Evidence map›Paper›PMID 29974224›Full record

ReviewZeitschrift fur Rheumatologie2018

[Rheumatoid arthritis].

E Neumann, K Frommer, M Diller, U Müller-Ladner

Abstract readReview
PubMed Publisher
In one paragraph

Review in Zeitschrift fur Rheumatologie, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Trial
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  5. [Tujia medicineNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
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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

4 authors at 2 institutions in 1 country.

E NeumannRheumatologie und Klinische Immunologie, Campus Kerckhoff, Justus-Liebig-Universität Gießen, Benekestr. 2-8, 61231, Bad Nauheim, Deutschland. e.neumann@kerckhoff-klinik.de.
K FrommerRheumatologie und Klinische Immunologie, Campus Kerckhoff, Justus-Liebig-Universität Gießen, Benekestr. 2-8, 61231, Bad Nauheim, Deutschland.
M DillerRheumatologie und Klinische Immunologie, Campus Kerckhoff, Justus-Liebig-Universität Gießen, Benekestr. 2-8, 61231, Bad Nauheim, Deutschland.
U Müller-LadnerRheumatologie und Klinische Immunologie, Campus Kerckhoff, Justus-Liebig-Universität Gießen, Benekestr. 2-8, 61231, Bad Nauheim, Deutschland.
Kerckhoff Klinik · DEUniversity of Giessen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is a chronic and progressive systemic disease of the connective tissue, which is particularly manifested with destructive alterations to the joints. Inflammatory reactions in the synovium lead to the influx of peripheral inflammatory cells as well as the activation of local cells. Released growth factors, chemokines and especially cytokines play a key role in chronic inflammatory responses. In addition to the central lymphocytes, the T and B cells and their subpopulations, locally resident cells, such as neutrophils, macrophages and fibroblasts as well as cells of bone metabolism are activated by the inflammatory milieu and contribute to and drive inflammation and tissue damage. The destruction of cartilage and bone substance by local tissue cells, synovial fibroblasts and osteoclasts is characteristic for this disease. Untreated, the local inflammatory and destructive processes as well as systemic inflammatory factors lead to progressive and irreversible joint destruction. Cellular and immunological processes in RA are closely interwoven; therefore, besides the general inhibition of immunological processes, specific inhibition of central key molecules can reduce or completely stop the inflammatory destructive processes; however, a high heterogeneity can be observed among RA patients and disease progression. Therefore, an expansion of the therapeutic options is desirable as not all patients are able to equally benefit from the therapeutic treatment. It is important to characterize new molecular mechanisms, which could lead to the development of new therapeutic options. Some of the more recent insights are summarized in this overview.

Indexed as

Arthritis, RheumatoidCytokinesFibroblastsHumansInflammationSynovial MembraneCytokinesCytokinesInflammationJoint erosionSynovitisTreatment options

Identifiers

PMID29974224
OpenAlexW4239444738

What OpenQuestion holds

Textmetadata
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.