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Hemolytic anemia in disorders of red cell metabolism

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TLDR
The Red Cell Structure, Red Cell Metabolism, and Other Pathways - 1.2.1 The Red Cell structure and Kinetic Properties.
Abstract
1 The Red Cell.- 1.1. Red Cell Structure.- 1.2. Red Cell Metabolism.- 1.2.1. Embden-Meyerhoff Pathway.- 1.2.2. Hexose Monophosphate Pathway.- 1.2.3. Other Pathways.- 1.2.4. ATPase Activity and Ion Movements.- 1.2.5. Methemoglobin Reduction.- References.- 2 Glucose-6-Phosphate Dehydrogenase Deficiency.- 2.1. History.- 2.2. Genetics and Population Distribution.- 2.3. Glucose-6-phosphate Dehydrogenase.- 2.3.1. Purification.- 2.3.2. Subunit Structure.- 2.3.3. Kinetic Properties.- 2.3.4. Biochemical Properties of Variants.- 2.4. Physiology and Pathophysiology.- 2.4.1. The Steady State.- 2.4.1.1. Red Cells.- 2.4.1.2. White Cells.- 2.4.1.3. Platelets.- 2.4.1.4. Other Tissues.- 2.4.2. Association of Various Disease States with G-6-PD Deficiency.- 2.4.2.1. Nonhematologic Changes.- 2.4.2.2. Drug-Induced Hemolytic Anemia.- 2.4.2.3. Hemolytic Anemia Induced by Infection.- 2.4.2.4. Hemolytic Anemia in Diabetic Acidosis.- 2.4.2.5. Neonatal Icterus.- 2.4.2.6. Favism.- 2.4.2.6a. The Predisposition to Favism.- 2.4.2.6b. The Active Factor.- 2.4.2.7. Hereditary Nonspherocytic Hemolytic Anemia.- 2.5. Diagnosis.- 2.6. Treatment.- References.- 3 Pyruvate Kinase Deficiency.- 3.1. History.- 3.2. Genetics.- 3.3. Acquired Pyruvate Kinase Deficiency.- 3.4. Pyruvate Kinase.- 3.4.1. The Normal Enzyme.- 3.4.2. Mutant Pyruvate Kinase.- 3.5. The Pyruvate Kinase-Deficient Red Cell.- 3.6. Clinical Manifestations.- 3.7. Diagnosis.- 3.8. Treatment.- References.- 4 Hemolytic Anemia Due to Other Enzyme Deficiencies.- 4.1. Hexokinase Deficiency.- 4.2. Glucose Phosphate Isomerase Deficiency.- 4.3. Phosphofructokinase Deficiency.- 4.4. Aldolase Deficiency.- 4.5. Triose Phosphate Isomerase Deficiency.- 4.6. Phosphoglycerate Kinase Deficiency.- 4.7. Glyceraldehyde Phosphate Dehydrogenase Deficiency.- 4.8. Diphosphoglycerate Mutase Deficiency.- 4.9. Diphosphoglycerate Phosphatase Deficiency.- 4.10. Enolase Deficiency.- 4.11. Defects in Glutathione Synthesis.- 4.12. Glutathione Reductase Deficiency.- 4.13. Glutathione Peroxidase Deficiency.- 4.14. Phosphogluconate Dehydrogenase Deficiency.- 4.15. Disorders of Nucleotide Metabolism.- 4.15.1. ATPase Deficiency.- 4.15.2. Adenylate Kinase Deficiency.- 4.15.3. "High ATP" Syndromes.- 4.15.4. Pyrimidine 5?-Nucleotidase Deficiency.- 4.15.5. Increased Adenosine Deaminase Activity.- References.

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Targeted disruption of the housekeeping gene encoding glucose 6-phosphate dehydrogenase (G6PD): G6PD is dispensable for pentose synthesis but essential for defense against oxidative stress

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Glucose-6-phosphate dehydrogenase deficiency: a historical perspective

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References
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Human Phosphoglycerate Kinase I. CRYSTALLIZATION AND CHARACTERIZATION OF NORMAL ENZYME

TL;DR: Human phosphoglycerate kinase (ATP:3-phospho-d-glycerate 1-Phosphotransferase, EC 2.7.3) was purified from red blood cells and indicated a homogeneous preparation.
Journal ArticleDOI

Familial Spinocerebellar Degeneration, Hemolytic Anemia, and Glutathione Deficiency

TL;DR: Preliminary studies indicate that this may be the only reported family with GSH deficiency due to γglutamyl-cysteine synthetase deficiency, and patients with autosomal recessive forms of spinocerebellar degeneration should be examined for disorders of GSH synthesis.
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