Megaloblastic anemia.

Most, but not all, megaloblastic anemia is produced by "ineffective erythropoiesis" in the bone marrow due to either folic acid or vitamin B12 deficiency. In folic acid deficiency the cause frequently is inadequate dietary intake, whereas vitamin B12 deficiency is almost always conditioned by some specific type of malabsorption. Anemia with oval macrocytes, few reticulocytes, moderate leukopenia, and thrombocytopenia is typical of both. Aplastic anemia, refractory anemias with cellular marrow, preleukemia, aleukemia, and erythroleukemia may have somewhat similar blood findings but are usually recognizable from bone marrow biopsy. Decreased levels of folate or vitamin B12 are the most reliable criteria of megaloblastic anemia. With these available in advance, therapy with the appropriate vitamin can be begun at once. If serum levels are unavailable or available only in retrospect, initial treatment, especially of severe anemia, should be with both vitamins. Differentiation between folate and vitamin B12 deficiency is important but impossible by blood and bone marrow morphology alone. Thus, if serum levels are unavailable, the distinction must be made, sometimes retrospectively, on the basis of other laboratory examinations, such as gastric analysis, small-bowel x-ray films, and the Schilling test.

Oxidant injury of caucasian glucose-6-phosphate dehydrogenase-deficient red blood cells by phagocytosing leukocytes during infection.

Patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency of red blood cells (RBC) may develop sudden hemolytic anemia during infection. Since phagocytizing polymorphonuclear leukocytes (PMN) are known to generate hydrogen peroxide, we explored the influence of this oxidant product of PMN on juxtaposed G6PD-deficient and normal RBC. The oxidant stress induced by phagocytosis depleted G6PD-deficient RBC of reduced glutathione (GSH) and this was associated with rapid removal of these cells from the circulation by the liver and spleen. No such effect was observed on normal RBC. Phagocytizing chronic granulomatous disease (CGD) PMN which lack hydrogen peroxide generation, failed to diminish GSH level in G6PD-deficient RBC. Thus, PMN can pose as a source of oxidant damage to G6PD-deficient RBC due to hydrogen peroxide generated during phagocytosis.