Anemias causing

Erythropoietin is a growth factor produced by interstitial cells of the kidney in response to hypoxia. Erythropoietin stimulates haematopoiesis in the bone marrow. Recombinant human erythropoietin is used to treat anemias, e.g. anemia caused by chronic renal failure and anemia in AIDS and cancer patients. 

Cyano- and hydroxocobalamin - both can be converted to the physiologically relevant coenzymes methyl- and 5 -deoxyadenosylcobalamin in the liver -are used for therapeutical applications. When pernicious anemia caused by chronic atrophic gastritis has been diagnosed, it is treated as follows During the first 7 days of treatment, 1000 pg of hydroxocobalamin/d are administered parenterally, usually intramuscularly. Then, the same dose is given once weekly for 4-6 weeks. The aim is to alleviate the deficiency symptoms and at the same time to replenish the stores. Afterwards, 1000 pg hydroxocobalamin should be given parenterally every 2 months lifelong to avoid relapse [1, 2]. 

It is an important intracellular reductant, helping to maintain essential SH groups of enzymes in their reduced state. This role is discussed in Chapter 20, and its involvement in the hemolytic anemia caused by deficiency of glucose-6-phosphate dehydrogenase is discussed in Ghapters 20 and 52. 

The causes of anemia can be divided into three main categories decreased production, increased destruction, and blood loss. Drug therapy is the mainstay of treatment for anemias caused by reduced production of erythrocytes and will be the focus of this chapter. 

EPOGEN Epoetin alfa Amgen also approved and marketed as PROCRIT by Ortho Biotech Anemia associated with chronic renal failure Anemia caused by chemotherapy... 

K12. Kanno, H Wei, D. C, C Chan, L. C., Mizoguchi, H., Ando, M., Nakahata, T Narisawa, K., Fujii, H., and Miwa, S., Hereditary hemolytic anemia caused by diverse point mutations of pyruvate kinase gene found in Japan and Hong Kong. Blood 84,3505-3509 (1994). 

N5. Neubauer, B., Lakomek, M., Winkler, H., Parke, M., Hofferbert, S., Schroter, W., Point mutations in the L-type pyruvate kinase gene of two children with hemolytic anemia caused by pyruvate kinase deficiency. Blood 77, 1871-1875 (1991). 

Latimer, K.S., A.V. Jain, H.B. Inglesby, W.D. Clarkson, and G.B. Johnson. 1989. Zinc-induced hemolytic anemia caused by ingestion of pennies by a pup. Jour. Amer. Veterin. Med. Assoc. 195 77-80. 

The hemolytic anemia caused in pregnant rabbits by diflunisal was severe enough to explain the concomitant axial skeletal malformations (Clark et ah, 1984). Acetazolamide-induced fetal malformations in mice are apparently related to maternal hypercapnia (Weaver and Scott, 1984a, b) and hypokalemia (Ellison and Maren, 1972). The increased resorption rate induced in rabbits by the antibiotic norfloxacin depends on exposure of the maternal gastrointestinal tract (Clark et ah,... 

Because of the possibility of hemolytic anemia caused by immature erythrocyte enzyme systems (glutathione instability), the drug is contraindicated in pregnant patients P.1001... 

Capsules/Tablets/Oral solution - Fatal and nonfatal Mis have been reported in patients with anemia caused by ribavirin. 

Flypersensitivity to TMP or SMZ megaloblastic anemia caused by folate deficiency ... 

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. 

Sickle-cell anemia causes red blood cells to assume a sickle shape. The abnormal blood cells disrupt blood circulation, which can lead to infections, organ damage, and chronic pain. 

Folate deficiency results in a megaloblastic anemia that is microscopically indistinguishable from the anemia caused by vitamin B12 deficiency (see above). However, folate deficiency does not cause the characteristic neurologic syndrome seen in vitamin B12 deficiency. In patients with megaloblastic anemia, folate status is assessed with assays for serum... 

In some drug reactions, several of these hypersensitivity responses may present simultaneously. Some adverse reactions to drugs may be mistakenly classified as allergic or immune when they are actually genetic deficiency states or are idiosyncratic and not mediated by immune mechanisms (eg, hemolysis due to primaquine in glucose-6-phosphate dehydrogenase deficiency, or aplastic anemia caused by chloramphenicol). 

There are examples where several genetic factors, including the acetylator phenotype, operate together. Hydralazine toxicity is one such example, which is discussed in detail in chapter 7. Another is the hemolytic anemia caused by the drug thiozalsulfone (Promizole), which occurs particularly in those individuals who are both glucose-6-phosphate dehydrogenase deficient and slow acetylators. Promizole is acetylated, and studies in rapid and slow acetylator mice confirmed that acetylation was a factor as well as an extent of hydroxylation. The latter may also be another factor in humans as is discussed below. 

Although sickle cell anemia causes problems in many organ systems, the chief cause of death of children with SCA is bacterial infection. Discuss. 

Yamamoto A, Katayama Y, Tomiyama K, Hosoai H, Hirata F, Kimura F, Fujita K, Yasuda H. Methimazole-induced aplastic anemia caused by hypocellular bone marrow with plasmacytosis. Thyroid 2004 14(3) 231-5. 

A number of toxic effects on the blood have been documented, including agranulocytosis caused by chlorpromazine, hemolytic anemia caused by methyldopa, and megaloblastic anemia caused by methotrexate. Toxic effects on the eye have been noted and range from retinotoxicity caused by thioridazine to glaucoma caused by systemic corticosteroids. 

Constriction of blood vessels, arrhythmia, and even aplastic anemia, caused by ethyl alcohol, methylene chloride, and benzene, respectively, are circulatory system diseases that result from misuse of these chemical substances. Methylene chloride, a paint solvent, reacts in the body to produce carbon monoxide, which replaces oxygen in the hemoglobin molecule. This can cause carbon monoxide poisoning, which can be fatal. 

The first approval of a therapeutic use for recombinant EPO was in 1989 for the treatment of anemia related to chronic renal failure. The treatment with EPO stimulates production of erythrocytes and improves the patient s quality of life, as well as reducing or eliminating the need for blood transfusion. There are other non-renal applications, such as the minimization of blood transfusion after surgery, the prevention of anemia after bone marrow transplantation, and the treatment of anemia caused by the use of antiretroviral drugs, by chemotherapy, and by prematurity. 

Zn Zn2+ 16 mg Over 200 e.g., carbonic anhydrase, carboxypeptidases Sickle cell anemia causes a Zn deficiency... 

Erythropoietin [ery throw PO eetin] is a glycoprotein, normally made by the kidney, that regulates red cell proliferation and differentiation in bone marrow. Human erythropoietin, produced by recombinant DNA technology, is effective in the treatment of anemia caused by end-stage renal disease, anemia associated with HIV-infected patients, and anemia in some cancer patients. Supplementation with iron may be required to assure an adequate response. The protein is usually administered intravenously in renal dialysis patients, but in others the subcutaneous route is preferred. Side effects such as iron deficiency and an elevation in blood pressure occur. [Note The latter may be due to increases in peripheral vascular resistance and/or blood viscosity.]... 

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