Glucose-6-phosphate dehydrogenase deficiency and pyruvate kinase deficiency are the two most common enzyme defects that cause hemolytic anemia. Glucose-6-phosphate dehydrogenase deficiency affects the pentose phosphate pathway, and pyruvate kinase deficiency affects the glycolytic pathway. The two variants of glucose-6-phosphate dehydrogenase deficiencies are African and Mediterranean. The Mediterranean variant has decreased enzyme activity in nearly all circulating RBCs. When cells are exposed to oxidant stress, a life-threatening hemolytic crisis ensues. In the African variant, only a limited portion of the RBC population is vulnerable at a given time; therefore, life-threatening complications are rare.
TTP is rare. Arteriolar lesions with localized platelet thrombi and fibrin deposits lead to thrombocytopenia and hemolytic anemia. The tissue hypoxia from occlusion of the vessels in the affected organ causes the symptoms of TTP. However, the cause of the occlusion remains unknown.
Autoimmune hemolytic anemia may be life-threatening. The disorder is seen in association with autoimmune diseases (eg, lupus, certain types of lymphomas and leukemias), or it may be drug-induced. In about 50% of cases, no identifiable etiology is found.
Nutritional etiologies of anemia include:
Vitamin B-12 deficiency
Starvation and generalized malnutrition
Read more about the etiology of anemia.
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Cite this: Emmanuel C. Besa. Fast Five Quiz: Anemia - Medscape - Feb 20, 2019.