Possible suppression of fetal erythropoiesis by the Kell blood group antibody anti-Kpa

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Immunohematology

American National Red Cross

Subject: Medical Laboratory Technology

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ISSN: 0894-203X
eISSN: 1930-3955

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VOLUME 27 , ISSUE 2 (June 2011) > List of articles

Possible suppression of fetal erythropoiesis by the Kell blood group antibody anti-Kpa

Michelle Tuson / Kim Hue-Roye / Karen Koval / Sherwin Imlay / Rajendra Desai / Gayatri Garg / Esam Kazem / Diane Stockman / Janis S. Hamilton / Marion E. Reid

Keywords : erythropoiesis—suppression, Kell blood group system, hemolytic disease of the newborn, Kpa

Citation Information : Immunohematology. Volume 27, Issue 2, Pages 58-60, DOI: https://doi.org/10.21307/immunohematology-2019-174

License : (Transfer of Copyright)

Published Online: 01-December-2019

ARTICLE

ABSTRACT

Antibodies to antigens in the Kell blood group system are usually immunoglobulin G, and, notoriously, anti-K, anti-k, and anti-Kpa can cause severe hemolytic transfusion reactions, as well as severe hemolytic disease of the fetus and newborn (HDFN). It has been shown that the titer of anti-K does not correlate with the severity of HDFN because, in addition to immune destruction of red blood cells (RBCs), anti-K causes suppression of erythropoiesis in the fetus, which can result in severe anemia. We report a case involving anti-Kpa in which one twin was anemic and the other was not. Standard hemagglutination and polymerase chain reaction (PCR)-based tests were used. At delivery, anti-Kpa was identified in serum from the mother and twin A, and in the eluate prepared from the baby’s RBCs. PCR-based assays showed twin A (boy) was KEL*841T/C (KEL*03/KEL*04), which is predicted to encode Kp(a+b+). Twin B (girl) was KEL*841C/C (KEL*04/ KEL*04), which is predicted to encode Kp(a–b+). We describe the first reported case of probable suppression of erythropoiesis attributable to anti-Kpa. One twin born to a woman whose serum contained anti-Kpa experienced HDFN while the other did not. Based on DNA analysis, the predicted blood type of the affected twin was Kp(a+b+) and that of the unaffected twin was Kp(a–b+). The laboratory findings and clinical course of the affected twin were consistent with suppression of erythropoiesis in addition to immune RBC destruction.

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