Linked Life Data

10957719

Source:http://linkedlifedata.com/resource/pubmed/id/10957719

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
13
pubmed:dateCreated
2000-9-27
pubmed:abstractText
The chronic immune activation state in HIV disease leads to increased activity of the rate-limiting tryptophan-kynurenine pathway enzyme indoleamine 2,3-dioxygenase (2,3-IDO), thereby increasing the formation of neurotoxic tryptophan metabolites such as kynurenine and quinolinic acid. We investigated whether highly active antiretroviral therapy (HAART) (median duration, 100 days; range, 50-188 days) lowers serum levels of these metabolites in HIV-infected individuals and if so, whether this was paralleled by changes in a surrogate marker for immune activation, i.e., soluble tumor necrosis factor receptor p75 (sTNFR p75) concentrations. Baseline quinolinic acid (848 nM, 95% CI 567-1130 vs. 303 nM, 95% CI 267.1-339.5) and kynurenine (4.1 microM, 95% CI 3.3-4.9 vs. 2.7 microM, 95% CI 2.4-2.9) concentrations as well as the mean kynurenine-to-tryptophan ratio (108.2, 95% CI 76.1-140.4 vs. 51.4, 95% CI 47.6-55.3) in 17 HIV-1-infected outpatients (7 with AIDS) were significantly higher than those in 55 healthy age-matched controls (p < 0.01), respectively. Serum quinolinic acid concentrations in 14 of 17 patients decreased (mean, -44.4%) during HAART in comparison with baseline (471.2 nM, 95% CI 288-654.3; p = 0. 022). Thirteen of these 14 patients also had decreases in sTNFR p75 concentrations. Overall, the mean sTNFR p75 concentration decreased by 36.3% (13.5 ng/ml, 95% CI 9.3-17.8 vs. 8.6 ng/ml, 95% CI 5.9-11. 4; p = 0.01, n = 17). Reduction in viral load through HAART and subsequent mitigation of the pathological immune activation state in HIV disease may have reduced 2,3-IDO over activation. This eventually led to a decrease in quinolinic acid formation. The parallel reduction of the immune activation marker sTNFR p75 supports this hypothesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0889-2229
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1215-21
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed-meshheading:10957719-Adult, pubmed-meshheading:10957719-Aged, pubmed-meshheading:10957719-Aged, 80 and over, pubmed-meshheading:10957719-Anti-HIV Agents, pubmed-meshheading:10957719-Antigens, CD, pubmed-meshheading:10957719-Drug Therapy, Combination, pubmed-meshheading:10957719-Female, pubmed-meshheading:10957719-HIV Infections, pubmed-meshheading:10957719-HIV-1, pubmed-meshheading:10957719-Humans, pubmed-meshheading:10957719-Kynurenine, pubmed-meshheading:10957719-Male, pubmed-meshheading:10957719-Middle Aged, pubmed-meshheading:10957719-Quinolinic Acid, pubmed-meshheading:10957719-RNA, Viral, pubmed-meshheading:10957719-Receptors, Tumor Necrosis Factor, pubmed-meshheading:10957719-Receptors, Tumor Necrosis Factor, Type II, pubmed-meshheading:10957719-Reverse Transcriptase Inhibitors, pubmed-meshheading:10957719-Treatment Outcome, pubmed-meshheading:10957719-Tryptophan, pubmed-meshheading:10957719-Viral Load
pubmed:year
2000
pubmed:articleTitle
Parallel decrease in neurotoxin quinolinic acid and soluble tumor necrosis factor receptor p75 in serum during highly active antiretroviral therapy of HIV type 1 disease.
pubmed:affiliation
Department of General Internal Medicine, University of Bonn, Germany. Look@Uni-Bonn.de
pubmed:publicationType
Journal Article, Clinical Trial