Transfusion · 2022
A case of Tn polyagglutination discovered by an ABO blood group discrepancy.
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Achram Robert, Denomme Gregory A, Stef Marianne A, Nguyen Thi Truc Anh, Delvadia Bhavesh, Thompson Louisa, Josephson Cassandra D, Roback John D, Sullivan H Cliff
Аннотация
BACKGROUND: Tn syndrome is an acquired form of polyagglutination arising from somatic mutations of hematopoietic stem cells. Tn red blood cells (RBCs) are agglutinable by naturally occurring anti-Tn antibodies in most adult sera. Current ABO typing reagents are monoclonal and do not detect polyagglutination on forward typing. However, herein we describe a case of Tn activation that was suspected due to cross-reactivity with a monoclonal anti-A reagent.
STUDY DESIGN AND METHODS: A 63-year-old man with myeloproliferative neoplasm, who historically typed as group O, demonstrated unexpected mixed field reactivity with anti-A reagent using a gel-based method. However, manual tube testing was consistent with the patient's historical group O type.
RESULTS: Lectin testing demonstrated reactivity with Salvia sclarea and Glycine soja, but not Arachis hypogea. The patient's RBCs produced positive crossmatches with healthy donor sera, but reactivity was eliminated by ficin pretreatment of the RBCs. Ficin treatment also resolved typing discrepancies on gel-based typing. No reactivity was noted using cord blood sera, and N antigen expression was diminished upon phenotyping. Tn activation was confirmed by detection of a novel 4-nucleotide deletion (c.395-398del) in exon 3 of C1GALT1C1 resulting in a truncated glycosyltransferase.
CONCLUSION: This case of acquired Tn polyagglutination due to a novel mutation was first suspected from an ABO phenotyping discrepancy. It highlights the cross-reactivity of anti-A reagent with Tn antigen when tested on a common gel-based method. Furthermore, the case demonstrates that review of patient history and test information can clarify discrepancies and guide resolution.
STUDY DESIGN AND METHODS: A 63-year-old man with myeloproliferative neoplasm, who historically typed as group O, demonstrated unexpected mixed field reactivity with anti-A reagent using a gel-based method. However, manual tube testing was consistent with the patient's historical group O type.
RESULTS: Lectin testing demonstrated reactivity with Salvia sclarea and Glycine soja, but not Arachis hypogea. The patient's RBCs produced positive crossmatches with healthy donor sera, but reactivity was eliminated by ficin pretreatment of the RBCs. Ficin treatment also resolved typing discrepancies on gel-based typing. No reactivity was noted using cord blood sera, and N antigen expression was diminished upon phenotyping. Tn activation was confirmed by detection of a novel 4-nucleotide deletion (c.395-398del) in exon 3 of C1GALT1C1 resulting in a truncated glycosyltransferase.
CONCLUSION: This case of acquired Tn polyagglutination due to a novel mutation was first suspected from an ABO phenotyping discrepancy. It highlights the cross-reactivity of anti-A reagent with Tn antigen when tested on a common gel-based method. Furthermore, the case demonstrates that review of patient history and test information can clarify discrepancies and guide resolution.