Evidence map›Paper›PMID 26062541›Full record

ArticleArthritis research & therapy2015

High mobility group box 1 levels in large vessel vasculitis are not associated with disease activity but are influenced by age and statins.

Alexandre W S de Souza, Kornelis S M van der Geest, Elisabeth Brouwer, Frederico A G Pinheiro, Ana Cecília Diniz Oliveira, Emília Inoue Sato, Luis Eduardo C Andrade, Marc Bijl, Johanna Westra, Cees G M Kallenberg

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 20% 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

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

  1. Pooled it
  2. The Role of HMGB1 in Rheumatic Diseases.Frontiers in immunology · 2022
    Review
  3. Observational
  4. High mobility group box 1 as a biomarker in critically ill patients.Journal of clinical laboratory analysis · 2018
    Article
  5. Lupus erythematosus revisited.Seminars in immunopathology · 2016
    Review
  6. Review
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

10 authors at 3 institutions in 2 countries.

Alexandre W S de SouzaDepartment of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700, RB, Groningen, The Netherlands. alexandre_wagner@uol.com.br.
Kornelis S M van der GeestDepartment of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700, RB, Groningen, The Netherlands. k.s.m.van.der.geest@umcg.nl.
Elisabeth BrouwerDepartment of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700, RB, Groningen, The Netherlands. e.brouwer@umcg.nl.
Frederico A G PinheiroRheumatology Division, Universidade Federal de São Paulo - Escola Paulista de Medicina, R. Botucatu, 720, 04023 900, São Paulo, SP, Brazil. fredagp1@yahoo.com.br.
Ana Cecília Diniz OliveiraRheumatology Division, Universidade Federal de São Paulo - Escola Paulista de Medicina, R. Botucatu, 720, 04023 900, São Paulo, SP, Brazil. medceci@hotmail.com.
Emília Inoue SatoRheumatology Division, Universidade Federal de São Paulo - Escola Paulista de Medicina, R. Botucatu, 720, 04023 900, São Paulo, SP, Brazil. eisato@unifesp.br.
Luis Eduardo C AndradeRheumatology Division, Universidade Federal de São Paulo - Escola Paulista de Medicina, R. Botucatu, 720, 04023 900, São Paulo, SP, Brazil. luis.andrade@unifesp.br.
Marc BijlDepartment of Internal Medicine and Rheumatology, Martini Hospital, Van Swietenplein 1, 9728, NT, Groningen, The Netherlands. m.bijl@mzh.nl.
Johanna WestraDepartment of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700, RB, Groningen, The Netherlands. johanna.westra@umcg.nl.
Cees G M KallenbergDepartment of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700, RB, Groningen, The Netherlands. c.g.m.kallenberg@umcg.nl.
University Medical Center Groningen · NLUniversidade Federal de São Paulo · BRMartini Ziekenhuis · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionTakayasu arteritis (TA) and giant cell arteritis (GCA) are large vessel vasculitides (LVV) that usually present as granulomatous inflammation in arterial walls. High mobility group box 1 (HMGB1) is a nuclear protein that acts as an alarmin when released by dying or activated cells. This study aims to evaluate whether serum HMGB1 can be used as a biomarker in LVV.

methodsTwenty-nine consecutive TA patients with 29 healthy controls (HC) were evaluated in a cross-sectional study. Eighteen consecutive GCA patients with 16 HC were evaluated at the onset of disease and some of them during follow-up. Serum HMGB1 levels were measured by enzyme-linked immunosorbent assay.

resultsIn GCA patients at disease onset mean serum HMGB1 levels did not differ from HC (5.74 ± 4.19 ng/ml vs. 4.17 ± 3.14 ng/ml; p = 0.230). No differences in HMGB1 levels were found between GCA patients with and without polymyalgia rheumatica (p = 0.167), ischemic manifestations (p = 0.873), systemic manifestations (p = 0.474) or relapsing disease (p = 0.608). During follow-up, no significant fluctuations on serum HMGB1 levels were observed from baseline to 3 months (n = 13) (p = 0.075), 12 months (n = 6) (p = 0.093) and at the first relapse (n = 4) (p = 0.202). Serum HMGB1 levels did not differ between TA patients and HC [1.19 (0.45-2.10) ng/ml vs. 1.46 (0.89-3.34) ng/ml; p = 0.181] and no difference was found between TA patients with active disease and in remission [1.31 (0.63-2.16) ng/ml vs. 0.75 (0.39-2.05) ng/ml; p = 0.281]. HMGB1 levels were significantly lower in 16 TA patients on statins compared with 13 patients without statins [0.59 (0.29-1.46) ng/ml vs. 1.93 (0.88-3.34) ng/ml; p = 0.019]. Age was independently associated with higher HMGB1 levels regardless of LVV or control status.

conclusionsPatients with TA and GCA present similar serum HMGB1 levels compared with HC. Serum HMGB1 is not useful to discriminate between active disease and remission. In TA, use of statins was associated with lower HMGB1 levels. HMGB1 is not a biomarker for LVV.

Indexed as

AgedAge FactorsArea Under CurveBiomarkersCross-Sectional StudiesEnzyme-Linked Immunosorbent AssayFemaleGiant Cell ArteritisHMGB1 ProteinHumansHydroxymethylglutaryl-CoA Reductase InhibitorsMaleMiddle AgedROC CurveSensitivity and SpecificityTakayasu ArteritisBiomarkersHMGB1 ProteinHMGB1 protein, humanHydroxymethylglutaryl-CoA Reductase Inhibitors

Identifiers

PMID26062541
PMCPMC4480896
OpenAlexW1484621988

What OpenQuestion holds

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LicenceCC BY
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.