Anti-G in a pregnant patient

Kevin L. Cash, T. Brown, A. Strupp, Joan Uehlinger

Research output: Contribution to journalArticle

15 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)531-533
Number of pages3
JournalTransfusion
Volume39
Issue number5
DOIs
StatePublished - 1999

Fingerprint

Dilatation and Curettage
Fetal Erythroblastosis
Bilirubin
Pregnancy
Antibodies
Rho(D) Immune Globulin
Fetal Monitoring
Coombs Test
Amniocentesis
Hemolysis
Hematocrit
Postpartum Period
Pregnant Women
Parturition
Acids
RHO(D) antibody
Therapeutics

ASJC Scopus subject areas

  • Hematology
  • Immunology

Cite this

Anti-G in a pregnant patient. / Cash, Kevin L.; Brown, T.; Strupp, A.; Uehlinger, Joan.

In: Transfusion, Vol. 39, No. 5, 1999, p. 531-533.

Research output: Contribution to journalArticle

Cash, KL, Brown, T, Strupp, A & Uehlinger, J 1999, 'Anti-G in a pregnant patient', Transfusion, vol. 39, no. 5, pp. 531-533. https://doi.org/10.1046/j.1537-2995.1999.39050531.x
Cash, Kevin L. ; Brown, T. ; Strupp, A. ; Uehlinger, Joan. / Anti-G in a pregnant patient. In: Transfusion. 1999 ; Vol. 39, No. 5. pp. 531-533.
@article{424a4e39fdc443d8b70a8651c1cf4aef,
title = "Anti-G in a pregnant patient",
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.",
author = "Cash, {Kevin L.} and T. Brown and A. Strupp and Joan Uehlinger",
year = "1999",
doi = "10.1046/j.1537-2995.1999.39050531.x",
language = "English (US)",
volume = "39",
pages = "531--533",
journal = "Transfusion",
issn = "0041-1132",
publisher = "Wiley-Blackwell",
number = "5",

}

TY - JOUR

T1 - Anti-G in a pregnant patient

AU - Cash, Kevin L.

AU - Brown, T.

AU - Strupp, A.

AU - Uehlinger, Joan

PY - 1999

Y1 - 1999

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0032901455&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032901455&partnerID=8YFLogxK

U2 - 10.1046/j.1537-2995.1999.39050531.x

DO - 10.1046/j.1537-2995.1999.39050531.x

M3 - Article

C2 - 10336005

AN - SCOPUS:0032901455

VL - 39

SP - 531

EP - 533

JO - Transfusion

JF - Transfusion

SN - 0041-1132

IS - 5

ER -