, low transferrin saturation and normal/high serum hepcidin values. The anemia appears in the post-natal period, although in some cases it is only diagnosed in adulthood. The disease is refractory to oral iron treatment but shows a slow response to intravenous iron injections and partial correction of the anemia. To date, 40 different Matriptase-2 mutations have been reported, affecting all the functional domains of the large ectodomain of the protein. In vitro experiments on transfected cells suggest that Matriptase-2 cleaves Hemojuvelin, a major regulator of hepcidin expression and that this function is altered in this genetic form of anemia. In contrast to the low/undetectable hepcidin levels observed in acquired iron deficiency, in patients with Matriptase-2 deficiency, serum hepcidin is inappropriately high for the low iron status and accounts for the absent/delayed response to oral iron treatment. A challenge for the clinicians and pediatricians is the recognition of the disorder among iron deficiency and other microcytic anemias commonly found in pediatric patients. The current treatment of iron refractory iron deficiency anemia is based on parenteral iron administration; in the future, manipulation of the hepcidin pathway with the aim of suppressing it might become an alternative therapeutic approach.
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Project description:Iron is essential for life because it is indispensable for several biological reactions, such as oxygen transport, DNA synthesis, and cell proliferation. Over the past few years, our understanding of iron metabolism and its regulation has changed dramatically. New disorders of iron metabolism have emerged, and the role of iron as a cofactor in other disorders has begun to be recognized. The study of genetic conditions such as hemochromatosis and iron-refractory iron deficiency anemia (IRIDA) has provided crucial insights into the molecular mechanisms controlling iron homeostasis. In the future, these advances may be exploited to improve treatment of both genetic and acquired iron disorders. IRIDA is caused by mutations in TMPRSS6, the gene encoding matriptase-2, which downregulates hepcidin expression under conditions of iron deficiency. The typical features of this disorder are hypochromic, microcytic anemia with a very low mean corpuscular volume of erythrocytes, low transferrin saturation, no (or inadequate) response to oral iron, and only a partial response to parenteral iron. In contrast to classic iron deficiency anemia, serum ferritin levels are usually low-normal, and serum or urinary hepcidin levels are inappropriately high for the degree of anemia. Although the number of cases reported thus far in the literature does not exceed 100, this disorder is considered the most common of the "atypical" microcytic anemias. The aim of this review is to share the current knowledge on IRIDA and increase awareness in this field.
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Project description:Expression of the yeast Cth2 protein stimulates degradation of mRNAs encoding proteins with Fe-dependent functions in metabolism, in iron storage and in other cellular processes. We demonstrate that in response to Fe deprivation, the Cth2-homologue, Cth1, stimulates specific degradation of mRNAs involved in mitochondrially localized activities that include respiration and amino acid biosynthesis. Furthermore, yeast cells grown under Fe deprivation accumulate mRNAs encoding proteins that function in glucose metabolism. These studies demonstrate a reprogramming of cellular metabolism during Fe-starvation dependent on the coordinated activities of two mRNA binding proteins. Keywords: Messenger RNAs down regulated by Cth1 and Cth2 proteins in response to Fe-limitation
2008-07-15 | GSE11236 | GEO