The University of Chicago Chicago, Illinois, United States
Background/Case Studies: The high-prevalence U antigen is part of the MNS blood group system and is carried on glycophorin B along with the S and s antigens. About 1.5% of the Black population has U-negative or U-variant phenotypes and can potentially develop IgG antibodies against the U antigen. Anti-U antibodies are associated with both transfusion reactions and hemolytic disease of the fetus and newborn (HDFN). While multiple case reports have described passively acquired anti-U in neonates at various maternal titers, the clinical significance and need for interventions are not very well established.
Study
Design/Methods: Here we present a 24-year-old G4P3003 AB-positive female with a history of anti-U alloimmunization. The patient had a reported anti-U titer of 1:16 identified during a second trimester antibody screen at an outside hospital. During the third trimester a repeat antibody titer had increased to 1:1024. The patient was transferred to our institution for further management. A middle cerebral artery (MCA) doppler was performed, revealing normal MCA peak systolic velocity for gestational age. The patient’s antibody screen was sent to the reference laboratory, confirming anti-U and Human Erythrocyte Antigen (HEA) Genotyping Panel confirmed the patient’s phenotype to be S-s-U-.
Results/Findings: At 37w0d a healthy female neonate was delivered via uncomplicated vaginal delivery and admitted to the intensive care unit for monitoring for HDFN. The infant was AB-positive with a positive antibody screen demonstrating panreactivity and a positive Direct Antiglobulin Test (DAT) (4+ with anti-IgG, 0 with anti-C3). An elution was performed at the reference lab where only anti-U was identified. Initial hemolysis labs post-birth were within normal limits (WNL) with a hemoglobin: 18.2 g/dL (RR: 13.2-19.1 g/dL ), hematocrit: 54.5% (RR: 42.0-60.0%), and an unconjugated bilirubin: 1.7 mg/dL (RR: 1.0-6.0 mg/dL). Hemoglobin/hematocrit, reticulocyte count, and bilirubin were closely monitored and remained WNL. Repeat DAT testing on day 1 and day 2 of life remained 4+ with anti-IgG. HEA Genotyping Panel performed at reference lab predicted a U+ phenotype. However, the neonate did not require phototherapy or transfusions and was discharged on day 2 of life in stable condition. Conclusions: This case demonstrates a passively acquired anti-U in a neonate, born to a mother with a high anti-U titer, who did not show any evidence of HDFN or require phototherapy or transfusions. To date, this appears to be the highest anti-U maternal titer reported in the literature in which the neonate did not receive any intervention. Yet, the clinical significance of anti-U in HDFN remains to be fully elucidated, and larger studies or case reports are needed to better understand its impact.
