K Cash1, T Brown, A Strupp, J Uehlinger. 1. Department of Pathology, Albert Einstein College of Medicine, Bronx, New York, USA. kcash@montefiore.org
Abstract
BACKGROUND: Anti-G is a red cell (RBC) antibody of the Rh system. It has been described in pregnant women only in association with anti-D or anti-C; therefore, the ability of this antibody alone to cause hemolytic disease of the newborn is uncertain. One case in which this antibody caused no clinical 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 units 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. Further evaluation by our laboratory revealed the presence of anti-G and possible 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 pregnancy. Amniocentesis performed at Weeks 28 and 32 showed no evidence of hemolytic disease of the newborn. A healthy 3.3-kg infant was delivered at 36 weeks' gestation. Prophylactic Rh immune globulin was administered antepartum and postpartum. The infant's RBCs were type O, D+, c+ C-, E-, and the direct 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 may be unnecessary if anti-G is the sole cause of fetomaternal RBC incompatibility.
BACKGROUND: Anti-G is a red cell (RBC) antibody of the Rh system. It has been described in pregnant women only in association with anti-D or anti-C; therefore, the ability of this antibody alone to cause hemolytic disease of the newborn is uncertain. One case in which this antibody caused no clinical 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 units 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. Further evaluation by our laboratory revealed the presence of anti-G and possible 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 pregnancy. Amniocentesis performed at Weeks 28 and 32 showed no evidence of hemolytic disease of the newborn. A healthy 3.3-kg infant was delivered at 36 weeks' gestation. Prophylactic Rh immune globulin was administered antepartum and postpartum. The infant's RBCs were type O, D+, c+ C-, E-, and the direct 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 may be unnecessary if anti-G is the sole cause of fetomaternal RBC incompatibility.