ArticleAnnals of hematology2026
Activated partial thromboplastin time prolongation without hemorrhagic dienhesis: a study of a chinese family coexisting with hereditary KNG1 p.Arg240 mutation and --SEA/αα genotype thalassemia.
Article in Annals of hematology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
High molecular weight kininogen (HK) deficiency is a rare autosomal recessive disorder caused by mutations in the KNG1 gene. This study reports a 66-year-old male Chinese patient who presented with significantly prolonged activated partial thromboplastin time (aPTT) and microcytic hypochromic anemia. Whole-exome sequencing revealed a homozygous nonsense mutation in exon 6 of the KNG1 gene (c.718 C > T, p.Arg240*) in the proband. This mutation results from a cytosine-to-thymine substitution, generating a premature termination codon that leads to truncated HK protein translation and loss of function. Additionally, genetic testing identified a concurrent heterozygous α-thalassemia --
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