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[Hydrops fetalis and G-6-PD deficiency]
1Service de soins intensifs néonatals et pédiatriques, hôpital Victor-Fouche, centre hospitalier régional et universitaire, Fort-de-France, France.
Summary
Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency can cause fetal anemia and hydrops fetalis. Early diagnosis through fetal blood enzyme studies is crucial for at-risk populations.
Area of Science:
- Perinatology
- Hematology
- Genetics
Background:
- Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is an uncommon cause of antenatal complications.
- Fetal hydrops and anemia can be manifestations of G-6-PD deficiency.
Observation:
- A male infant presented with hydrops fetalis (HF) and moderate anemia at 34 weeks gestation.
- Fetal blood sampling revealed erythroblastosis, and HF spontaneously resolved then recurred.
- Neonatal anemia and hydrops were successfully managed with aspiration and transfusion.
Findings:
- Postnatal investigations at 4 months revealed low G-6-PD enzyme activity.
- The child exhibited appropriate growth and development by 12 months.
Implications:
- G-6-PD deficiency should be suspected in cases of unexplained fetal anemia and hydrops fetalis, particularly in at-risk populations.
- Fetal red blood cell enzyme studies can confirm G-6-PD deficiency antenatally.
- Timely diagnosis and management can lead to favorable outcomes for affected infants.