Evidence map›Paper›PMID 20686829›Full record

ReviewInflammation2011

Does dehydroepiandrosterone influence the expression of urticaria?-a mini review.

A Kasperska-Zajac

Open access · hybridAbstract readReview
In one paragraph

Review in Inflammation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Stress, pseudoallergens, autoimmunity, infection and inflammation in chronic spontaneous urticaria.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2019
    Review
  4. Article
  5. Article
  6. Article
  7. Article
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

1 author at 1 institution in 1 country.

A Kasperska-ZajacClinical Department of Internal Diseases, Allergology and Clinical Immunology, Medical University of Silesia, ul. Ceglana 35, 40-952, Katowice, Poland. kasperska@plusnet.pl
Medical University of Silesia · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic urticaria is a challenging problem since the exact cause and mechanism involved in the disease development have still remained unknown. This disease is associated with mast cells activation and immunoinflammatory processes. Interestingly, dysfunctions of the neuroendocrine-immune system due to stress and other factors seem to appear as a very interesting theory for urticaria pathogenesis. Dehydroepiandrosterone and its sulfate derivative (DHEA-S) appear to have regulatory effects in immune homeostasis and are regulated by the nervous system, and it is suggested that they may be an integral element of neuroimmunomodulation. Our studies showed substantially decreased serum concentration of DHEA-S in patients with chronic urticaria. However, current knowledge prevents answering whether lower circulating DHEA-S concentration is a primary phenomenon or just an accompanying one which appears as a response of different systems to the course of the illness and may not be of any importance for the pathogenesis of urticaria whatsoever. This review is a summary of clinical research on the role of DHEA in chronic urticaria.

Indexed as

Chronic DiseaseDehydroepiandrosteroneDehydroepiandrosterone SulfateFemaleHumansInterleukin-6MaleNeuroimmunomodulationUrticariaDehydroepiandrosteroneDehydroepiandrosterone SulfateIL6 protein, humanInterleukin-6

Identifiers

PMID20686829
PMCPMC3170459
OpenAlexW2142066386

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.