Erythrocyte production anemia from

Anemia from vitamin BI2 or folic acid deficiency is treated effectively by replacing the missing nutrient. Both folic acid and vitamin B12 are essential for erythrocyte production and maturation. Replacing these factors allows for normal DNA synthesis and, consequently, normal erythropoiesis. 

Some other examples of free radical formation in various pathologies are discussed below. (Of course, they are only few examples among many others, which can be found in literature.) Mitochondrial diseases are associated with superoxide overproduction [428] and cytochrome c release [429], For example, mitochondrial superoxide production apparently contributes to hippocampal pathology produced by kainate [430]. It has been found that erythrocytes from iron deficiency anemia are more susceptible to oxidative stress than normal cells but have a good capacity for recovery [431]. The beneficial effects of treatment of iron deficiency anemia with iron dextran and iron polymaltose complexes have been shown [432,433]. 

This vitamin is not made by plants or animals and can be synthesized only by a few species of microorganisms. It is required by healthy people in only minute amounts, about 3 p.g day. The severe disease pernicious anemia results from failure to absorb vitamin B12 efficiently from the intestine, where it is synthesized by intestinal bacteria or obtained from digestion of meat. Individuals with this disease do not produce sufficient amounts of intrinsic factor, a glycoprotein essential to vitamin B12 absorption. The pathology in pernicious anemia includes reduced production of erythrocytes, reduced levels of hemoglobin, and severe, progressive impairment of the central nervous system Administration of large doses of vitamin B12 alleviates these symptoms in at least some cases. ... 

Erythropoietin. Erythropoietin is a heavily glycosylated protein containing 166 amino acid residues. It is produced primarily by the peritubular cells in the cortex of the kidney, and up to 15% is produced in the liver. Il is the principal hormone responsible for stimulating the production of red blood cells from eryihroid progenitor cells, erythrocyte bursl-forming units, and erythrocyte colony-forming units. Small amounts of erylhropoielin are delectable in the plasma however, most of (he hormone is secreted by the kidneys in respon.se (o hypoxia or anemia, when levels of the hormone ean ri.se more than KX)-fold. 

Polycythemia is characterized by an increase in the number, and in the hemoglobin content, of circulating red cells. In patients who have chronic anoxia from impaired pulmonary ventilation or congenital or acquired heart disease, the increase in plasma erythropoietin leads to secondary polycythemia. Some renal cell carcinomas, hepatocarcinomas, and other tumors, which produce physiologically inappropriate amounts of erythropoietin, may also cause secondary polycythemia. Conversely, anemia can result from renal insufficiency and from chronic disorders that depress erythropoietin production. In polycythemia vera (primary polycythemia), which is a malignancy of erythrocyte stem cells of unknown cause, erythropoietin levels are normal or depressed. 

In vitamin B12 or folate deficiency anemia, megaloblastosis results from interference in fohc acid-and vitamin B -interdependent nucleic acid synthesis in the immature erythrocyte. The rate of RNA and cytoplasm production exceeds the rate of DNA production. The maturation process is retarded, resulting in immature large RBCs (macrocytosis). Synthesis of the RNA and DNA necessary for cell division depends on a series of reactions catalyzed by vitamin B12 and folic acid, as they have a role in the conversion of midine to thymidine. As shown in Fig. 99-4, dietary folates are absorbed in this process and converted (A) to 5-methyl tetrahydrofolate, which is then converted via a Bi2-dependent reaction (B) to tetrahydrofolate (C). After gaining a carbon, tetrahydrofolate is converted to a folate cofactor (D), 5,10-methyl-tetrahydrofolate, used by thymidylate synthetase (E) in the... 

ACD is a hypoprolrferative anemia that has traditionally been associated with infectious or inflammatory processes, tissue injury, or conditions associated with the release of proinflammatory cytokines. Alternative names include anemia of inflammation and cytokine-mediated anemia. The pathogenesis of the anemia of chronic disorders is based on three abnormalities shortened erythrocyte survival, impaired marrow response, and disturbance of iron metabolism. Pathologically, the RBCs have a shortened life span, and the bone marrow s capacity to respond to EPO is inadequate to maintain normal Hgb concentration. The cause of this defect is still uncertain, but appears to involve a block in the release of iron from the reticuloendothelial cells of the marrow. Various cytokines, such as interleukin-1, interferon-y, and tumor necrosis factor released during these illnesses may inhibit the production or action of EPO or the production of RBCs. ... 

Erythropoietin is a protein produced by the kidneys that stimulates the production of erythrocytes. Epoetin is mainly used in patients suffering from anemia associated with chronic renal failure or cancer. Three forms of epoetin are commercially... 

CDC, 1978, 1991, 2005 U.S. EPA, 1977, 1986, 2006). The purely lead-associated anemia is taken to be mildly hypochromic or normochromic and nor-mocytic. With severe exposures, one occasionally sees basophilic stippling from deranged erythropoietic activity and accumulation of pyrimidine nucleotides. Reticulocytosis is seen subsequent to reduced erythrocyte survival time. Lead toxicity induces the anemia via the combined effects of reduced hemoglobin production and increased erythrocyte destruction. 

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