At the first prenatal visit, a blood type and antibody screen are routinely assessed, and unbound antibodies in maternal serum are detected by the indirect Coombs test (Chap. 9, p. 160). When the result is positive, the specific antibodies are identified, their immunoglobulin subtype is determined as either immunoglobulin G (IgG) or M (IgM) , and the titer is quantiied. Only IgG antibodies are a concern because IgM antibodies do not cross the placenta. Selected antibodies and their potential to cause fetal hemolytic anemia are listed in Table he critical titer is the level at which significant fetal anemia could potentially develop. This may be diferent for each antibody, is determined individually by each laboratory, and usually ranges between 1:8 and 1 :32. If the critical titer for anti-D antibodies is 1: 16, a titer : 1: 16 indicates the possibility of severe hemolytic disease. An important exception is Kell sensitization, which is discussed on page 302.
he CDE system includes ive red cell proteins or antigens:
C, c, D, E, and e. here is no "d" antigen, and D-negativity is deined as the absence of the D antigen. Although most people are D positive or negative, more than 200 D antigen variants exist (Daniels, 2013). h was formerly termed rhesus because of
TABLE 15-1. Selected Red Cell Antigens and Their Relationship to Fetal Hemolytic Disease
CDE (Rh) 0,E, Bea, Ce, Cw, Cx, ce, c Ow, Evans, e, G, Goal, Hr, Hro, JAL, HOFM,
LOCR, Riv. Rh29, Rh32,
Rh42, Rh46, STEM, Tar k, Kp3, Kpb, K1s1, K22 Ku, Jsa, Jsb, Ula
Jkb, Jk3
MNS M, N, S, s, U, Mtd, Ena, Far, Hil, Hut, Mia, Mit, Mut, Mur, Mv, sO, Vw
Colton Cd, C03 Severe disease risk
Severe disease infrequent, mild disease risk
Severe disease infrequent, mild disease risk
Severe disease infrequent, mild disease risk Not associated with fetal hemolytic disease Severe disease infrequent, mild disease risk Mild disease possible
Severe disease infrequent, mild disease risk
Severe disease infrequent, mild disease risk
Severe disease infrequent, mild disease risk
Dd, Gy3, Hy, Joa Mild disease possible , Ge3, Ge4 , Lsa Mild disease possible
I I, i Not associated with fetal hemolytic disease
Lewis Lea, Leb Not associated with fetal hemolytic disease
From de Haas, 2015; Moise, 2008; Weinstein, 1982.
a misconception that red cells from rhesus monkeys expressed human blood group antigen. In transfusion medicine, "rhesus" is no longer used (Sandler, 2017).
CDE antigens are clinically important. D-negative individuals may become sensitized after a single exposure to as little as 0.1 mL of fetal erythrocytes (Bowman, 1988). The two responsible genes-RHD and RHCE-are located on the short arm of chromosome 1 and are inherited together, independent of other blood group genes. The incidence of antigen positivity varies according to racial and ethnic origin. Nearly 85 percent of non-Hispanic white Americans are D-positive. The incidence approximates 90 percent for Native Americans, 93 percent for frican Americans and Hispanic Americans, and at least 99 percent for Asian individuals (Garratty, 2004).