Evidence map›Paper›PMID 35344299›Full record

ArticleClinical and translational allergy2022

Comorbidities in hereditary angioedema-A population-based cohort study.

Linda Sundler Björkman, Barbro Persson, David Aronsson, Lillemor Skattum, Patrik Nordenfelt, Arne Egesten

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational allergy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
6.9field-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

36 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Mast cell mediators in hereditary angioedema.Orphanet journal of rare diseases · 2026
    Article
  6. Therapeutic Potential of C1-Inhibitor in Vascular Diseases and Beyond.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Comorbidities in Canadian patients with hereditary angioedema: a quantitative survey study.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2025
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Observational
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

6 authors at 3 institutions in 1 country.

Linda Sundler BjörkmanRespiratory Medicine & Allergology, Department of Clinical Sciences Lund, Lund University and Skåne University Hospital, Lund, Sweden.ORCID https://orcid.org/0000-0003-4146-9983
Barbro PerssonDepartment of Immunology, Genetics and Pathology, The Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
David AronssonRespiratory Medicine & Allergology, Department of Clinical Sciences Lund, Lund University and Skåne University Hospital, Lund, Sweden.
Lillemor SkattumDepartment of Laboratory Medicine, Section of Microbiology, Immunology and Glycobiology, Lund University and Clinical Immunology and Transfusion Medicine, Lund, Sweden.
Patrik NordenfeltRespiratory Medicine & Allergology, Department of Internal Medicine, County Hospital of Ryhov, Jönköping, Sweden.
Arne EgestenRespiratory Medicine & Allergology, Department of Clinical Sciences Lund, Lund University and Skåne University Hospital, Lund, Sweden.
Lund University · SERyhov Hospital Jönköping · SEUppsala University · SE

Funding

CSL-Behring (unrestricted grant)Swedish Government Funds for Clinical Research (ALF)
6 · The paper itself

Abstract

backgroundIn hereditary angioedema (HAE), low levels (type 1) or defect in function (type 2) of the serine-protease inhibitor C1 Inhibitor protein results in activation of the classical pathway of the complement system as well as the contact system. Here, we investigated the risk of comorbidities in HAE.

methodsIndividuals with HAE (n = 239; identified through a physician made diagnosis) and a control cohort from the general population (n = 2383; matched for age, gender, and county of residence) were compared with the Swedish inpatient, cause of death, cancer, and prescription registers. Conditional logistic regression was used to analyze the data.

resultsIncreased risk of cardiovascular disease (odds ratio [OR] 1.83; 95% confidence interval [CI] 1.32-2.54), including arterial (OR 6.74; 95% CI 1.89-24.06) and venous thromboembolic disease (OR 4.20; 95% CI 2.42-7.23) as well as hypertension (OR 1.64; 95% CI 1.12-2.39) was seen in HAE. There was also an increased number of individuals diagnosed with hyperlipidemia (OR 2.01; 95% CI 1.16-3.50) among HAE patients. Furthermore, the risk of autoimmune disease was increased (OR 1.65; 95% CI 1.15-2.35) being particularly pronounced for systemic lupus erythematosus (OR 71.87; 95% CI 8.80-586.7). The risk of having two or more autoimmune diseases was also higher among HAE patients (p = 0.017). In contrast, the risk of cancer was not increased. Data from the prescription register revealed higher prescription rates of drugs against hypertension, hypothyroidism, and hyperlipidemia among HAE patients.

conclusionsThe results warrant for awareness and prevention of comorbid conditions, in particular, thromboembolic and autoimmune diseases in HAE. Future prophylactic interventions may modify these risks.

Indexed as

autoimmunitycardiovascular diseasecomplementepidemiologyhereditary angioedema (HAE)

Identifiers

PMID35344299
PMCPMC8967273
OpenAlexW4220843497

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.