Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162316 (iron deficiency anemia)
 3,806 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Repeated blood donors manifest clinical, subclinical, and biochemical signs of iron deficiency anemia, have significantly higher erythropoietin and vascular endothelial growth factor (VEGF) concentrations, and decreased tissue oxygen saturation, oxygenated tissue hemoglobin, and regional cerebral oxygen saturation. Erythropoietin and VEGF are potent retinal angiogenic factors which may initiate and promote the retinal angiogenesis process independently or simultaneously. Increases in circulating levels of erythropoietin and VEGF are proportionate to the levels of hematocrit, hypoxemia, and tissue hypoxia. It is suggested that higher erythropoietin production following iron deficiency anemia-induced chronic hypoxemia/ hypoxia may, hypothetically, enhance the risk of retinal angiogenesis and/or neovascularization, possibly by inducing hypoxia inducible factor-1 alpha, which consequently upregulates genes stimulating angiogenesis, resulting in formation of a new vasculature, possibly by modulation of signal transducer and activator of transcription 3 signaling in the retina. Implications of this hypothesis cover erythropoietin doping, chronic hypoxia, and hypoxemic situations, such as angiogenesis-related cardiac and pulmonary diseases.
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PMID:Possibility of enhanced risk of retinal neovascularization in repeated blood donors: blood donation and retinal alteration. 2194 50

Hereditary hemorrhagic telangiectasia (HHT) also known as Rendu Osler syndrome is a vascular hereditary autosomal dominant disease, leading to a dysfunction in the development of arteriovenous capillaries, usually resulting in epistaxis, gastrointestinal (GI) bleeding, and iron deficiency anemia. It is believed that by interfering and stopping angiogenesis, anti-vascular endothelial growth factor molecules could be an option for HHT patients. Indeed, an intranasal treatment regime of diluted Avastin (bevacizumab; recombinant humanized antivascular epithelial growth factor immunoglobin G1) has proven clinically efficacious in patients with HHT1. However, there are no data available regarding bevacizumab's effect in patients with HHT and GI bleeding. We report here the case of an 85-year-old woman, suffering from life-threatening GI bleeding due to HHT with an impressive clinical response using anti-vascular endothelial growth factor infusion.
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PMID:Bevacizumab as rescue treatment for severe recurrent gastrointestinal bleeding in hereditary hemorrhagic telangiectasia. 2316 83

The mechanisms underlying thrombocytosis in patients with iron deficiency anemia remain unknown. Here, we present findings that support the hypothesis that low iron biases the commitment of megakaryocytic (Mk)-erythroid progenitors (MEPs) toward the Mk lineage in both human and mouse. In MEPs of transmembrane serine protease 6 knockout (Tmprss6-/-) mice, which exhibit iron deficiency anemia and thrombocytosis, we observed a Mk bias, decreased labile iron, and decreased proliferation relative to wild-type (WT) MEPs. Bone marrow transplantation assays suggest that systemic iron deficiency, rather than a local role for Tmprss6-/- in hematopoietic cells, contributes to the MEP lineage commitment bias observed in Tmprss6-/- mice. Nontransgenic mice with acquired iron deficiency anemia also show thrombocytosis and Mk-biased MEPs. Gene expression analysis reveals that messenger RNAs encoding genes involved in metabolic, vascular endothelial growth factor, and extracellular signal-regulated kinase (ERK) pathways are enriched in Tmprss6-/- vs WT MEPs. Corroborating our findings from the murine models of iron deficiency anemia, primary human MEPs exhibit decreased proliferation and Mk-biased commitment after knockdown of transferrin receptor 2, a putative iron sensor. Signal transduction analyses reveal that both human and murine MEP have lower levels of phospho-ERK1/2 in iron-deficient conditions compared with controls. These data are consistent with a model in which low iron in the marrow environment affects MEP metabolism, attenuates ERK signaling, slows proliferation, and biases MEPs toward Mk lineage commitment.
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PMID:Low iron promotes megakaryocytic commitment of megakaryocytic-erythroid progenitors in humans and mice. 3169 43