ArticleClinical and experimental medicine2016
Growth factors and IL-17 in hereditary angioedema.
Article in Clinical and experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- The Hereditary Angioedema Frailty and Inflammation Score (HAE-FIS): A Preliminary Study on the Inter-Attack Chronic Burden.Journal of clinical medicine · 2026Article
- Mast cell mediators in hereditary angioedema.Orphanet journal of rare diseases · 2026Article
- Unveiling the Complexities of Hereditary Angioedema.Biomolecules · 2024Review
- Determining biomarkers for evaluation and diagnosis of hereditary angioedema.Clinical and translational allergy · 2022Article
- Roles of Immune Cells in Hereditary Angioedema.Clinical reviews in allergy & immunology · 2021Review
- Biomarkers in Hereditary Angioedema.Clinical reviews in allergy & immunology · 2021Review
- Proteomic Analysis of the Acid-Insoluble Fraction of Whole Saliva from Patients Affected by Different Forms of Non-histaminergic Angioedema.Journal of clinical immunology · 2020Article
- The complex alteration in the network of IL-17-type cytokines in patients with hereditary angioedema.Clinical and experimental medicine · 2018Article
- Genetics of Hereditary Angioedema Revisited.Clinical reviews in allergy & immunology · 2016Review
- "Nuts and Bolts" of Laboratory Evaluation of Angioedema.Clinical reviews in allergy & immunology · 2016Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hereditary angioedema (HAE) is a rare autosomal dominant disorder, due to C1-inhibitor deficiency, which causes episodic swellings of subcutaneous tissues, bowel walls and upper airways which are disabling and potentially life-threatening. We evaluated n = 17 patients with confirmed HAE diagnosis in basal and crisis state and n = 19 healthy subjects. The samples were tested for IL-17, FGFb, G-CSF and GM-CSF, using Bio-plex kit. Data analysis was performed via nonparametric Spearman's correlations and two sets of linear mixed models. When comparing HAE subjects during basal and crisis states, we found out significantly (i.e., p value <0.05) higher values in crisis states rather than in basal states for the three growth factors and cytokine IL-17. When comparing healthy subjects versus HAE patients at basal state, we found out significantly higher values in HAE subjects only for GM-CSF, FGFb and IL-17, but not for G-CSF. In HAE patients, there is a connection between IL-17 and growth factors. The low-grade inflammation in absence of attacks is demonstrated by constant higher amount of IL-17, FGFb and GM-CSF with respect to healthy patients. This could indicate that in this disease there is a level of activation that maintains the system in a "tick-over state," that can be activate by several stimuli that are able to induce a increase in inflammatory mediators during the acute attack.
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