Evidence map›Paper›PMID 29657867›Full record

ArticleEuropean journal of rheumatology2018

The relationship of serum endocan levels and anti-TNF-alpha therapy in patients with ankylosing spondylitis.

Fatma Zehra Kadayıfçı, Makbule Gezmen Karadağ

Open access · diamondAbstract read
In one paragraph

Article in European journal of rheumatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

0 citing papers in PubMed, 6 citations in OpenAlex.

No citing paper in PubMed yet.

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

2 authors at 1 institution in 2 countries.

Fatma Zehra KadayıfçıDepartment of Nutrition and Dietetic, Gazi University, Ankara, Turkey.ORCID http://orcid.org/0000-0003-4618-3853
Makbule Gezmen KaradağDepartment of Nutrition and Dietetic, Gazi University, Ankara, Turkey.ORCID http://orcid.org/0000-0003-3202-3250
California Baptist University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveEndocan is a marker for vascular pathogenesis and important mediator of angiogenesis that strongly associates with inflammation and vascular diseases. Growing evidence suggest that inflammatory cytokine tumor necrosis factor (TNF-alpha) plays a role in its regulation and secretion, whereas TNF-alpha inhibitors may have the opposite influence. The aim of this research is to investigate the association between serum endocan and anti-TNF-alpha drug treatment in patients with ankylosing spondylitis (AS).

methodsSerum endocan levels were analyzed in 42 patients with AS under anti-TNF-alpha usage. Control group consisted of 37 patients with AS who are not receiving anti-TNF drugs. Endocan is analyzed using ESM-1 ELISA kits. The blood glucose and lipid measurements of patients were also assessed.

resultsThere was no significant change in serum endocan levels among groups. The total cholesterol, triglyceride, and LDL-C levels were higher in patients receiving anti-TNF-alpha; however, differences were not significant. There was no significant correlation between serum endocan levels and blood lipid measurements.

conclusionAnti-TNF-alpha treatment does not affect serum endocan levels in patients with AS. This research has been first to evaluate the relationship between serum endocan and anti-TNF-alpha therapy in AS. Future studies are necessary to verify the exact role of anti-TNF-alpha therapy on serum endocan levels in patients with AS.

Indexed as

ankylosing spondylitisAnti-TNF-alpha treatmentendocan

Identifiers

PMID29657867
PMCPMC5895144
OpenAlexW2770080283

What OpenQuestion holds

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Registered trials

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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.