BACKGROUND: Anti-G is a red cell (RBC) antibody of the Rh system. It has be
en described in pregnant women only in association with anti-D or anti-G; t
herefore, the ability of this antibody alone to cause hemolytic disease of
the newborn is uncertain. One case in which this antibody caused no clinica
l sequelae is reported.
CASE REPORT: The patient was a 35-year-old primigravida with type O, D-, C-
, E-, c+ RBCs who was given 4 units of type O, D- allogeneic RBCs and 2 uni
ts of autologous RBCs 2 years antepartum. She was found to have anti-D and
anti-C by an outside laboratory as part of a routine prenatal work-up. Furt
her evaluation by our laboratory revealed the presence of anti-G and possib
le anti-C without anti-D Titers at 22 weeks' gestation were 64 against r'r
RBCs and 16 against R2R2 RBCs; these remained unchanged throughout the preg
nancy. Amniocentesis performed at Weeks 28 and 32 showed no evidence of hem
olytic disease of the newborn. A healthy 3.3-kg infant was delivered at 36
weeks' gestation. Prophylactic Rh immune globulin was administered antepart
um and postpartum. The infant's RBCs were type O, D+, c+ C-, E-, and the di
rect antiglobulin test was positive. An acid eluate prepared from the baby'
s RBCs revealed anti-G. The total bilirubin was 5.5 mg per dL at birth, and
the hematocrit was 66 percent. Total bilirubin peaked on Day 5 at 11.9 mg
per dL, and no therapeutic intervention was required.
CONCLUSIONS: Anti-G alone caused little if any fetal or neonatal hemolysis
in this case. Although further study is needed, invasive fetal monitoring m
ay be unnecessary if anti-G is the sole cause of fetomaternal RBC incompati
bility.