Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Institutionalized aged subjects, considered free of evolutive disease and whose body weight was stable, were studied. They were divided into two groups depending on their body mass index: controls (BMI greater than or equal to 24) and depleted (BMI less than or equal to 21). The depleted group, as judged by anthropometric measurements, showed dramatically reduced body muscle and adipose masses. Usual blood parameters were normal in both groups. Biochemical markers of the protein and energy status, viz. albumin, transthyretin, transferrin, somatomedin-C, as well as serum levels of osteocalcin and apolipoproteins AI, AII, B, CII, CIII and E, were not affected in the depleted group. However, moderate iron deficiency and marked zinc deficiency were found in this group. It is concluded that in the elderly, biochemical markers of the protein and energy status are not related to the nutritional status assessed by anthropometry.
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PMID:Discrepancy between anthropometry and biochemistry in the assessment of the nutritional status of the elderly. 191 1

We determined the influence of undernutrition on blood soluble transferrin receptor (sTfR) concentrations, an indicator of iron deficiency, in 99 Zairean women (aged 16-45 y) without inflammation. They were recruited during a survey on iron deficiency in rural Bas-Zaire. sTfR was measured by enzyme immunoassay, and indicators of nutritional status [albumin, transthyretin (or prealbumin), and retinol binding protein] were measured by radial immunodiffusion. Undernutrition was diagnosed if the concentration of any one of the indicators was below normal: albumin < 35 g/L, transthyretin < 160 mg/L, and retinol binding protein < 30 mg/L. The sTfR concentration ranged from 1.89 to 19.1 mg/L (mean: 8.7 mg/L). Mean values for indicators of nutritional status, serum ferritin, and transferrin saturation were within the normal range for health subjects. Regardless of the iron status (iron sufficiency, anemia, or iron deficiency with or without anemia) and whether women were pregnant or nonpregnant, undernutrition did not significantly reduce sTfR concentrations. A higher percentage (80%) of iron-deficient women with two or three protein values below normal had sTfR concentrations > 8 mg/L (which are suggestive of iron-deficiency erythropoiesis) compared with iron-deficient women with no (72.7%) or one (66.7%) protein value below normal, anemic women (46-60%) and iron-sufficient women (18.2-36.8%). Results suggest that sTfR can be used as an indicator of iron deficiency in field studies without in-depth assessment of nutritional status. However, the effect of severe malnutrition on this index requires further investigation.
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PMID:Serum transferrin receptor concentrations in women with mild malnutrition. 859 25

We recently reported the hemochromatosis-like phenotype observed in our Usf2 knockout mice. In these mice, as in murine models of hemochromatosis and patients with hereditary hemochromatosis, iron accumulates in parenchymal cells (in particular, liver and pancreas), whereas the reticuloendothelial system is spared from this iron loading. We suggested that this phenotypic trait could be attributed to the absence, in the Usf2 knockout mice, of a secreted liver-specific peptide, hepcidin. We conjectured that the reverse situation, namely overexpression of hepcidin, might result in phenotypic traits of iron deficiency. This question was addressed by generating transgenic mice expressing hepcidin under the control of the liver-specific transthyretin promoter. We found that the majority of the transgenic mice were born with a pale skin and died within a few hours after birth. These transgenic animals had decreased body iron levels and presented severe microcytic hypochromic anemia. So far, three mosaic transgenic animals have survived. They were unequivocally identified by physical features, including reduced body size, pallor, hairless and crumpled skin. These pleiotropic effects were found to be associated with erythrocyte abnormalities, with marked anisocytosis, poikylocytosis and hypochromia, which are features characteristic of iron-deficiency anemia. These results strongly support the proposed role of hepcidin as a putative iron-regulatory hormone. The animal models devoid of hepcidin (the Usf2 knockout mice) or overexpressing the peptide (the transgenic mice presented in this paper) represent valuable tools for investigating iron homeostasis in vivo and for deciphering the molecular mechanisms of hepcidin action.
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PMID:Severe iron deficiency anemia in transgenic mice expressing liver hepcidin. 1193 10

After more than a decade of relatively modest advancements, heart failure therapeutic development has accelerated, with the PARADIGM-HF trial and the SHIFT trial demonstrated significant reductions in cardiovascular death and heart failure hospitalization for sacubitril-valsartan and in heart failure hospitalization alone for ivabradine. Several heart failure therapies have since received or stand on the verge of market approval and promise substantive advances in the treatment of chronic heart failure. Some of these improve clinical outcomes, whereas others improve functional or patient-reported outcomes. In light of these rapid advances in the care of adults living with chronic heart failure, in this review we seek to update the general practitioner on novel heart failure therapies. Specifically, we will review recent data on the implementation of sacubitril-valsartan, treatment of functional mitral regurgitation, sodium-glucose co-transporter-2 (SGLT-2) inhibitor therapy, agents for transthyretin amyloid cardiomyopathy, treatment of iron deficiency in heart failure, and the use of biomarkers or remote hemodynamic monitoring to guide heart failure therapy.
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PMID:Recent advances in the treatment of chronic heart failure. 3194 37