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Red cell 2,3-diphosphoglycerate levels in children with hereditary haemolytic anaemias
Insights
Red blood cell 2,3-diphosphoglycerate (2,3-DPG) levels were normal in neonatal jaundice but elevated in various hereditary hemolytic anemias. This impacts hemoglobin oxygen availability in these conditions.
Area of Science:
- Biochemistry
- Pediatrics
- Hematology
Background:
- Red blood cell 2,3-diphosphoglycerate (2,3-DPG) is crucial for regulating hemoglobin's oxygen affinity.
- Neonatal jaundice and hereditary hemolytic anemias can affect oxygen transport.
- Understanding 2,3-DPG levels is vital for managing these conditions.
Purpose of the Study:
- To investigate the role of 2,3-DPG in neonatal jaundice and hereditary hemolytic anemias.
- To determine how 2,3-DPG levels influence hemoglobin oxygen availability in these patient groups.
Main Methods:
- Measured 2,3-DPG levels in 58 normal children, 6 normal adults, 18 jaundiced newborns, and 57 patients with hereditary hemolytic anemias.
- Included conditions such as beta-thalassemia major, alpha-thalassemia, sickle-cell disease, favism, and hereditary spherocytosis.
Main Results:
- 2,3-DPG levels were normal in jaundiced newborns (14.51 mumol/g Hb) compared to normal controls (14.90 mumol/g Hb).
- Elevated 2,3-DPG levels were observed in patients with beta-thalassemia major, alpha-thalassemia, sickle-cell disease, favism, and hereditary spherocytosis.
- Normal 2,3-DPG levels were found in beta-thalassemia heterozygotes with increased HbA2 and in sickle cell trait.
Conclusions:
- 2,3-DPG levels do not significantly change in neonatal jaundice.
- Hereditary hemolytic anemias, particularly those with increased hemoglobin F, are associated with elevated 2,3-DPG.
- These findings highlight the adaptive role of 2,3-DPG in compensating for reduced oxygen-carrying capacity in hemolytic anemias.
Abstract:
The role of red cell 2,3-diphosphoglycerate (2,3-DPG) in increasing the availability of haemoglobin oxygen in neonatal jaundice and hereditary haemolytic anaemias was investigated. Measurements of 2,3-DPG were carried out on 58 normal children and six normal adults, 18 full-term newborns with neonatal jaundice and 57 cases (51 children and six adults) with hereditary haemolytic anaemias. In normal children and adults, with a mean haemoglobin of 12.69 g/dl, mean 2,3-DPG was 14.90 mumol/g Hb. In jaundiced newborns with a mean haemoglobin of 16.04 g/dl mean 2,3-DPG levels were 14.51 mumol/g Hb, i.e. normal. 2,3-DPG levels were increased in patients with beta-thalassaemia major, alpha-thalassaemia, sickle-cell disease, favism, hereditary spherocytosis and in heterozygotes for beta-thalassaemia with increased haemoglobin F. In heterozygotes for beta-thalassaemia with increased haemoglobin A2 only and in sickle cell trait 2,3-DPG levels were normal.