Читать книгу Neonatal Haematology - Barbara J. Bain, Irene Roberts - Страница 20

There are major differences between the metabolism of fetal or neonatal red blood cells and that of adult red blood cells. These differences affect not only the functional properties of the red cells of healthy fetuses and neonates but also the clinical impact of inherited and acquired red cell disorders. Both the glycolytic pathway and the pentose phosphate pathway are affected (see Table 1.1). Overall, glycolysis and glucose consumption are lower in neonatal red blood cells than in adult red blood cells. This occurs despite the increased activity of most glycolytic pathway enzymes, such as glucose‐6‐phosphate dehydrogenase (G6PD), pyruvate kinase and lactate dehydrogenase (LDH), and is thought to be the result of reduced phosphofructokinase activity. Neonatal red cells also have less ability to generate the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) via the pentose phosphate pathway and have lower levels of glutathione peroxidase than adult red blood cells. The net result is that neonatal red blood cells are more susceptible than adult cells to oxidant‐induced injury.⁴⁶

In addition, neonatal red blood cells have a lower level of methaemoglobin reductase (about 60% of that in adult red blood cells). Methaemoglobin levels are therefore slightly higher in neonates than in adults (mean 4.3 g/l in preterm neonates, 2.2 g/l in term neonates and 1.1 g/l in adults).³⁵ Neonates are also more likely to develop methaemoglobinaemia because they are susceptible to the toxic effects of chemicals, such as nitric oxide and local anaesthetics, that oxidise haemoglobin‐derived iron more rapidly than the maximal possible rate of methaemoglobin reduction (see Chapter 2, Case 2.7).