Linked Life Data

16395269

Source:http://linkedlifedata.com/resource/pubmed/id/16395269

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-2-9
pubmed:abstractText
Intravenous iron is commonly used in conjunction with erythropoietic agents to treat anemia in patients with chronic kidney disease. Iron has been proposed to promote oxidative stress and endothelial dysfunction in vascular tissues. We studied the acute effects of intravenous iron sucrose on homocysteine-induced endothelial dysfunction in the brachial artery of normal human subjects. In all, 40 healthy subjects received intravenous iron sucrose 100 mg or placebo over 30 min immediately before ingestion of 100 mg/kg of oral methionine in a double-blind, randomized study. Flow- and nitroglycerin-mediated dilation in the brachial artery, serum markers of iron stores, and homocysteine and nitrotyrosine levels were measured before and after study drug administration. Intravenous iron significantly increased transferrin saturation and non-transferrin-bound iron (NTBI) when compared with placebo. Flow-mediated dilation significantly decreased from baseline 1 h after administration of iron sucrose when compared with placebo (from 6.66+/-0.47 to 1.93+/-0.35% after iron sucrose vs from 6.00+/-0.40 to 5.61+/-0.46% after placebo, P<0.001), but did not differ between groups at 4 h (1.10+/-0.39 vs 1.33+/-0.51%). Nitroglycerin-mediated vasodilation, and homocysteine and 3-nitrotyrosine levels did not differ after administration of iron sucrose and placebo. Intravenous administration of iron sucrose in the setting of transient hyperhomocysteinemia induced by methionine ingestion significantly increased transferrin saturation and plasma levels of NTBI and significantly attenuated flow-mediated dilation in the brachial artery when compared with placebo. This potential mechanistic link between intravenous iron and endothelial dysfunction warrants further study of cardiovascular effects of intravenous iron in anemic chronic kidney disease populations.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0085-2538
pubmed:author
pubmed:issnType
Print
pubmed:volume
69
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
679-84
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:16395269-Adult, pubmed-meshheading:16395269-Anemia, Iron-Deficiency, pubmed-meshheading:16395269-Brachial Artery, pubmed-meshheading:16395269-Cardiovascular Diseases, pubmed-meshheading:16395269-Chelating Agents, pubmed-meshheading:16395269-Double-Blind Method, pubmed-meshheading:16395269-Endothelium, Vascular, pubmed-meshheading:16395269-Female, pubmed-meshheading:16395269-Ferric Compounds, pubmed-meshheading:16395269-Ferritins, pubmed-meshheading:16395269-Homocysteine, pubmed-meshheading:16395269-Humans, pubmed-meshheading:16395269-Iron, pubmed-meshheading:16395269-Male, pubmed-meshheading:16395269-Methionine, pubmed-meshheading:16395269-Nitroglycerin, pubmed-meshheading:16395269-Oxidative Stress, pubmed-meshheading:16395269-Razoxane, pubmed-meshheading:16395269-Regional Blood Flow, pubmed-meshheading:16395269-Risk Factors, pubmed-meshheading:16395269-Transferrin, pubmed-meshheading:16395269-Tyrosine, pubmed-meshheading:16395269-Vasodilation
pubmed:year
2006
pubmed:articleTitle
Iron sucrose augments homocysteine-induced endothelial dysfunction in normal subjects.
pubmed:affiliation
Department of Medicine, Yale University School of Medicine, New Haven, Conneticut 06510, USA.
pubmed:publicationType
Journal Article, Randomized Controlled Trial, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural