Blood
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We determined the prevalence and optimal methods for laboratory diagnosis of iron deficiency anemia in patients with sickle cell disease. Laboratory investigations of 38 nontransfused and 32 transfused patients included transferrin saturation, serum ferritin, mean corpuscular volume (MCV), and free erythrocyte protoporphyrin (FEP). Response to iron supplementation confirmed the diagnosis of iron deficiency anemia in 16% of the nontransfused patients. ⋯ The high FEP was in part due to protoporphyrin IX and not completely due to zinc protoporphyrin, which is elevated in iron deficiency. We conclude that iron deficiency anemia is a potential problem in young nontransfused sickle cell patients. Serum ferritin below 25 ng/ml and low MCV are the most useful screening tests.
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The preservation of red cells "hard packed" to a hematocrit of over 80% from blood collected in citrate-phosphate-dextrose (CPD) or CPD-adenine (CPDA-1) has been investigated. After 21 days of storage, cells that had been collected in CPD solution had consumed most or all of the available glucose and manifested markedly impaired viability after reinfusion into the normal donor. In contrast, red cells prepared from blood collected in CPDA-1, a medium containing supplementary adenine and an increased amount of glucose, maintained higher glucose and adenosine triphosphate levels and, in most instances, manifested satisfactory posttransfusion viability. We emphasize that in addition to providing longer shelf life of stored blood, CPDA-1 provides a better hard-packed red cell concentrate for transfusion at 21 days.
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The pathophysiology of the occurrence and resolution of sickle cell crisis is unknown. The molecular abnormality is constant, while crisis is episodic. ⋯ Recovery from sickle crisis is associated with an increased filterability of the circulating red cell and a decreased susceptibility of the red cell to sickle with deoxygenation (p less than 0.05). The possibility that these changes are responsible for the resolution of crisis is suggested.
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Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. ⋯ Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.