Hereditary α tryptasemia is a valid genetic biomarker for severe mediator-related symptoms in mastocytosis
Open accessAbstract
Mastocytosis is a hematopoietic neoplasm characterized by expansion of KIT D816V-mutated clonal mast cells in various organs and severe or even life-threatening anaphylactic reactions. Recently, hereditary α-tryptasemia (HαT) has been described as a common genetic trait with increased copy numbers of the α-tryptase encoding gene, TPSAB1, and associated with an increased basal serum tryptase level and a risk of mast cell activation. The purpose of our study was to elucidate the clinical relevance of HαT in patients with mastocytosis. TPSAB1 germline copy number variants were assessed by digital polymerase chain reaction in 180 mastocytosis patients, 180 sex-matched control subjects, 720 patients with other myeloid neoplasms, and 61 additional mastocytosis patients of an independent validation cohort. α-Tryptase encoding TPSAB1 copy number gains, compatible with HαT, were identified in 17.2% of mastocytosis patients and 4.4% of the control population (P < .001). Patients with HαT exhibited higher tryptase levels than patients without HαT (median tryptase in HαT+ cases: 49.6 ng/mL vs HαT− cases: 34.5 ng/mL, P = .004) independent of the mast cell burden. Hymenoptera venom hypersensitivity reactions and severe cardiovascular mediator-related symptoms/anaphylaxis were by far more frequently observed in mastocytosis patients with HαT than in those without HαT. Results were confirmed in an independent validation cohort. The high prevalence of HαT in mastocytosis hints at a potential pathogenic role of germline α-tryptase encoding TPSAB1 copy number gains in disease evolution. Together, our data suggest that HαT is a novel emerging robust biomarker in mastocytosis that is useful for determining the individual patient´s risk of developing severe anaphylaxis.
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There is a consensus that HαT is a risk modifier of severe anaphylaxis.
“There is a consensus that HαT is a risk modifier of severe anaphylaxis [21,48,49,50,51,52,53].”
From Diagnostic Significance of Tryptase for Suspected Mast Cell Disorders (2023) · cites this paper as [51]
The Discussion reports a three- to fourfold increased risk of severe cardiovascular mediator-related symptoms, mainly anaphylaxis, associated with HαT in patients with mastocytosis, and notes a parallel study with a similar finding. This supports HαT as a risk modifier in mastocytosis, but the paper does not establish a general consensus or an unqualified risk across populations. (LLM, conf=0.83)
Experimental — accuracy not yet measuredIn patients with systemic mastocytosis, the risk for developing severe or life-threatening anaphylaxis is high, especially when a concomitant IgE-dependent allergy or Hereditary α-tryptasemia is present.
“In patients with systemic mastocytosis (SM), the risk for developing severe or even life-threatening anaphylaxis is high, especially when a concomitant IgE-dependent allergy or the genetic trait Hereditary a -tryptasemia (H a T) is present.”
From Selecting the Right Criteria and Proper Classification to Diagnose Mast Cell Activation Syndromes: A Critical Review (2021) · cites this paper as [25]
The Discussion reports a three- to fourfold higher risk of severe cardiovascular symptoms, mainly anaphylaxis, in mastocytosis patients with hereditary α-tryptasemia. The Introduction also describes life-threatening anaphylaxis in systemic mastocytosis. The paper records allergies, particularly hymenoptera venom allergy, but the cited passages do not establish concomitant IgE-dependent allergy as a separate factor increasing anaphylaxis risk in these patients. (LLM, conf=0.84)
Experimental — accuracy not yet measuredAn approximately two to three times higher prevalence of hereditary alpha-tryptasemia has been reported in two large cohorts of systemic mastocytosis patients, and hereditary alpha-tryptasemia concurrently occurring with MCAS has been reported.
“However, an approximately two to three times higher prevalence of H a T has been reported in two large cohorts of SM patients 25,129 ; also, H a T concurrently occurring with MCAS has been reported. 130,131”
From Selecting the Right Criteria and Proper Classification to Diagnose Mast Cell Activation Syndromes: A Critical Review (2021) · cites this paper as [25]
Split into 2 atoms — 0 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredHereditary alpha-tryptasemia may be associated with an increased severity of anaphylactic reactions and other mediator-induced symptoms in patients with mastocytosis and venom allergy.
“Further, H a T may be associated with an increased severity of anaphylactic reactions and other mediator-induced symptoms in patients with mastocytosis and venom allergy. 25,129”
From Selecting the Right Criteria and Proper Classification to Diagnose Mast Cell Activation Syndromes: A Critical Review (2021) · cites this paper as [25]
The prevalence of HαT in patients with SM can reach up to 12%-20%.
“in patients with SM, where it can reach up to 12%–20% (17, 19, 22, 23).”
From Defining “Normal” basal serum tryptase levels: a context-dependent approach to improve diagnostics in systemic mastocytosis (2025) · cites this paper as [22]
HαT is enriched in patients with SM, Hymenoptera-allergic patients with severe anaphylaxis, and patients with idiopathic anaphylaxis.
“HαT is enriched in patients with SM,42,43 in Hymenoptera-allergic patients with severe anaphylaxis,44,45 and in patients with idiopathic anaphylaxis.42,43,45,46”
From Mast cell activation syndrome: Current understanding and research needs (2024) · cites this paper as [43]
MCAS has been reported in patients with hereditary alpha-tryptasemia, an autosomal dominant genetic trait caused by increased copy-number of the alpha-tryptase gene TPSAB1, resulting in increased baseline serum tryptase levels.
“Furthermore, MCAS has been reported in patients with hereditary a-tryptasemia (HaT), an autosomal dominant genetic trait caused by an increased copy-number of the atryptase gene TPSAB1, resulting in increased baseline serum tryptase levels.7,8”
From Low Prevalence of Idiopathic Mast Cell Activation Syndrome Among 703 Patients With Suspected Mast Cell Disorders (2024) · cites this paper as [7]
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“In patients with systemic mastocytosis (SM), the risk for developing severe or even life-threatening anaphylaxis is high, especially when a concomitant IgE-dependent allergy or the genetic trait Hereditary a-tryptasemia (HaT) is present.(22-25) When MCA-related symptoms are severe and recurrent, the diagnosis of MCA s…”
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World Health Organization Classification and Diagnosis of Mastocytosis
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Severe food allergy reactions are associated with α-tryptase
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Review and updates on systemic mastocytosis and related entities
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Bone Marrow Mastocytosis: A Diagnostic Challenge
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Clinically accessible amplitude-based multiplex ddPCR assay for tryptase genotyping
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Self-citationState-of-the-Art on Biomarkers for Anaphylaxis in Obstetrics
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What the clinician should know when ordering a mast cell tryptase test
Michel, M., Giusti, D., Klingebiel, C., Pham, B., & Vitte, J. (2025) · Annals of Allergy Asthma & Immunology · doi:10.1016/j.anai.2025.03.003 · Cited by 8 · see citing works
Expanding the Immunologic and Neuronal Landscape of IgE‐Mediated Anaphylaxis
Biswas, R., Fried, J. M., & de Lafaille, M. A. C. (2025) · Immunological Reviews · doi:10.1111/imr.70078 · Cited by 8 · see citing works
Tryptase and tumor angiogenesis
Ribatti, D. (2024) · Frontiers in Oncology · doi:10.3389/fonc.2024.1500482 · Cited by 8 · see citing works
Genetic Variants Leading to Urticaria and Angioedema and Associated Biomarkers
Lyons, J. J., Farkas, H., Germenis, A. E., Rijavec, M., Smith, T., & Valent, P. (2023) · The Journal of Allergy and Clinical Immunology In Practice · doi:10.1016/j.jaip.2023.05.031 · Cited by 8 · see citing works
Self-citation
- Authors
- Greiner, G., Sprinzl, B., Górska, A., Ratzinger, F., Gurbisz, M., Witzeneder, N., Schmetterer, K. G., Gisslinger, B., Uyanik, G., Hadzijusufovic, E., Esterbauer, H., Gleixner, K. V., Krauth, M. T., Pfeilstöcker, M., Keil, F., Gisslinger, H., Nedoszytko, B., Niedoszytko, M., Sperr, W. R., Valent, P., & Hoermann, G.
- Affiliations
- Ludwig Boltzmann Institute for Hematology and Oncology (AT)
- Hanusch Hospital (AT)
- Gdańsk Medical University (PL)
- Ihr Labor, Medical Diagnostic Laboratories, Vienna, Austria;
- Medical University of Vienna (AT)
- Sigmund Freud Privatuniversität Wien (AT)
- University of Veterinary Medicine Vienna (AT)
- Department of Dermatology, Medical University of Gdańsk, Gdańsk, Poland;
- Innsbruck Medical University (AT)
- Corresponding author
- Hoermann, Gregor
- ORCID
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2021-01-14
- Volume
- 137
- Issue
- 2
- Pages
- 238-247
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC7116780
- OpenAlex
- W3048592971
- Cited by
- 189
- References
- 59
- Citations by year
- 2026: 24 · 2025: 31 · 2024: 28 · 2023: 29 · 2022: 33 · 2021: 40 · 2020: 3
- FWCI
- 9.18
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal Tumor Research and Treatment
- Health Sciences › Medicine › Surgery › Congenital gastrointestinal and neural anomalies
- Keywords
- hereditary alpha-tryptasemia, mastocytosis, TPSAB1, copy number gain, genetic biomarkers, anaphylaxis, KIT D816V mutation, mast cell activation, myeloid neoplasms
- MeSH terms
- Adolescent, Adult, Aged, Aged, 80 and over, Child, Female, Genetic Markers, Humans, Male, Mastocytosis, Middle Aged, Tryptases, Young Adult, DNA Copy Number Variations
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