Anemias deficiency causing

Deficiency conditions Pernicious anemia, deficiency caused by inadequate diet or intestinal malabsorption, hemolytic anemia, hyperthyroidism, bowel and pancreatic malignancies, gastrectomy, GI lesions, neurologic damage, malabsorption syndrome, metabolic disorders, renal disease... 

Fohc acid is a precursor of several important enzyme cofactors required for the synthesis of nucleic acids (qv) and the metaboHsm of certain amino acids. Fohc acid deficiency results in an inabiUty to produce deoxyribonucleic acid (DNA), ribonucleic acid (RNA), and certain proteins (qv). Megaloblastic anemia is a common symptom of folate deficiency owing to rapid red blood cell turnover and the high metaboHc requirement of hematopoietic tissue. One of the clinical signs of acute folate deficiency includes a red and painhil tongue. Vitamin B 2 folate share a common metaboHc pathway, the methionine synthase reaction. Therefore a differential diagnosis is required to measure foHc acid deficiency because both foHc acid and vitamin B 2 deficiency cause... 

Macrocytic or magaloblastic anemia is caused by disturbances of DNA synthesis. It occurs, for example, in both folic acid and vitamin B12 deficiencies. Hematopoesis is slowed down due to reduced DNA synthesis and a reduced number of abnormally large (macrocytic) and hemaglobin-rich (hyperchromic) erythrocytes is released. 

Evidence of iron overload known hypersensitivity to iron sucrose or any of its inactive components anemia not caused by iron deficiency. 

T8. Relationship between Folic Acid Deficiency and Anemia Folic acid deficiency, believed to be the most common vitamin deficiency, causes a type of anemia in which hemoglobin synthesis is impaired and erythrocytes do not mature properly. What is the metabolic relationship between hemoglobin synthesis and folic acid deficiency ... 

Folic acid Precursor of the coenzyme tetrahydrofolic acid. Deficiency causes anemias. 

The richest sources of vitamin C are citrus fruits (e.g., lemon, oranges), tomatoes, potatoes, green chilies, and human milk. Severe deficiency causes scurvy and is prevalent in malnourished infants, children, adults, alcoholics, and drug addicts. Symptoms such as bleeding gums, deformed teeth, brittle bones, impaired wound healing, anemia, and growth retardation are observed. 

Regulation of homocysteine metabolism appears to be especially important in the central nervous system, presumably because of the critical role of methyl transfer reactions in the production of neurotransmitters and other methylated products. It has been known for decades that mental retardation is a feature of the genetic diseases, such as CBS deficiency, that cause severe hyperhomocysteinemia and ho-mocystinuria. Impaired cognitive function is also seen in pernicious anemia, which causes hyperhomocysteinemia due to deficiency of cobalamin (see Chapter 28). Hyperhomocysteinemia also may be linked to depression, schizophrenia, multiple sclerosis, and Alzheimer s disease. The molecular mechanisms underlying these clinical associations have not yet been delineated. 

Cardiovascular Disorders and Copper. Sudden cardiac failure has been associated with copper deficiency (91J. There are two attractive mechanisms. First, the coronary arteries and aorta may become weakened from an inability to synthesize elastin due to a decrease in lysyl oxidase activity. Rupture of these major blood vessels has been shown to cause sudden death in animals suffering from copper deficiency. Second, a decrease in cytochrome oxidase activity during copper deficiency Impairs aerobic metabolism of the heart and increases the risk of hypertrophy. Hypertrophy, which may lead to high output congestive heart failure, is exacerbated by hypochromic anemia also caused by copper deficiency. 

In premature infants, whose reserves of the vitamin are inadequate, vitamin E deficiency causes a shortened half-life of erythrocytes, which can progress to increased intravascular hemolysis, and hence hemolytic anemia. In infants treated with hyperbaric oxygen, there is a risk of damage to the retina (retro-lental fibroplasia), and vitamin E supplements may be protective, although this is not firmly established (Phelps, 1987). 

In other reports from Canada and the UK, patients typically developed sudden worsening of anemia unresponsive to increasing doses of epoetin alfa or any other form of erythropoietin and became transfusion dependent (85). In patients who develop sudden lack of efficacy or worsening of anemia, typical causes of non-response (for example deficiencies of iron, folate, and vitamin B12, infection or inflammation, blood loss, hemolysis, and aluminium intoxication) should be investigated. If pure red cell aplasia is suspected and no cause can be identified, erythropoietin antibodies should be sought. 

Although there was no evidence for blood loss, the anemia was caused by iron deficiency. We concluded that this may have been attributable to a lack of availability of iron from the bread, greater iron loss attributable to excessive sweating in hot climate, and adverse effect of geophagia on iron absorption. In every case, the anemia completely corrected by administration of oral iron. 

A. Pernicious anemia occurs when the stomach does not produce adequate intrinsic factor for absorption of vitamin B12, which is required for the conversion of methylmalonyl CoA to succinyl CoA and homocysteine to methionine. A vitamin B12 deficiency results in the excretion of methylmalonic acid and an increased dietary requirement for methionine. The methyl group transferred from vitamin B12 to homocysteine to form methionine comes from 5 -methyl tetrahydrofolate, which accumulates in a vitamin B12 deficiency, causing a decrease in folate levels and symptoms of folate deficiency, including increased levels of FIGLU and decreased purine biosynthesis. 

Iron is used to regenerate hemoglobin. Iron is absorbed in the intestine and enters plasma as heme. Iron is stored as ferritin in the liver, spleen, and bone marrow. Five to twenty milligrams of iron are required daily. Iron deficiency causes anemia. Iron is found in liver, lean meats, egg yolks, dried beans, green vegetables (i.e., spinach), and fruit. Women who are pregnant should increase their iron intake as specified by the healthcare provider. Large doses of iron are prescribed in the second and third trimesters. The patient must adhere to the... 

A number of other enzymopathic substances (e.g., pyruvate kinase. Chapter 13 and pyrimidine-5 -nucleotidase. Chapter 27), abnormal hemoglobins (Chapter 28), and abnormalities of the erythrocyte cytoskeleton (Chapter 10) may cause hemolytic anemia. Because many enzymes in the red cell are identical to those in other tissues, defects in these enzymes may have pleiotropic effects. Thus, in addition to hemolytic anemia, triose phosphate isomerase deficiency causes severe neuromuscular disease, and phospho-fructokinase deficiency causes a muscle glycogen storage disease (Chapter 13). Mutations that result in decreased enzyme stability are usually most strongly expressed in erythrocytes because of their inability to synthesize proteins. 

Vitamin B12 is stable to temperatures up to 250°C (482°F) in acidic or neutral solutions. Dietary B12 deficiency is rare among meat eaters but not in strict vegetarians. The average total body content of vitamin B12 is about 2.5 mg, most of which is in the liver (1 /u,g of Bi2 per gram of hepatic tissue). There is extensive reutilization of cobalamin and an active enterohepatic circulation. The principal disease caused by vitamin B12 deficiency is megaloblastic anemia. Deficiency also causes neurological abnormalities that become irreversible if allowed to persist. 

B. Megaloblastic anemia is caused by a decrease in the synthesis of deoxythymidylate and the purine bases usually caused by a deficiency in either THF or cobalamin or both. This results in decreased DNA synthesis, which results in abnormally large hematopoietic cells created by perturbed cell division and DNA replication and repair. This patient exhibits signs of chronic alcoholism, which often leads to a folate deficiency. This can occur due to poor dietary intake, decreased absorption of folate due to damage of the intestinal brush border cells and resulting conjugase deficiency, and poor renal resorption of folate. 

Be aware of how folate deficiency causes megaloblastic anemia. 

The occurrence of anemia in clinical scorbutics does not necessarily suggest that ascorbic acid deficiency causes anemia. This possibility... 

Cobalt is found in vitamin Bn, its only apparent biological site. The vitamin is a cyano complex, but a methyl or methylene group replaces CN in native enzymes. Vitamin-Bi2 deficiency causes the severe disease of pernicious anemia in humans, which indicates the critical role of cobalt. The most common type of reaction in which cobalamin enzymes participate results in the reciprocal exchange of hydrogen atoms if they are on adjacent carbon atoms, yet not with hydrogen in solvent water ... 

Animals and plants cannot synthesize vitamin B12. In fact, only a few microorganisms can synthesize it. Humans must obtain all their vitamin B12 from their diet, particularly from meat. Because vitamin B12 is needed in only very small amounts, deficiencies caused by consumption of insufficient amounts of the vitamin are rare, but have been found in vegetarians who eat no animal products. Deficiencies are most commonly caused by an inability to absorb the vitamin in the intestine. The deficiency causes pernicious anemia. The following are examples of enzyme-catalyzed reactions that require coenzyme B12 ... 

Glucose 6-phosphate Dehydrogenase Deficiency Causes a Drug-Induced Hemolytic Anemia... 

Jean Ann s serum folic acid level was 3.1 ng/mL (reference range =6-15), and her serum B12 level was 154 pg/mL (reference range = 150-750). Her serum iron level was normal. It was clear, therefore, that Jean Ann s megaloblastic anemia was caused by a folate deficiency (although her B12 levels were in the low range of normal). The management of a pure folate deficiency in an alcoholic patient includes cessation of alcohol intake and a diet rich in folate. 

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