Evidence map›Paper›PMID 31836943›Full record

ReviewClinical reviews in allergy & immunology2020

Eczema Herpeticum: Clinical and Pathophysiological Aspects.

Alexia Damour, Magali Garcia, Julien Seneschal, Nicolas Lévêque, Charles Bodet

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
8.0field-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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Dermatologic Toxicities Induced by JAK Inhibitors.American journal of clinical dermatology · 2026
    Review
  7. Article
  8. Woman with a Painful Rash.Clinical practice and cases in emergency medicine · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Pruritus in Pregnancy.Journal of obstetrics and gynaecology of India · 2024
    Review
  15. Article
  16. Journal of virology · 2023
    Article
  17. Article
  18. Review
  19. Review
  20. Skin of colour: essentials for the non-dermatologist.Clinical medicine (London, England) · 2023
    Review
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

5 authors at 2 institutions in 1 country.

Alexia DamourLaboratoire Inflammation Tissus Epithéliaux et Cytokines EA 4331, Université de Poitiers, Poitiers, France.
Magali GarciaLaboratoire Inflammation Tissus Epithéliaux et Cytokines EA 4331, Université de Poitiers, Poitiers, France.
Julien SeneschalINSERM U1035, BMGIC, Immuno-dermatologie ATIP-AVENIR, Bordeaux, France.
Nicolas LévêqueLaboratoire Inflammation Tissus Epithéliaux et Cytokines EA 4331, Université de Poitiers, Poitiers, France.
Charles BodetLaboratoire Inflammation Tissus Epithéliaux et Cytokines EA 4331, Université de Poitiers, Poitiers, France. charles.bodet@univ-poitiers.fr.ORCID http://orcid.org/0000-0002-8016-0324
Université de Poitiers · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atopic dermatitis (AD) is the most common chronic inflammatory skin disease in the world. AD is a complex pathology mainly characterized by an impaired skin barrier, immune response dysfunction, and unbalanced skin microbiota. Moreover, AD patients exhibit an increased risk of developing bacterial and viral infections. One of the most current, and potentially life-threatening, viral infection is caused by herpes simplex virus (HSV), which occurs in about 3% of AD patients under the name of eczema herpeticum (EH). Following a first part dedicated to the clinical features, virological diagnosis, and current treatments of EH, this review will focus on the description of the pathophysiology and, more particularly, the presently known predisposing factors to herpetic complications in AD patients. These factors include those related to impairment of the skin barrier such as deficit in filaggrin and anomalies in tight and adherens junctions. In addition, low production of the antimicrobial peptides cathelicidin LL-37 and human β-defensins; overexpression of cytokines such as interleukin (IL)-4, IL-13, IL-25, IL-33, and thymic stromal lymphopoietin (TSLP); or downregulation of type I to III interferons as well as defect in functions of immune cells such as dendritic, natural killer, and regulatory T cells have been involved. Otherwise, genetic polymorphisms and AD topical calcineurin inhibitor treatments have been associated with an increased risk of EH. Finally, dysbiosis of skin microbiota characterized in AD patients by Staphylococcus aureus colonization and toxin secretion, such as α-toxin, has been described as promoting HSV replication and could therefore contribute to EH.

Indexed as

Dermatitis, AtopicDisease SusceptibilityDysbiosisFilaggrin ProteinsHerpesviridae InfectionsHumansKaposi Varicelliform EruptionMicrobiotaSimplexvirusSkinFilaggrin ProteinsAtopic dermatitisHerpes simplex virusImmune responseMicrobiota dysbiosisPredisposing factorsSkin barrier

Identifiers

PMID31836943
OpenAlexW2996587996

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.