Evidence map›Paper›PMID 23947678›Full record

ReviewExperimental dermatology2013

What causes alopecia areata?

K J McElwee, A Gilhar, D J Tobin, Y Ramot, J P Sundberg, M Nakamura, M Bertolini, S Inui, Y Tokura, L E King and 7 more

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Experimental dermatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04793945 (The Efficacy of Combining 308 Nm-Excimer Light and Topical Steroid in the Treatment of Alopecia Areata), which is not on this map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
13.5field-weighted citation impact, top 1% 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.

NCT04793945 phase4unknown statusnot on this mapstarted 2021, after this paper: background citation

The Efficacy of Combining 308 Nm-Excimer Light and Topical Steroid in the Treatment of Alopecia Areata

TypeinterventionalSponsorAssiut UniversityRan2021 to 2022Enrolled30ConditionsAlopecia AreataArmstopical steroid and 308nm-Excimer light therapy
3 · Its place in the literature

Who cites it

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 176 citations in OpenAlex.

  1. Pooled it
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  4. Review
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  8. Review
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  14. Phloroglucinol Enhances Anagen Signaling and Alleviates HJournal of microbiology and biotechnology · 2024
    Article
  15. Review
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  17. Review
  18. Article
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  20. Article

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

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

17 authors at 12 institutions in 6 countries.

K J McElweeDepartment of Dermatology and Skin Science, University of British Columbia, Vancouver, BC, Canada. kmcelwee@mail.ubc.ca
A Gilhar
D J Tobin
Y Ramot
J P Sundberg
M Nakamura
M Bertolini
S Inui
Y Tokura
L E King
B Duque-Estrada
A Tosti
A Keren
S Itami
Y Shoenfeld
A Zlotogorski
R Paus
Hadassah Medical Center · ILOsaka Gakuin University · JPTechnion – Israel Institute of Technology · ILUniversity of Lübeck · DEHamamatsu University School of Medicine · JPJackson Laboratory · USTel Aviv University · ILUniversity of Bradford · GBUniversity of British Columbia · CAUniversity of Miami · USUniversity of Occupational and Environmental Health Japan · JPVanderbilt University Medical Center · US

Funding

Genetics of Alopecia Areata in the C3H/HeJ MouseR01AR056635 · NIAMS · JACKSON LABORATORY · PI SUNDBERG, JOHN PAUL · 2010 to 2014
$1.9M
NIAMS NIH HHS R01 AR056635
6 · The paper itself

Abstract

The pathobiology of alopecia areata (AA), one of the most frequent autoimmune diseases and a major unsolved clinical problem, has intrigued dermatologists, hair biologists and immunologists for decades. Simultaneously, both affected patients and the physicians who take care of them are increasingly frustrated that there is still no fully satisfactory treatment. Much of this frustration results from the fact that the pathobiology of AA remains unclear, and no single AA pathogenesis concept can claim to be universally accepted. In fact, some investigators still harbour doubts whether this even is an autoimmune disease, and the relative importance of CD8(+) T cells, CD4(+) T cells and NKGD2(+) NK or NKT cells and the exact role of genetic factors in AA pathogenesis remain bones of contention. Also, is AA one disease, a spectrum of distinct disease entities or only a response pattern of normal hair follicles to immunologically mediated damage? During the past decade, substantial progress has been made in basic AA-related research, in the development of new models for translationally relevant AA research and in the identification of new therapeutic agents and targets for future AA management. This calls for a re-evaluation and public debate of currently prevalent AA pathobiology concepts. The present Controversies feature takes on this challenge, hoping to attract more skin biologists, immunologists and professional autoimmunity experts to this biologically fascinating and clinically important model disease.

Indexed as

Alopecia AreataAnimalsAutoimmune DiseasesDisease Models, AnimalHumansMiceModels, ImmunologicalTranslational Research, Biomedical

Identifiers

PMID23947678
PMCPMC4094373
OpenAlexW1482434502

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.