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Fetal liver dysfunction in Rh alloimmunization.

U Nicolini1, P Nicolaidis, Y Tannirandorn

  • 1Royal Postgraduate Medical School, Institute of Obstetrics & Gynaecology, Queen Charlotte's and Chelsea Hospital, London.

British Journal of Obstetrics and Gynaecology
|March 1, 1991
PubMed
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Severe Rh alloimmunization causes liver dysfunction in fetuses. Transfusion therapy temporarily increases liver enzymes like gamma glutamyl transpeptidase (GGT) due to extramedullary erythropoiesis and potential portal hypertension.

Area of Science:

  • Perinatal Medicine
  • Fetal Physiology
  • Hematology

Background:

  • Rh alloimmunization is a serious condition causing fetal anemia and hydrops.
  • Liver enzyme alterations are observed in affected fetuses, but their dynamics and causes are not fully understood.

Purpose of the Study:

  • To investigate fetal liver enzyme levels (AST, ALT, GGT, ALP) in relation to Rh alloimmunization and intravascular transfusions.
  • To explore the correlation between liver enzymes, gestational age, fetal condition (hydropic vs. non-hydropic), and transfusion response.

Main Methods:

  • Blood samples were collected from 25 fetuses with Rh alloimmunization undergoing transfusions and 17 comparison fetuses.
  • Liver enzymes (AST, ALT, GGT, ALP) were measured at serial transfusions.
  • Correlations with gestational age, nucleated red cell count, and hematocrit were analyzed.

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Main Results:

  • Hydropic fetuses showed higher ALT levels than non-hydropic fetuses.
  • Transaminases (AST, ALT) normalized after transfusions, while GGT significantly increased, correlating with hematocrit.
  • GGT elevation was transitory and linked to extramedullary erythropoiesis and possibly portal hypertension.

Conclusions:

  • Rh alloimmunization induces fetal liver dysfunction, characterized by elevated transaminases.
  • Intravascular transfusions transiently increase GGT, likely due to increased erythropoiesis and portal hypertension.
  • These findings highlight liver involvement in severe Rh alloimmunization pathophysiology.