Evidence map›Paper›PMID 20703489›Full record

ArticleZeitschrift fur Rheumatologie2010

[IL-1 antagonists].

I Kötter, G Horneff

Abstract read
PubMed Publisher
In one paragraph

Article in Zeitschrift fur Rheumatologie, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

2 authors at 2 institutions in 1 country.

I KötterInterdisziplinäres Zentrum für Rheumatologie, Klinische Immunologie und Autoimmunerkrankungen (INDIRA) und Medizinische Universitätsklinik Abt. II, Universistätsklinikum Tübingen, 72076 Tübingen, Deutschland. ina.koetter@med.uni-tuebingen.de
G Horneff
Asklepios Klinik Sankt Augustin · DEUniversitätsklinikum Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin (IL)-1 plays an important role not only in the mediation of inflammation but also in the destruction of cartilage and bone. Together with TNF-alpha it is one of the most important cytokines in the pathogenesis of rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA). The first IL-1 antagonist to be approved for RA was Anakinra, an IL-1 receptor antagonist. Anakinra appears to be less effective for RA than TNF blockers. Hence, Anakinra is rarely used for the treatment of RA, but more for the treatment of IL-1-mediated diseases such as autoinflammatory syndromes, adult-onset Still's disease and systemic onset JIA. Two newer IL-1 antagonists have recently been approved for the treatment of CAPS (cryopyrin-associated periodic syndromes): Canakinumab, a fully human IL-1beta antibody, and rilonacept, a fusion protein consisting of the ligand-binding domain of the IL-1 receptor and the IL-1-receptor accessory protein, bound to human IgG1. For RA, there is only one proof-of-concept study to date with canakinumab. There are no prospective data for the treatment of patients with RA who did not respond to or tolerate TNF antagonists; in a retrospective analysis, only 8% of anti-TNF pretreated patients achieved an ACR 20 response.

Indexed as

AdultAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntirheumatic AgentsHumansInterleukin-1Interleukin 1 Receptor Antagonist ProteinRecombinant Fusion ProteinsRheumatic DiseasesAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntirheumatic AgentscanakinumabInterleukin-1Interleukin 1 Receptor Antagonist ProteinRecombinant Fusion Proteinsrilonacept

Identifiers

PMID20703489
OpenAlexW1597370399

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.