Evidence map›Paper›PMID 22674016›Full record

ReviewClinical reviews in allergy & immunology2013

Pathogenic intracellular and autoimmune mechanisms in urticaria and angioedema.

Katherine Altman, Christopher Chang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
3.5field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 85 citations in OpenAlex.

  1. Efficacy and safety ofPharmaceutical biology · 2023
    Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Identification of key genes and molecular mechanisms of chronic urticaria based on bioinformatics.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024
    Article
  6. Immunological signature of chronic spontaneous urticaria (Review).Experimental and therapeutic medicine · 2022
    Review
  7. Review
  8. Eosinophils in skin diseases.Seminars in immunopathology · 2021
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Emerging Therapies in Chronic Spontaneous Urticaria.Allergy, asthma & immunology research · 2019
    Review
  14. Causal Relationship Between Anti-TPO IgE and Chronic Urticaria byAllergy, asthma & immunology research · 2019
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Leukotriene receptor antagonists for chronic urticaria: a systematic review.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2014
    Review
  20. 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

2 authors at 2 institutions in 1 country.

Katherine Altman1015 Belmont Pl E, Seattle, WA 98102, USA. Katherine.altman@gmail.com
Christopher Chang
Seattle University · USThomas Jefferson University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Urticaria and angioedema are common disorders. Chronic urticaria is defined as lasting longer than 6 weeks. Causes of chronic urticaria fall into the following categories: physical, allergic, hereditary, autoimmune, and idiopathic. Basophils and mast cells are the primary effector cells responsible for clinical symptoms and signs. These cells produce and secrete a variety of mediators including histamine, leukotrienes, prostaglandins, cytokines, chemokines, and other pro-inflammatory mediators. This leads to vasodilation, fluid exudation, increased vascular permeability, and accumulation of additional secondary inflammatory cells. Two mechanisms have been investigated as possibly contributing to the pathogenesis of chronic urticaria. One is the development of autoantibodies to FcεRI or IgE on mast cells and basophils. This appears to be responsible for 30-50 % of cases. The other is dysregulation of intracellular signaling pathways involving Syk, SHIP-1, or SHIP-2 in basophils and mast cells. The primary treatment for chronic urticaria is to treat the underlying pathology, if any can be identified. Otherwise, in idiopathic cases, H1 antihistamines, H2 antihistamines, antileukotrienes, and corticosteroids constitute the main pharmacologic treatment modalities. In severe and recalcitrant cases of chronic and autoimmune urticaria, immunosuppressive drugs have been used, most commonly cyclosporin. More recent experimental studies have also suggested that omalizumab, an anti-IgE therapy, may be of benefit. Currently, inhibitors of Syk are also being developed and tested in the laboratory and in animal models. As our understanding of the pathogenesis of idiopathic urticaria increases, development of additional drugs targeting these pathways may provide relief for the significant physical and psychological morbidity experienced by patients with this disorder.

Indexed as

AngioedemaAnimalsAntibodies, Anti-IdiotypicAntibodies, Monoclonal, HumanizedAutoantibodiesAutoimmunityBasophilsCyclosporineHistamine AntagonistsHumansImmunoglobulin EIntracellular Signaling Peptides and ProteinsMast CellsOmalizumabProtein-Tyrosine KinasesReceptors, IgEAntibodies, Anti-IdiotypicAntibodies, Monoclonal, HumanizedAutoantibodiesCyclosporineFCER1A protein, humanHistamine AntagonistsImmunoglobulin EIntracellular Signaling Peptides and ProteinsOmalizumabProtein-Tyrosine KinasesReceptors, IgESyk KinaseSYK protein, human

Identifiers

PMID22674016
OpenAlexW2076465943

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.