Evidence map›Paper›PMID 21366849›Full record

ArticleJournal of clinical hypertension (Greenwich, Conn.)2011

Determinants of vascular function in patients with chronic gout.

Robert D Brook, Srilakshmi Yalavarthi, James D Myles, Shokoufeh Khalatbari, Rita Hench, Susan Lustig, Wendy Marder, Adam Neidert, Mariana J Kaplan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of clinical hypertension (Greenwich, Conn.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Review
  6. Article
  7. Gout and Metabolic Syndrome: a Tangled Web.Current rheumatology reports · 2017
    Review
  8. Article
  9. Serum uric acid still carries controversies about its role in endothelial dysfunction.Journal of clinical hypertension (Greenwich, Conn.) · 2013
    Article
  10. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Robert D BrookDivisions of Rheumatology and Cardiology, Department of Internal Medicine; the Michigan Institute for Clinical Research, University of Michigan Medical School, 1150 W. Medical Center Drive, Ann Arbor, MI 48109, USA.
Srilakshmi Yalavarthi
James D Myles
Shokoufeh Khalatbari
Rita Hench
Susan Lustig
Wendy Marder
Adam Neidert
Mariana J Kaplan
Center for Rheumatology · USUniversity of Michigan–Ann Arbor · US

Funding

MICHIGAN INSTITUTE FOR CLINICAL AND HEALTH RESEARCH (MICHR) (UL1): (BPCA)UL1RR024986 · NCRR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHANLEY, THOMAS P. · 2007 to 2011
$51.2M
NCRR NIH HHS UL1 RR024986NCRR NIH HHS UL1RR024986
6 · The paper itself

Abstract

Epidemiologic studies have proposed a relationship between hyperuricemia and cardiovascular (CV) risk. However, it is unclear whether uric acid (UA) is an independent risk factor for CV disease (CVD) after controlling for other predisposing conditions. Gout patients might have persistent systemic inflammation, which, in addition to hyperuricemia, may potentiate CVD. This study examined vascular function and markers of CV damage in gout patients when compared with healthy controls. Brachial artery flow-mediated dilatation, arterial compliance, and microvascular function were measured. Circulating apoptotic endothelial cells and endothelial progenitor cells were quantified by FACS and circulating biomarkers of CVD by enzyme-linked immunosorbent assay. Gout patients displayed significant increases in body mass index, C-reactive protein, UA, and triglycerides and decreases in high-density lipoprotein. There were no significant differences in other CV traditional risk factors, adhesion molecules, or chemokines. Gout patients did not differ from controls in vascular function. In univariate and multivariate analysis, UA was not associated with the quantified CV risk parameters. Despite an increase in several CV risk factors, inflammation, and UA, gout patients display normal endothelial function and no increases in biomarkers of CVD. These results do not support the notion that gout is an independent risk factor for premature CVD.

Indexed as

AdultApoptosisBiomarkersCardiovascular SystemCase-Control StudiesChronic DiseaseCross-Sectional StudiesEndothelium, VascularFemaleGoutHealth Status IndicatorsHumansHyperuricemiaMaleMicrovesselsMiddle AgedBiomarkers

Identifiers

PMID21366849
PMCPMC3076024
OpenAlexW2114435234

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.