Evidence map›Paper›PMID 23283143›Full record

ArticleThe World Allergy Organization journal2011

Hereditary angioedema caused by c1-esterase inhibitor deficiency: a literature-based analysis and clinical commentary on prophylaxis treatment strategies.

Richard G Gower, Paula J Busse, Emel Aygören-Pürsün, Amin J Barakat, Teresa Caballero, Mark Davis-Lorton, Henriette Farkas, David S Hurewitz, Joshua S Jacobs, Douglas T Johnston and 2 more

Abstract read
In one paragraph

Article in The World Allergy Organization journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Trial
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Assessment and management of disease burden and quality of life in patients with hereditary angioedema: a consensus report.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Subcutaneous C1 inhibitor for prevention of attacks of hereditary angioedema: additional outcomes and subgroup analysis of a placebo-controlled randomized study.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2019
    Article
  15. Article
  16. A Case of Type 2 Hereditary Angioedema With SERPING1 Mutation.Allergy, asthma & immunology research · 2017
    Article
  17. Observational
  18. Article
  19. The first probable case of hereditary angioedema in Vietnam.Allergy, asthma & immunology research · 2012
    Article
  20. 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

12 authors.

Richard G GowerClinical Associate Professor of Medicine, University of Washington, Marycliff Allergy Specialists, PS, Spokane, WA.
Paula J Busse
Emel Aygören-Pürsün
Amin J Barakat
Teresa Caballero
Mark Davis-Lorton
Henriette Farkas
David S Hurewitz
Joshua S Jacobs
Douglas T Johnston
William Lumry
Marcus Maurer

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hereditary angioedema (HAE) caused by C1-esterase inhibitor deficiency is an autosomal-dominant disease resulting from a mutation in the C1-inhibitor gene. HAE is characterized by recurrent attacks of intense, massive, localized subcutaneous edema involving the extremities, genitalia, face, or trunk, or submucosal edema of upper airway or bowels. These symptoms may be disabling, have a dramatic impact on quality of life, and can be life-threatening when affecting the upper airways. Because the manifestations and severity of HAE are highly variable and unpredictable, patients need individualized care to reduce the burden of HAE on daily life. Although effective therapy for the treatment of HAE attacks has been available in many countries for more than 30 years, until recently, there were no agents approved in the United States to treat HAE acutely. Therefore, prophylactic therapy is an integral part of HAE treatment in the United States and for selected patients worldwide. Routine long-term prophylaxis with either attenuated androgens or C1-esterase inhibitor has been shown to reduce the frequency and severity of HAE attacks. Therapy with attenuated androgens, a mainstay of treatment in the past, has been marked by concern about potential adverse effects. C1-esterase inhibitor works directly on the complement and contact plasma cascades to reduce bradykinin release, which is the primary pathologic mechanism in HAE. Different approaches to long-term prophylactic therapy can be used to successfully manage HAE when tailored to meet the needs of the individual patient.

Identifiers

PMID23283143
PMCPMC3666183

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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.