Related Experiment Videos
Soluble transferrin receptor in sickle cell diseases: correlation with spleen function.
H Z Grotto1, E M Kimura, M V Carneiro
1Department of Clinical Pathology, School of Medical Sciences, Universidade Estadual de Campinas (UNICAMP), Campinas, Brazil. grotto@fem.unicamp.br
Sao Paulo Medical Journal = Revista Paulista De Medicina
|November 24, 1999
Summary
Soluble transferrin receptor (sTfR) levels and red cell ferritin (RCF) in sickle cell disease patients were evaluated. High sTfR is not linked to spleen function, but RCF accumulation may stem from spleen exocytosis deficiency.
Area of Science:
- Hematology
- Pediatrics
- Internal Medicine
Background:
- Sickle cell disease (SCD) is a group of inherited red blood cell disorders.
- SCD is characterized by chronic hemolysis, vaso-occlusion, and organ damage.
- Spleen function is often impaired in SCD patients, affecting their susceptibility to infections and disease severity.
Purpose of the Study:
- To investigate the relationship between spleen function and biomarkers of erythropoiesis and iron metabolism in SCD.
- To correlate soluble transferrin receptor (sTfR) levels and red cell ferritin (RCF) values with spleen function in SCD patients.
Main Methods:
- A prospective study was conducted involving 60 SCD patients and 28 healthy controls.
- Measurements included serum iron, transferrin-binding capacity, serum ferritin, RCF, and sTfR.
- Spleen function was assessed by quantifying pitted erythrocytes.
Main Results:
- SCD patients exhibited significantly higher sTfR and RCF levels compared to controls.
- sTfR levels showed an inverse correlation with fetal hemoglobin (HbF) levels.
- RCF values correlated with the presence of pitted erythrocytes, suggesting impaired spleen function.
Conclusions:
- Elevated sTfR levels in SCD are associated with increased erythropoiesis, potentially modulated by HbF.
- High sTfR levels do not directly reflect the degree of spleen dysfunction in SCD.
- Reduced spleen exocytosis may contribute to RCF accumulation in SCD patients, highlighting a potential mechanism for iron dysregulation.