By Philip Lanzkowsky
Completely up-to-date to mirror smooth pondering and protocols, the guide of Pediatric Hematology and Oncology offers concise info wanted for the day by day administration of kids with pediatric hematologic and oncologic ailments. The transparent kind permits readers to make a correct analysis and allows him/her to regard sufferers no matter if they've got no longer had broad past hematologic or oncologic event. Pertinent advances in molecular genetics, cytogenetics, immunology, transplantation and biochemistry are the results of forty years of sensible event by way of the writer within the administration of sufferers and contains a variety of participants who've had huge scientific event. * good points quite a few tables, movement diagrams, protocols, and algorithms for fast entry of crucial scientific info precious for the analysis and administration of those ailments in kids* Designed as a concise, effortless to take advantage of advisor for clinical scholars, citizens, fellows, pediatric hematologists/oncologists, pediatric nurses and nurse practitioners* a lot of the sensible details contained during this handbook isn't really present in general textbooks* elementary kind with none redundant phrases or references
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Extra info for Manual of Pediatric Hematology and Oncology, Fourth Edition
A concentration of less than 12 ng/mL is considered diagnostic of iron deficiency. Normal ferritin levels, however, can exist in iron deficiency when bacterial or parasitic infection, malignancy, or chronic inflammatory conditions coexist because ferritin is an acute-phase reactant. Figure 3-1 depicts the normal range of serum ferritin concentrations at different ages. 8. Serum iron and iron saturation percentage: Serum iron estimation as a measure of iron deficiency has serious limitations. It reflects the balance between several factors, including iron absorbed, iron used for hemoglobin synthesis, iron released by red cell destruction, and the size of iron stores.
Decreased red cell survival (normal when injected into asplenic subjects) 3. Increased autohemolysis 4. Increased red cell rigidity 5. Increased susceptibility to sulfhydryl inhibitors 6. Decreased heme production 7. Decreased globin and α-chain synthesis 8. Precipitation of α-globin monomers to cell membrane 9. Decreased glutathione peroxidase and catalase activity a. Inefficient H2O2 detoxification b. Greater susceptibility to H2O2 hemolysis c. Oxidative damage to cell membrane d. Increased cellular rigidity (Continues) 38 Hematology and Oncology Table 3-6.
Mild (type II): Crigler–Najjar (autosomal dominant) 3. Gilbert disease B. Inhibitors of bilirubin glucuronyl transferase 1. Drugs: novobiocin 2. Breast milk: pregnane-3α, 20β-diol 3. Familial: transient familial hyperbilirubinemia VI. Metabolic Hypothyroidism, maternal diabetes mellitus, galactosemia VII. , pyloric stenosis, annular pancreas, duodenal atresia) VIII. , homozygous sickle cell hemoglobinopathy) IX. Idiopathic a Not usually a cause of jaundice in the newborn because of the predominance of Hgb F (unless associated with concomitant G6PD deficiency).