Pediatr Blood Cancer 2005;45:861–862

LETTER TO THE EDITORHemolytic Disease of the Newborn Caused by a High Titer

Anti-Group B IgG From a Group A Mother

To the Editor: A 3-day-old infant presented withjaundice. Hewas a term infant and first child of a 29-year-old black female whose pregnancy was complicated byupper respiratory infections and premature labor. Hismother brought him to the hospital from home on histhird day of life concerned about jaundice. He had nofever or evidence of birth trauma. He had not stooledsince birth (3 days) and was having 2–3 wet diaperseach day. Family history was notable for a lack ofhemoglobinopathy, spherocytosis, anemia, or neonataljaundice. On physical examination, he had dry mucusmembranes and scleral icterus. He did not have a palpablespleen or liver. His total bilirubin was 28.6 mg/dl with anindirect bilirubin of 28.0 mg/dl. His white blood-cellcount was 6,100/mm3, hemoglobin 12.9 GMS%, hema-tocrit 37%, MCV 109.9 fl, RDW 17.6%, and plateletcount 382,000 mm3. The reticulocyte count was 9.8%.The peripheral blood smear revealed moderate numbersof spherocytes, ovalocytes, and macrocytes. His bloodgroup was Bþ. He had a negative direct antiglobulin test,but weak positive indirect Coombs when tested on Bcells. Maternal anti-B IgG titer was >1:1,024 and herblood group was Aþ.

The patient received intravenous hydration, 5 days ofphototherapy, no packed red blood cell transfusion, andcontinued breast-feeding. Returning to Hematology clinicat 17 months of age, he had a hemoglobin of 12.3 GMS%,hematocrit 36.5%,MCV 73.6 fL, RDW 14%, reticulocytecount 1.1%, total bilirubin of 0.2 mg/dl, and a peripheralsmear without spherocytes. Osmotic fragility testing onboth he and his sister was normal. He had no jaundice orhepatosplenomegaly, and was growing and developingnormally.

Anti-B IgG from a group A mother is an infrequentcause of hemolytic disease of the newborn (HDN) [1].This is not surprising because the development of anti-AorB IgG from group A or B mothers is rare [2–4].Isohemaglutinins are naturally occurring antibodies andare usually IgM, and people who develop IgG isohema-glutinins are typically group O. Since there are fewer Aand B antigenic sites on a newborn’s RBCmembrane, andalternative antigenic sites in other tissues to which theseantibodies could bind, anti-A or B IgG infrequently causesclinically apparent HDN [5].

After considering physiologic jaundice and the jaun-dice associated with poor feeding and dehydration aspotential causes of our patient’s hyperbilirubinemia, webelieve that our patient’s mother’s high titer anti-group BIgG is pathologic. There are no clinical or laboratory cri-teria available to predict the severity of ABO associatedHDN. Chen et al. [6] reported thatmaternal titers of anti-Aor B IgG>1:512 correlated with increased risk of HDN ingroup Omothers. Our patient’s mother’s titer of>1:1,024is unique, and another similar clinical case does not exist inthe literature. Our experience leads us believe that hightiter anti-B IgG fromagroupAmother can causeHDNandshould be considered when there is an otherwise un-explained indirect hyperbilirubinemia in a newborn.

Michael Wang, MD*Taru Hays, MD

Dan R. Ambruso, MD

Christopher C. Silliman, MD, PhDDivision of Hematology/Oncology/

Bone Marrow TransplantationThe Children’s HospitalUniversity of Colorado

Health Sciences Center Denver, Colorado

William C. Dickey, MD

Christopher C. Silliman, MD, PhDDan R. Ambruso, MD

Bonfils Blood CenterDenver, Colorado

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2. Dufour DR,MonaghanWP. ABO hemolytic disease of the newborn.

Am J Clin Path 1980;73:369.

� 2005 Wiley-Liss, Inc.DOI 10.1002/pbc.20503

——————*Correspondence to: Michael Wang, Hematology/Oncology/Bone

Marrow Transplantation, The Children’s Hospital, 1056 East 19th

Avenue, B115, Denver, CO 80218. E-mail: wang.michael@tchden.org

Received 6 January 2005; Accepted 7 January 2005

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JL, editors. Hematologic problems in the newborn, 2nd edn.

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862 Wang et al.