ArticleEJHaem2021
Facilitating EMA binding test performance using fluorescent beads combined with next-generation sequencing.
Article in EJHaem, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Decoding the Ektacytometric Landscape of Hereditary Spherocytosis: Insights from 204 Cases.Diagnostics (Basel, Switzerland) · 2026Article
- Identification and functional analysis of novel SPTB and ANK1 mutations in hereditary spherocytosis patients.Scientific reports · 2024Article
- DAHEAN: A Danish nationwide study ensuring quality assurance through real-world data for suspected hereditary anemia patients.Orphanet journal of rare diseases · 2024Article
- Article
- Glucose phosphate isomerase deficiency demasked by whole-genome sequencing: a case report.Journal of medical case reports · 2024Article
- Hematological characteristics and hepatobiliary complications of hereditary spherocytosis in a tertiary care pediatric center: optimizing diagnosis and care through local and international networks.Frontiers in pediatrics · 2023Article
- Acquired spherocytosis in the setting of myelodysplasia.Leukemia research reports · 2022Article
- Facilitating EMA binding test performance using fluorescent beads combined with next-generation sequencing.EJHaem · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The eosin-5'-maleimide (EMA) binding test is widely used as diagnostic test for hereditary spherocytosis (HS), one of the most common haemolytic disorders in Caucasian populations. We recently described the advantages of replacing the use of healthy control blood samples with fluorescent beads in a modified EMA binding assay. In this study we further explore this novel approach. We performed targeted next-generation sequencing, modified EMA binding test and osmotic gradient ektacytometry on consecutive individuals referred to our laboratory on the suspicion of HS. In total, 33 of 95 carried a (likely) pathogenic variant, and 24 had variants of uncertain significance (VUS). We identified a total 79 different (likely) pathogenic variants and VUS, including 43 novel mutations. Discarding VUS and recessive mutations in
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