Evidence map›Paper›PMID 25931325›Full record

ReviewClinical reviews in allergy & immunology2016

Mediators of Chronic Pruritus in Atopic Dermatitis: Getting the Itch Out?

Nicholas K Mollanazar, Peter K Smith, Gil Yosipovitch

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed, 3 pooled it
25.8field-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.

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

142 citing papers in PubMed, 3 syntheses or guidelines pooled it, 348 citations in OpenAlex.

  1. European S2k Guideline on Chronic PruritusActa dermato-venereologica · 2025
    Guideline
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  14. Skin pain in pediatric atopic dermatitis: mechanisms and management.Current opinion in allergy and clinical immunology · 2026
    Review
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82 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

3 authors at 2 institutions in 2 countries.

Nicholas K MollanazarDepartment of Dermatology and Itch Center, Temple University School of Medicine, 3322 North Broad Street, Medical Office Building, Suite 212, Philadelphia, PA, 19140, USA.
Peter K SmithClinical Medicine, Griffith University, Southport, Australia.
Gil YosipovitchDepartment of Dermatology and Itch Center, Temple University School of Medicine, 3322 North Broad Street, Medical Office Building, Suite 212, Philadelphia, PA, 19140, USA. gil.yosipovitch@tuhs.temple.edu.
Temple University · USGriffith University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

For centuries, itch was categorized as a submodality of pain. Recent research over the last decade has led to the realization that itch is in fact a separate and distinct, albeit closely related, sensation. Chronic itch is a common complaint and has numerous etiologies. Various receptors (TRPA1, TRPV1, PAR2, gastrin-releasing peptide receptor (GRPR), Mas-related G proteins), secreted molecules (histamine, nerve growth factor (NGF), substance P (SP), proteases), and cytokines/chemokines (thymic stromal lymphopoietin (TSLP), IL-2, IL-4, IL-13, and IL-31) are implicated as mediators of chronic pruritus. While much remains unknown regarding the mechanisms of chronic itch, this much is certain: there is no singular cause of itch. Rather, itch is caused by a complex interface between skin, keratinocytes, cutaneous nerve fibers, pruritogenic molecules, and the peripheral and central nervous systems. Atopic dermatitis is one of the most itchy skin dermatoses and affects millions worldwide. The sensation of atopic itch is mediated by the interplay between epidermal barrier dysfunction, upregulated immune cascades, and the activation of structures in the central nervous system. Clinicians are in possession of an arsenal of different treatment options ranging from moisturizers, topical immunomodulators, topical anesthetic ion channel inhibitors, systemic immunomodulators, as well as oral drugs capable of reducing neural hypersensitization. Emerging targeted therapies on the horizon, such as dupilumab, promise to usher in a new era of highly specific and efficacious treatments. Alternative medicine, stress reduction techniques, and patient education are also important treatment modalities. This review will focus on the mediators of chronic pruritus mainly associated with atopic dermatitis (atopic itch), as well as numerous different therapeutic options.

Indexed as

BasophilsCombined Modality TherapyCytokinesDermatitis, AtopicDrug DiscoveryEpidermisHistamineHumansInflammation MediatorsNeuropeptidesPerceptionPruritusSensory Receptor CellsSignal TransductionSynaptic TransmissionThymic Stromal LymphopoietinCytokinesHistamineInflammation MediatorsNeuropeptidesThymic Stromal LymphopoietinAlternative itch therapiesAtopic dermatitisBarrier disruptionChronic pruritusImmunomodulatorsNeural hypersensitizationNeuropeptidesNonhistaminergic itchPatient educationPruritus receptor unit

Identifiers

PMID25931325
OpenAlexW2060891980

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.