Evidence map›Paper›PMID 30508136›Full record

ReviewRheumatology (Oxford, England)2019

Clinical significance of Janus Kinase inhibitor selectivity.

Ernest H Choy

Erratum issuedOpen access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Rheumatology (Oxford, England), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 130 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed, 9 pooled it
7.7field-weighted citation impact, top 2% 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

130 citing papers in PubMed, 9 syntheses or guidelines pooled it, 276 citations in OpenAlex.

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70 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Ernest H ChoyCREATE Centre, Section of Rheumatology, Division of Infection and Immunity, Cardiff University School of Medicine, Cardiff, UK.
Cardiff University · GB

Funding

Arthritis Research UK
6 · The paper itself

Abstract

Cytokines are key drivers of inflammation in RA, and anti-cytokine therapy has improved the outcome of RA. Janus Kinases (JAK) are intracellular tyrosine kinases linked to intracellular domains of many cytokine receptors. There are four JAK isoforms: JAK1, JAK2, JAK3 and TYK2. Different cytokine receptor families utilize specific JAK isoforms for signal transduction. Phosphorylation of JAK when cytokine binds to its cognate receptor leads to phosphorylation of other intracellular molecules that eventually leads to gene transcription. Oral JAK inhibitors (JAKi) have been developed as anti-cytokine therapy in RA. Two JAKi, tofacitinib and baricitinib, have been approved recently for the treatment of RA, and many JAKi are currently in development. JAKi inhibit JAK isoforms with different selectivity. This review discusses the efficacy and safety of JAKi in RA, in particular the potential clinical significance of JAKi selectivity.

Indexed as

Antirheumatic AgentsArthritis, RheumatoidAzetidinesHumansInflammationJanus Kinase InhibitorsPiperidinesPurinesPyrazolesPyrimidinesPyrrolesSulfonamidesAntirheumatic AgentsAzetidinesbaricitinibJanus Kinase InhibitorsPiperidinesPurinesPyrazolesPyrimidinesPyrrolesSulfonamidestofacitinibDMARDsJanus Kinaserheumatoid arthritistargeted synthetic DMARDstreatment

Identifiers

PMID30508136
PMCPMC6532440
OpenAlexW2903436036

What OpenQuestion holds

Textmetadata
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.