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Growth differentiation factor-15 in young sickle cell disease patients: relation to hemolysis, iron overload and
Azza Abdel Gawad Tantawy1, Amira Abdel Moneam Adly1, Eman Abdel Rahman Ismail2
1Pediatrics Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
Insights
Growth Differentiation Factor-15 (GDF-15) is elevated in children with sickle cell disease (SCD), reflecting ineffective erythropoiesis and hemolysis. Higher GDF-15 levels correlate with iron overload and may predict thrombotic events in SCD patients.
Area of Science:
- Hematology
- Pediatrics
- Genetics
Background:
- Growth Differentiation Factor-15 (GDF-15) is implicated in pathological iron overload in thalassemia.
- Sickle cell syndromes involve increased erythropoiesis and erythrocyte destruction.
Purpose of the Study:
- To measure serum GDF-15 in pediatric sickle cell disease (SCD) patients versus healthy controls.
- To assess GDF-15's relationship with hemolysis, iron overload, and vascular complications in SCD.
Main Methods:
- Serum GDF-15 levels were measured in 35 children/adolescents with SCD and 35 controls.
- GDF-15 was correlated with SCD genotype, sickling crisis frequency, hydroxyurea use, and serum ferritin.
Main Results:
- SCD patients exhibited significantly higher GDF-15 levels than controls (p<0.001).
- Elevated GDF-15 was associated with high serum ferritin (≥2500 μg/L), prior cerebral stroke, and splenectomy.
- GDF-15 was not significantly linked to crisis frequency, pulmonary hypertension, or hydroxyurea therapy; transfusion index, LDH, and ferritin independently predicted GDF-15 levels.
Conclusions:
- Increased GDF-15 in SCD highlights the role of ineffective erythropoiesis in disease severity and anemia.
- GDF-15 levels correlate with hemolysis and iron overload in SCD.
- GDF-15 may aid in identifying SCD patients at higher risk for thrombotic events.
Background:
High expression of growth differentiation factor-15 (GDF-15) contributes to pathological iron overload in thalassemia. Sickle cell syndromes are characterized by increased levels of erythropoiesis, although the primary defect involves the destruction of mature erythrocytes.
Aim:
To determine serum GDF-15 in 35 children and adolescents with sickle cell disease (SCD) compared to 35 healthy controls and assess its relation to markers of hemolysis, iron overload and vascular complications.
Methods:
GDF-15 was measured and correlated to genotype, frequency of sickling crises, hydroxyurea therapy and serum ferritin.
Results:
GDF-15 levels were increased in SCD patients whether sickle cell anemia or sickle β° thalassemia compared with controls (p<0.001) with no significant difference between patients' groups. GDF-15 was significantly higher in patients who had serum ferritin ≥2500 μg/L, previous cerebral stroke, and splenectomy. GDF-15 was not significantly related to frequency of sickling crises, pulmonary hypertension, or hydroxyurea therapy. On regression analysis, transfusion index, lactate dehydrogenase and serum ferritin were independently related to GDF-15.
Conclusion:
Increased GDF-15 in SCD reflects the importance of ineffective erythropoiesis in the pathophysiology and severity of anemia in SCD. GDF-15 levels are related to hemolysis and iron overload and may provide utility for identifying patients at increased risk of thrombotic events.
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