Associated Papers
Global prevalence of hereditary thrombotic thrombocytopenic purpura determined by genetic analysis.
Seidizadeh O et al.
Blood Advances, 2024
38935915 (PubMed )
Supplement: BLOODA_ADV-2024-013421-mmc1.pdf
The effects of pathogenic and likely pathogenic variants for inherited hemostasis disorders in 140 214 UK Biobank participants.
Stefanucci L et al.
Blood, 2023
37647632 (PubMed )
Supplement: BLOOD_BLD-2023-020118-mmc3.xlsx › ST3.5
Hypercoagulability and Inflammatory Markers in a Case of Congenital Thrombotic Thrombocytopenic Purpura Complicated by Fetal Demise.
Skeith L et al.
Journal of Clinical Medicine, 2022
Morbidities and mortality in patients with hereditary thrombotic thrombocytopenic purpura.
Borogovac A et al.
Blood Advances, 2022
34807988 (PubMed )
Supplement: advancesADV2021005760-suppl1.pdf
The global carrier frequency and genetic prevalence of Upshaw-Schulman syndrome.
Zhao T et al.
Bmc Genomic Data, 2021
34789164 (PubMed )
Supplement: 12863_2021_1010_MOESM10_ESM.xlsx › HGMD
Pathophysiology of thrombotic thrombocytopenic purpura and hemolytic uremic syndrome.
Kremer Hovinga JA et al.
Journal of Thrombosis and Haemostasis : Jth, 2018
Multiple in silico tools predict phenotypic manifestations in congenital thrombotic thrombocytopenic purpura.
Hing ZA et al.
British Journal of Haematology, 2013
Drop of residual plasmatic activity of ADAMTS13 to undetectable levels during acute disease in a patient with adult-onset congenital thrombotic thrombocytopenic purpura.
Lotta LA et al.
Blood Cells, Molecules & Diseases, 2013
Residual plasmatic activity of ADAMTS13 is correlated with phenotype severity in congenital thrombotic thrombocytopenic purpura.
Lotta LA et al.
Blood, 2012
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