Anemia defined

Aplastic anemia, defined by the presence of pancytopenia and a hypocellular bone marrow in the absence of any abnormal blood cells, is a serious reaction that has been attributed to perphenazine in a single case (2). 

According to the World Health Organization, anemia is second only to tuberculosis as the world s most prevalent and costly public health issue. Anemia defined as Hgb <13 g/dL in men or <12 g/dL in women (as recommended by the World Health Organization) occurs in... 

The anemias discussed in this chapter include iron deficiency anemia, anemia in patients witii chronic renal disease pernicious anemia, and anemia resulting from a folic acid deficiency. Table 45-1 defines these anemias. Drugp used in treatment of anemia are summarized in die Summary Drug Table Drugp Used in die Treatment of Anemia. 

CoAd Blood Testing oa Sickle Cell Anemia and Related Vl6-oAdeAS by AlienachAomatogAaphlc Methods. The CM-Sephadex procedure easily detects Hb-S and Hb-C at birth but the diffuse zone of Hb-A has on occasion been difficult to see. Substitution of CM-Cellulose for CM-Sephadex has yielded a superior mlcrochromatographlc method, and the compact, well-defined zones of the CM-Cellulose column facilitate the Interpretation of the results even though the amount of sample Is only 20% as great. The CM-Cellulose method Is as simple and rapid as the original CM-Sephadex procedure (27. 28). 

Current NKF guidelines define anemia as a hemoglobin (Hgb) level less than 11 g/dL (6.8 mmol/L).31 A number of factors can contribute to the development of anemia, including deficiencies in vitamin B12 or folate, hemolysis, bleeding, or bone marrow suppression. Many of these can be detected by alterations in RBC indices, which should be included in the evaluation for anemia. A complete blood cell count is also helpful in evaluating anemia to determine overall bone marrow function. 

The Nobel Prize chemist Linus Pauling related the mechanism of sickle cell anemia to a genetic defect in hemoglobin synthesis and thus defined the first molecular disease. Pauling s groundbreaking paper in 1949 was boldly titled Sickle Cell Anemia A Molecular Disease. Many claim that this discovery laid the foundation for molecular biology. What is the chemistry that is at the heart of this pioneering work ... 

Molecular medicine was a term used by two-time Nobel laureate in chemistry and peace Linus Pauling, Ph.D., in his landmark article on the mechanism of production of sickle cell anemia published in 1949.1 It defined a new perspective on the origin of disease based upon the recognition that specific mutations of the genes can create an altered "molecular environment" and therefore the modified physiological function associated with specific diseases. 

Like folate and vitamin C, vitamin B6 (pyroxidine) is water soluble and like folate has several vitamers. Vitamin B6 may be involved in more bodily functions than any other nutrient (Tambasco-Studart et al., 2005), is a cofactor for many enzymes, especially those involved in protein metabolism, and is also a cofactor for folate metabolism. Vitamin B6 has anticancer activity (Theodoratou et al., 2008), is a strong antioxidant (Denslow et al., 2005), is involved in hemoglobin biosynthesis, lipid and glucose metabolism and immune and nervous system function. Possible consequences of deficiency include anemia, impaired immune function, depression, confusion, and dermatitis (Spinneker et al., 2007). Vitamin B6 deficiency is generally not a problem in the developed world, but there could be as yet poorly defined consequences of suboptimal intake particularly for the elderly. 

Once a diagnosis of megaloblastic anemia is made, it must be determined whether vitamin B12 or folic acid deficiency is the cause. (Other causes of megaloblastic anemia are very rare.) This can usually be accomplished by measuring serum levels of the vitamins. The Schilling test, which measures absorption and urinary excretion of radioactively labeled vitamin B12, can be used to further define the mechanism of vitamin Bi2 malabsorption when this is found to be the cause of the megaloblastic anemia. 

Hemoglobinopathies have traditionally been defined as a family of dis orders caused by production of a structurally abnormal hemoglobin molecule, synthesis of insufficient quantities of normal hemoglobin, or, rarely, both. Sickle-cell anemia (HbS), hemoglobin C disease (HbC), and the thalassemia syndromes are representative hemoglobinopathies that can have severe clinical consequences. The first two conditions result from production of hemoglobin with an altered amino acid sequence, whereas the thalassemias are caused by decreased produc tion of normal hemoglobin. 

Ania BJ, Suman VJ, Fairbanks VF, Rademacher DM, Melton LJ 3rd. Incidence of anemia in older people An epidemiologic study in a well defined population. J Am Geriatr Soc 1997 45 825-31. 

Osgood demonstrated that pernicious anemia serum delays maturation of megaloblastic bone marrow (see LI). The work of Callender and Lajtha (see G20) points out that addition of normal gastric juice potentiates the effect of vitamin B12 in counteracting this maturation-delaying effect of pernicious anemia serum. A B12 binder separated from normal gastric juice by electrophoresis or ammonium sulfate precipitation was also shown to enhance the B12 effect on maturation of the erythro-blasts, when added to bone marrow (P2, P3). The relation of this maturation-promoting factor to Castle s intrinsic factor is not clearly defined (see G20). 

The combination of a-thalassemia with chain variants has frequently been observed w hen associated with Hb-E a well-defined clinical syndrome is present which is primarily found in Thailand (Til, T13, W5). The combination of two a-thalassemia genes (a-Thi and o-Thj) and a single Hb E gene results in a thalassemia intermedia with moderate anemia and hepatosplenomegaly. At time of birth these patients produce some 25% Hb-Bart s, Hb-A, Hb-F, and small amounts of Hb-E. At a later age the disease is characterized by the presence of an increased y chain production and a decreased chain production the hemoglobin phenotype shows some 15% Hb-E, 5-15% Hb-Bart s, and the remainder Hb-A. Hb-H i t) is hardly present as is the tetramer of the yS chain. 

Vitamin Bjj deficiency is a dearly defined condition that tends to be somewhat common in the older population, due to gastric atrophy and pernicious anemia. Moderate increases in plasma homocysteine can ciccur with B j deficiency, and these levels can be cut in half by supplements of this vitamin (Brattstrom el al, 1988 Sumner el ai., 1996). Researchers interested in the mechanisms by which plasma homocysteine can influence metabolism need to con.sider the possible effects of other sulfhydryl compounds (K—Sf f) that occur in plasma. These sulf-hydryl compounds include cysteine (10-100 pM) (Hiramatsu et ai, 1994 Fuka-gawa, 1996), glutathione (2 pAi in humans 20 pM in rats) (Halliwell and Gut-teridge, 1990), and the free sulfhydryl in albumin (640 pM) (E>eMaster et al., 1995). The micromolar levels of cysteine, glutathione, and the albumin in plasma are indicated. 

Anemia in infants is defined as an Hb level below 109 mg/ml of whole blood and a hematocrit less than Extensive surveys conducted in the United States have revealed that the incidence of anemia in lower-income families is about 6%. The lower-income family was defined as that participating in the WIC (Women, Infants, Children) program. The decline in infant anemia in the decade prior to 1985 is attributed to an increase in the use of iron-fortified formulas and cereals. 

PER see Prohdn efficiency ratio Perilipirv 383,401 Periportal hepatocytes, 253 Perivenous hepatocytes, 253 Permeability, defined, 119 Pernicious anemia as cancer risk factor. 519 folic acid and, 516 parietal cells and, 83 vitamin Biz deficieiKy and, 434,518-519, 523... 

In a double-blind, placebo-controlled study of the safety and efficacy of methotrexate therapy combined with glucocorticoids in patients with giant cell arteritis over 24 months, adverse events were defined as a new diagnosis of any condition during treatment (39). The combination of methotrexate plus prednisolone reduced the number of relapses and improved the course of the disease. Methotrexate was withdrawn in three patients who had adverse events that were clearly drug-related. One had leukopenia, anemia, and mucositis, one developed pancytopenia, and one oral ulcers. These patients were not taking folic acid or folinic acid supplements. 

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