Evidence map›Paper›PMID 38345154›Full record

ReviewThe British journal of dermatology2024

Prurigo nodularis: new insights into pathogenesis and novel therapeutics.

Viviane Liao, Hannah L Cornman, Emily Ma, Shawn G Kwatra

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The British journal of dermatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 3 pooled it
26.7field-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

41 citing papers in PubMed, 3 syntheses or guidelines pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. European S2k Guideline on Chronic PruritusActa dermato-venereologica · 2025
    Guideline
  3. Pooled it
  4. Rapid improvement of itch with nemolizumab in atopic dermatitis and prurigo nodularis phase 3 studies.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026
    Trial
  5. Review
  6. Immunopathogenesis of itch: an integrative framework for chronic pruritus.JID innovations : skin science from molecules to population health · 2026
    Review
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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

4 authors at 2 institutions in 1 country.

Viviane LiaoDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0001-9355-1298
Hannah L CornmanDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0003-1462-2479
Emily MaDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0001-6022-6659
Shawn G KwatraDepartment of Dermatology.ORCID 0000-0003-3736-1515
Johns Hopkins University · USUniversity of Maryland, Baltimore · US

Funding

Racial Differences in Biomarkers and Therapeutic Targets for Chronic ItchK23AR077073 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI KWATRA, SHAWN GAURAV · 2021 to 2025
$873k
NIAMS NIH HHS K23 AR077073NIH HHS K23AR077073-01A1
6 · The paper itself

Abstract

Prurigo nodularis (PN) is an inflammatory skin condition characterized by intensely pruritic nodules on the skin. Patients with PN suffer from an intractable itch-scratch cycle leading to impaired sleep, psychosocial distress and a significant disruption in quality of life. The pathogenesis of PN is associated with immune and neural dysregulation, mediated by inflammatory cytokines [such as interleukin (IL)-4, -13, -17, -22 and -31] and neuropeptides (such as substance P and calcitonin gene-related peptide). There is a role for type 2 inflammation in PN in addition to T-helper (Th)17 and Th22-mediated inflammation. The neuroimmune feedback loop in PN involves neuropeptides released from nerve fibres that cause vasodilation and further recruitment of inflammatory cells. Inflammatory cells, particularly mast cells and eosinophils, degranulate and release neurotoxins, as well as nerve growth factor, which may contribute to the neuronal hyperplasia seen in the dermis of patients with PN and neural sensitization. Recent studies have also indicated underlying genetic susceptibility to PN in addition to environmental factors, the existence of various disease endotypes centred around degrees of type 2 inflammation or underlying myelopathy or spinal disc disease, and significant race and ethnicity-based differences, with African Americans having densely fibrotic skin lesions. Dupilumab became the first US Food and Drug Administration-approved therapeutic for PN, and there are several other agents currently in development. The anti-IL-31 receptor A inhibitor nemolizumab is in late-stage development with positive phase III data reported. In addition, the oral Janus kinase (JAK) 1 inhibitors, abrocitinib and povorcitinib, are in phase II trials while a topical JAK1/2 inhibitor, ruxolitinib, is in phase III studies.

Indexed as

PrurigoAntibodies, Monoclonal, HumanizedCytokinesHumansJanus Kinase InhibitorsNitrilesPyrazolesPyrimidinesReceptors, InterleukinAntibodies, Monoclonal, HumanizedCytokinesdupilumabIL31RA protein, humanJanus Kinase InhibitorsnemolizumabNitrilesPyrazolesPyrimidinesReceptors, Interleukinruxolitinib

Identifiers

PMID38345154
PMCPMC11099982
OpenAlexW4391746574

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.