Premium
Anti‐G in a pregnant patient
Author(s) -
Cash K.,
Brown T.,
Strupp A.,
Uehlinger J.
Publication year - 1999
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1046/j.1537-2995.1999.39050531.x
Subject(s) - hemolytic disease of the newborn (abo) , medicine , gestation , rh isoimmunization , amniocentesis , pregnancy , hematocrit , rh blood group system , antibody , fetus , obstetrics , coombs test , bilirubin , hemolytic anemia , gastroenterology , immunology , prenatal diagnosis , biology , genetics
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, Dñ, Cñ, Eñ, c+ RBCs who was given 4 units of type O, Dñ 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 weeksí gestation were 64 against r′r RBCs and 16 against R 2 R 2 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 weeksí gestation. Prophylactic Rh immune globulin was administered antepartum and postpartum. The infantís RBCs were type O, D+, c+ Cñ, Eñ, and the direct antiglobulin test was positive. An acid eluate prepared from the babyís 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.