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Red Cell 2,3‐Diphosphoglycerate Levels in Children with Hereditary Haemolytic Anaemias
Author(s) -
Haidas S.,
ZannosMariolea L.,
Matsaniotis N.
Publication year - 1975
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1975.tb00887.x
Subject(s) - diphosphoglycerate , hereditary spherocytosis , jaundice , medicine , red cell , sickle cell trait , heterozygote advantage , beta thalassaemia , hemoglobinopathy , hemolytic anemia , hemoglobin , pediatrics , thalassemia , endocrinology , disease , biology , genotype , genetics , gene
S ummary . 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 μmol/g Hb. In jaundiced newborns with a mean haemoglobin of 16.04 g/dl mean 2,3‐DPG levels were 14.51 μmol/g Hb, i.e. normal. 2,3‐DPG levels were increased in patients with β‐thalassaemia major, α‐thalassaemia, sickle‐cell disease, favism, hereditary spherocytosis and in heterozygotes for β‐thalassaemia with increased haemoglobin F. In heterozygotes for β‐thalassaemia with increased haemoglobin A 2 only and in sickle cell trait 2,3‐DPG levels were normal.