ArticleLeukemia & lymphoma2013
Bone marrow mast cell burden and serum tryptase level as markers of response in patients with systemic mastocytosis.
Article in Leukemia & lymphoma, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Management of skeletal-related events and fracture prevention in systemic mastocytosis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026Review
- Secretory and Membrane-Associated Biomarkers of Mast Cell Activation and Proliferation.International journal of molecular sciences · 2023Review
- Article
- Pharmacological treatment options for mast cell activation disease.Naunyn-Schmiedeberg's archives of pharmacology · 2016Review
- Determination of plasma heparin level improves identification of systemic mast cell activation disease.PloS one · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Two important response criteria in systemic mastocytosis (SM) are the elimination or reduction in percentage of bone marrow mast cells (MCs) and the reduction of serum tryptase levels. We investigated the accuracy of a single time point reduction of bone marrow MCs and serum tryptase level as response criteria in 50 patients with SM with available serial assessments. Bone marrow MC percentage varied significantly, with an average coefficient of variation (CV) of 65% (range, 6-173%) and 44% of patients having a CV higher than the average. The average CV for serum tryptase level was 19% (range, 0-96%), with 36% of patients having a CV higher than average. These wide variations in bone marrow MC burden and serum tryptase level were independent of the administration of SM-directed therapy, type of therapy or disease subtype. Furthermore, the achievement of a single time point therapy-induced bone marrow complete response (no histological evidence of malignant bone marrow MCs) did not correlate with tryptase level or symptomatic improvement. In conclusion, the value of single measurements of bone marrow MC percentage and serum tryptase level as response criteria in SM is not supported by clinical data. Incorporation of an assessment of the degree in reduction of MCs and tryptase, and assessment of response durability, would make response criteria more clinically meaningful.
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Registered trials
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