Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology
October 15, 2026 · via Europe PMC
Hereditary α-tryptasemia is associated with response to omalizumab in severe allergic asthma.
Rijavec M, Svetina M, Škrgat S, +9 more, Kopač P.
AI summary — for doctors, generated from the abstract only
Hereditary alpha-tryptasemia was independently associated with poor response to omalizumab in severe allergic asthma.
What was studied
A cohort of 181 patients with severe allergic asthma treated with omalizumab at two tertiary centres (Slovenia and UK) who underwent tryptase genotyping, comparing clinical features between those with and without hereditary alpha-tryptasemia (HaT).
Key findings
- Limited benefit from omalizumab occurred in 22.7% of patients, and HaT was found in 8.3% overall
- HaT was present in 20% of poor responders versus 5% of responders (OR 4.6; 95% CI 1.5-12.3; P = .0068)
- After adjustment, HaT remained independently associated with poor response (OR 4.56; 95% CI 1.24-16.74; P = .022)
- Among patients with HaT, 4 of 15 had basal serum tryptase below 8 ng/mL
Clinical relevance
Tryptase genotyping might eventually help predict who is less likely to benefit from anti-IgE therapy. Because some patients with HaT had a normal-range serum tryptase, serum levels alone may miss them.
Who should care
Limitations
Observational cohort with a modest number of patients with HaT, wide confidence intervals and no information in the abstract on prospective validation. Association does not prove HaT causes poor response.
HaT is linked to poorer omalizumab response, but this needs confirmation before it guides treatment choice.
This is an AI-generated summary of the published abstract, not a clinical recommendation. It may not reflect the full text or subsequent updates — verify against the original source before acting on it.
Abstract
Background
Higher basal serum tryptase (BST) levels have been associated with increased asthma severity that correlated with active tryptase allele number and was linked to poor clinical responses to anti-IgE treatment (omalizumab). However, the commonest cause of elevated BST is hereditary α-tryptasemia (HαT) caused by increased α-tryptase-encoding Tryptase alpha/beta 1 (TPSAB1) copy number, and its relationship to omalizumab response in asthma remains unclear.
Objective
Our aim was to assess the relative contribution of tryptase genotype and HαT to the clinical efficacy of omalizumab treatment in patients with severe allergic asthma.
Methods
A cohort (N=181) of severe allergic asthma patients treated with omalizumab from 2 tertiary referral centres in Slovenia and the UK underwent tryptase genotyping, and clinical features were subsequently compared between groups with and without HαT.
Results
Limited benefit from omalizumab therapy was demonstrated in 22.7% of patients. Overall, HαT was identified in 8.3% of patients with severe allergic asthma treated with omalizumab. HαT was found in 20% of individuals with poor clinical responses to omalizumab, compared to 5% of those with positive responses (OR = 4.6 [95% CI 1.5-12.3]; P = .0068). In multivariable analysis, adjusted for study site and other covariates, HαT remained independently associated with poor response to omalizumab (OR = 4.56; [95% CI, 1.24-16.74]; P = .022). Among patients with HαT, 4 of 15 had BST below 8 ng/mL.
Conclusion
HαT is associated with poorer clinical response to anti-IgE treatment in patients with severe allergic asthma.
DOI
10.1016/j.anai.2026.10.014
PMID
42880632
Research metadata (titles, abstracts, authors, publication dates) is sourced from Europe PMC, which aggregates content from PubMed/MEDLINE, PubMed Central, and other providers under the U.S. National Library of Medicine (NLM/NCBI). NLM does not claim copyright on abstracts; the original journal publishers or authors may hold rights to the full articles. AI-generated summaries are derived only from the abstract, never the full text, and are always labeled as AI-generated.
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