Hemolytic anemia oxidative

As the above mentioned studies with high supplementation dosages exemplarily show, there is no known toxicity for phylloquinone (vitamin Kl), although allergic reactions are possible. This is NOT true for menadione (vitamin K3) that can interfere with glutathione, a natural antioxidant, resulting in oxidative stress and cell membrane damage. Injections of menadione in infants led to jaundice and hemolytic anemia and therefore should not be used for the treatment of vitamin K deficiency. 

Genetic deficiency of glucose-6-phosphate dehydrogenase, with consequent impairment of the generation of NADPH, is common in populations of Mediterranean and Afro-Caribbean origin. The defect is manifested as red cell hemolysis (hemolytic anemia) when susceptible individuals are subjected to oxidants, such as the an-timalarial primaquine, aspirin, or sulfonamides or when... 

McMillan, D.C., et al.. Role of oxidant stress in lawsone-induced hemolytic anemia,... 

Hemolytic anemia results from decreased RBC survival time due to destruction in the spleen or circulation. The most common etiologies are RBC membrane defects (e.g., hereditary spherocytosis), altered Hb solubility or stability (e.g., sickle cell anemia [see Chap. 34] and thalassemias), and changes in intracellular metabolism (e.g., glucose-6-phosphate dehydrogenase deficiency). Some drugs cause direct oxidative damage to RBCs (see Appendix 3). 

Treatment of hemolytic anemia should focus on correcting the underlying cause. There is no specific therapy for glucose-6-phosphate dehydrogenase deficiency, so treatment consists of avoiding oxidant medications and chemicals. Steroids, other immunosuppressants, and even splenectomy can be indicated to reduce RBC destruction. 

Drugs Associated with Oxidative Hemolytic Anemia... 

Regarding its effect on hemolysis and formation of Heinz bodies, methemaglobinemia, and hemolytic anemia, it is likely that either additive or S5mergistic interaction would occur with other oxidants, such as aniline and acrolein, which are known to inhibit G6PD. 

The presence of precipitates of oxidized, denatured hemoglobin (Heinz bodies) helps distinguish the hemolytic anemia caused by of G6PD deficiency from that caused by pyruvate kinase deficiency. 

Hemolytic anemia can be caused by eating foods (such as fava beans) or taking drugs (such as anti-malarial agents or acetaminophen) that have oxidizing properties. 

Acute inorganic lead poisoning is uncommon today. It usually results from industrial inhalation of large quantities of lead oxide fumes or, in small children, from ingestion of a large oral dose of lead in the form of lead-based paint chips small objects, eg, toys coated or fabricated from lead or contaminated food or drink. The onset of severe symptoms usually requires several days or weeks of recurrent exposure and manifests as signs and symptoms of encephalopathy or colic. Evidence of hemolytic anemia (or anemia with basophilic stippling if exposure has been subacute), and elevated hepatic aminotransferases may be present. 

Most individuals who have inherited one of the many G6PD mutations do not show clinical manifestations (Figure 13.12. However, some patients with G6PD deficiency develop hemolytic anemia if they are treated with an oxidant drug, ingest fava beans, or contract a severe infection. 

Oxidant drugs Commonly used drugs that produce hemolytic anemia in patients with G6PD deficiency are best remembered from the mnemonic AAA = Antibiotics (for example, sulfa-... 

Mechanism of primaquine-induced hemolytic anemia. GSH, reduced glutathione GSSG, oxidized glutathione NADPH, reduced nicotinamide adenine dinucleotide phosphate. 

Nitrofurantoin prodnces oxidant stress and cellnlar damage by different mechanisms (43). It can distnrb folate metabolism, leading to a megaloblastic component in pre-existing (mostly hemolytic) anemia, which responds to folic acid treatment. 

---