Download PDF
Am J Perinatol 2008; 25(9): 541-545
DOI: 10.1055/s-0028-1085072
© Thieme Medical Publishers

Hemolytic Disease of the Fetus and Newborn Due to Anti-Ge3: Combined Antibody-Dependent Hemolysis and Erythroid Precursor Cell Growth Inhibition

Douglas P. Blackall1 , Gina D. Pesek1 , Matthew M. Montgomery1 , Krishna K. Oza1 , Patricia A. Arndt2 , George Garratty2 , Ali Shahcheraghi3 , Gregory A. Denomme3
  • 1University of Arkansas for Medical Sciences College of Medicine, Little Rock, Arkansas
  • 2American Red Cross Blood Services, Pomona, California
  • 3Mount Sinai Hospital, University of Toronto and Canadian Blood Services, Toronto, Canada
Further Information

Publication History

Publication Date:
21 August 2008 (online)

    Permissions and Reprints

ABSTRACT

The Gerbich (Ge) antigens are a collection of high-incidence antigens carried on the red blood cell membrane glycoproteins, glycophorins C and D. Antibodies against these antigens are uncommon, and there have been only rare case reports of hemolytic disease of the fetus and newborn due to anti-Ge. In this case report, we present a neonate with severe anemia and hyperbilirubinemia due to anti-Ge3. Routine and special laboratory studies undertaken in this case suggested two mechanisms for the patient's hemolysis and persistent anemia. Antibody-dependent hemolysis was associated with early-onset hyperbilirubinemia, anemia, and a mild reticulocytosis, and inhibition of erythroid progenitor cell growth was associated with late anemia and normal bilirubin and reticulocyte values. Though rare, anti-Ge3 can be a dangerous antibody in pregnancy. Affected neonates may require intensive initial therapy and close follow-up for at least several weeks after delivery.

KEYWORDS

Gerbich - hemolysis - hemolytic disease of the newborn - red blood cells

REFERENCES

  • 1 Reid M E, Spring F A. Molecular basis of glycophorin C variants and their associated blood group antigens.  Transfus Med. 1994;  4 139-146
    CrossrefPubMedGoogle Scholar
  • 2 Reid M E, Lomas-Francis C. The Blood Group Antigen Factsbook. 2nd ed. San Diego, CA; Academic Press 2004: 403-418
    Google Scholar
  • 3 Rosenfield R E, Haber G V, Kissmeyer-Nielsen F, Jack J A, Sanger R, Race R R. Ge, a very common red-cell antigen.  Br J Haematol. 1960;  6 344-349
    CrossrefPubMedGoogle Scholar
  • 4 Peddle L J, Josephson J E, Lawton A. Auto-donation in the management of placenta previa and erythroblastosis in a pregnancy complicated by Gerbich iso-immunization.  Vox Sang. 1970;  18 547-550
    PubMedGoogle Scholar
  • 5 Reid M, Rector D, Danneskiold T. Anti-Gerbich: a case report.  Immunohematology. 1984;  1 7-8
    PubMedGoogle Scholar
  • 6 Sacks D A, Johnson C S, Platt L D. Isoimmunization in pregnancy to Gerbich antigens.  Am J Perinatol. 1985;  2 208-210
    PubMedGoogle Scholar
  • 7 Pinder L, Coleman R, Woodfield D G. Polynesian patients of the Gerbich-negative phenotype Ge:-2–3.  Vox Sang. 1992;  63 74
    PubMedGoogle Scholar
  • 8 Miller R, Volny M, Unger P, Shapiro A, Sirota R, Engel M. A mild case of hemolytic disease of the newborn due to anti-Ge2,3 subclass IgG3.  Transfusion. 1996;  36 25S
    PubMedGoogle Scholar
  • 9 Arndt P A, Garratty G, Daniels G et al.. Late onset neonatal anemia due to maternal anti-Ge: possible association with destruction of erythroid progenitors.  Transfus Med. 2005;  15 125-132
    CrossrefPubMedGoogle Scholar
  • 10 Bowman J M, Pollock J M, Manning F A, Harman C R, Menticoglou S. Maternal Kell blood group alloimmunization.  Obstet Gynecol. 1992;  79 239-244
    PubMedGoogle Scholar
  • 11 Vaughan J I, Manning M, Warwick R M, Letsky E A, Murray N A, Roberts I A. Inhibition of erythroid progenitor cells by anti-Kell antibodies in fetal alloimmune anemia.  N Engl J Med. 1998;  338 798-803
    CrossrefPubMedGoogle Scholar
  • 12 Daniels G, Hadley A, Green C A. Causes of fetal anemia in hemolytic disease due to anti-K.  Transfusion. 2003;  43 115-116
    CrossrefPubMedGoogle Scholar
  • 13 Denomme G A, Shahcheraghi A, Blackall D P, Oza K K, Garratty G. Inhibition of erythroid progenitor cell growth by anti-Ge3.  Br J Haematol. 2006;  133 443-444
    CrossrefPubMedGoogle Scholar
  • 14 Brecher ME AABB Technical Manual. 15th ed. Bethesda, MD; American Association of Blood Banks 2005
    Google Scholar
  • 15 Arndt P A, Garratty G. A retrospective analysis of the value of monocyte monolayer assay results for predicting the clinical significance of blood group alloantibodies.  Transfusion. 2004;  44 1273-1281
    CrossrefPubMedGoogle Scholar
  • 16 Sacks D A, Nance S J, Garratty G, Petrucha R A, Horenstein J A, Fotheringham N. The monocyte monolayer assay as a predictor of severity of hemolytic disease of the fetus/newborn.  Am J Perinatol. 1993;  10 428-431
    PubMedGoogle Scholar
  • 17 Klein H G, Anstee D J. Mollison's Blood Transfusion in Clinical Medicine. 11th ed. Oxford; Blackwell Publishing 2005: 496-498
    Google Scholar
  • 18 Luban N L. Hemolytic disease of the newborn: progenitor cells and late effects.  N Engl J Med. 1998;  338 830-831
    PubMedGoogle Scholar
  • 19 Bony V, Gane P, Bailly P, Cartron J P. Time-course expression of polypeptides carrying blood group antigens during human erythroid differentiation.  Br J Haematol. 1999;  107 263-274
    CrossrefPubMedGoogle Scholar
  • 20 Head D J, Lee Z E, Poole J, Avent N D. Expression of phosphatidylserine (PS) on wild-type and Gerbich variant erythrocytes following glycophorin-C (GPC) ligation.  Br J Haematol. 2005;  129 130-137
    CrossrefPubMedGoogle Scholar

Douglas P BlackallM.D. 

Department of Pathology, Arkansas Children's Hospital

800 Marshall Street, Little Rock, AR 72202

Email: blackalldouglasp@uams.edu

      >