Evidence map›Paper›PMID 31559260›Full record

ReviewInflammatory intestinal diseases2019

Mechanism-Based Treatment Strategies for IBD: Cytokines, Cell Adhesion Molecules, JAK Inhibitors, Gut Flora, and More.

Philipp Schreiner, Markus F Neurath, Siew C Ng, Emad M El-Omar, Ala I Sharara, Taku Kobayashi, Tadakazu Hisamatsu, Toshifumi Hibi, Gerhard Rogler

Open access · goldAbstract readReview
In one paragraph

Review in Inflammatory intestinal diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
7.9field-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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

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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

9 authors at 7 institutions in 6 countries.

Philipp SchreinerDepartment of Gastroenterology and Hepatology, University Hospital Zurich, Zurich, Switzerland.
Markus F NeurathMedizinische Klinik 1, Universitätsklinikum Erlangen-Nürnberg, Erlangen, Germany.
Siew C NgDepartment of Medicine and Therapeutics, Institute of Digestive Disease, LKS Institute of Health Science, State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, China.
Emad M El-OmarSt. George and Sutherland Clinical School, University of New South Wales, Sydney, New South Wales, Australia.
Ala I ShararaDivision of Gastroenterology, Department of Internal Medicine, American University of Beirut, Beirut, Lebanon.
Taku KobayashiCenter for Advanced IBD Research and Treatment, Kitasato University Kitasato Institute Hospital, Tokyo, Japan.
Tadakazu Hisamatsu3rd Department of Internal Medicine, Kyorin University, Tokyo, Japan.
Toshifumi HibiCenter for Advanced IBD Research and Treatment, Kitasato University Kitasato Institute Hospital, Tokyo, Japan.
Gerhard RoglerDepartment of Gastroenterology and Hepatology, University Hospital Zurich, Zurich, Switzerland.
Kitasato Institute Hospital · JPUniversity Hospital of Zurich · CHAmerican University of Beirut · LBChinese University of Hong Kong · HKKyorin University · JPSutherland Hospital · AUUniversitätsklinikum Erlangen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough TNF inhibitors revolutionized the therapy of inflammatory bowel disease (IBD), we have been reaching a point where other therapies with different mechanisms of action are necessary. A rising number of elderly IBD patients with contraindications to established therapies and a growing group of patients losing response to anti-TNF therapy compel us to find safer, better-tolerated, and, ideally, personalized treatment options. However, in order to choose the right drug to fit a patient, it is indispensable to understand the pathomechanism involved in IBD. SUMMARY: The aim of this review is to explain the inflammatory signaling pathways in IBD and how to inhibit them with current and future therapeutic approaches. Next to biologic agents targeting inflammatory cytokines (anti-TNF agents, anti-IL-12/-23 agents, and specific inhibitors of IL-23), biologics blocking leukocyte trafficking to the gut (anti-integrin antibodies) are available nowadays. More recently, small molecules inhibiting the JAK-STAT pathway (JAK inhibitors) or preventing lymphocyte trafficking (sphingosine-1-phosphate modulators) have been approved or are under investigation. Furthermore, modifying the microbiota has potential therapeutic effects on IBD, and autologous hematopoietic or mesenchymal stem cell transplantation may be considered for a highly selected group of IBD patients. KEY MESSAGE: Physicians should understand the different mechanisms of action of the potential therapies for IBD to select the right drug for the right patient.

Indexed as

BiologicsCrohn's diseaseInflammatory bowel diseaseSmall moleculesUlcerative colitis

Identifiers

PMID31559260
PMCPMC6751442
OpenAlexW2961464090

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.