Iron deficiency anemia consequences

Pollitt E (2001) The developmental and probabilistic nature of the functional consequences of iron-deficiency anemia in childhood. J Nutr 131 669S-675S. 

In hypogonadal dwarfism, reported by Prasad et al. [47], adolescents in Iran and Egypt became zinc-deficient in consequence of high phytate content in the diet making zinc unavailable for absorption. This disease results in dwarfism, retarded sexual maturation, iron deficiency anemia, and hepatosplenomegaly. 

One of the main consequences of iron deficiency is the reduced synthesis of hemoglobin, leading to the appearance of small (microcytic) erythrocytes poor in hemoglobin (hypochromic) in the blood. Since there is no interference with division and maturation of the mother cell of the erythrocyte, it is not surprising that the bone marrow cells attempt to compensate for the reduced concentration of hemoglobin per cell by increasing the number of cells. Thus, the bone marrow becomes hyperplastic. In fact, vicarious hematopoiesis often appears in spleen and liver of patients with iron deficiency anemia. 

Anemia is defined by abnormally low circulating hemoglobin concentrations. A variety of etiologies exist for anemia, including dietary deficiencies of folate or vitamin B12 (pernicious or macrocytic anemia), infections and inflammatory states (anemia of chronic disease), and conditions that result in insufficient production of red blood cells (aplastic anemia) or excessive destruction of red blood cells (hemolytic anemia). However, worldwide, the most prevalent form of anemia is that of iron deficiency, which causes anemia characterized by hypochromic and normo- or microcytic red blood cells. Iron deficiency anemia remains a health problem in both the developed and the developing world. This article discusses the metabolism of iron the assessment of iron deficiency iron requirements across the life span and the consequences, prevention, and treatment of iron deficiency and iron deficiency anemia. 

Consequences of Iron Deficiency and Iron Deficiency Anemia... 

Secondary hemochromatosis is the consequence of the uicreased administration and absorption of iron. The administration of iron includes that given with the transfusions that are required in certain anemic patients and the ill-advised and unfortunate administration of iron to anemic patients who are not actually iron deficient. The most common causes of secondary hemochromatosis are thalassemia major and acquired myelodysplastic states, but there are many other circumstances in which secondary iron overload occurs, including pyruvate kinase deficiency and congenital dyserythropoietic anemias. 

In the later stages of IDA, the Hgb and Hct fall below normal values, and a microcytic, hypochromic anemia develops. Microcytosis may precede hypochromia, as erythropoiesis is programmed to maintain normal Hgb concentration in deference to ceU size. As a consequence, even slightly abnormal Hgb and Hct levels may indicate significant depletion of iron stores and should not be ignored. In terms of RBC indices, MCV reduction occurs earlier in iron-deficient hematopoiesis than reduction in Hgb concentration. 

A dietary deficiency of calcium can lead to osteoporosis, a disease in which bones are insufficiently mineralized and consequently are fragile and easily fractured. Osteoporosis is a particularly common problem among elderly women. Deficiency of phosphorus results in bone loss along with weakness, anorexia, malaise, and pain. Iron deficiencies lead to anemia, a decrease in the concentration of hemoglobin in the blood. 

Ann O Rexia has a hypochromic anemia, which means that her red blood cells are pale because they contain low levels of hemoglobin. Because of her iron deficiency, she is not producing adequate amounts of heme. Consequently, elF2 is phosphorylated in her reticulocytes and cannot activate initiation of globin translation. 

Deficiencies of electron transport In cells, complete transfer of electrons from NADH and FAD(2H) through the chain to O2 is necessary for ATP generation. Impaired transfer through any complex can have pathologic consequences. Fatigue can result from iron-defeciency anemia, which decreases Fe for Fe-S centers and cytochromes Cytochrome Cj oxidase, which contains the O2 binding site, is inhibited by cyanide Mitochondrial DNA (mtDNA), which is maternally inherited, encodes some of the subunits of the electron transport chain complexes and ATP synthase. Oxphos diseases are caused by mutations in nuclear DNA or mtDNA that decrease mitochondrial capacity for oxidative phosphorylation. 

Consequently, the body hoards iron and uses it efficiently. Its only significant loss is through bleeding. Nonetheless, iron deficiency can occur and results in the body s inability to make enough Hb, which in turn causes anemia-a condition in which the patient feels tired, apathetic, and susceptible to cold temperatures. 

Iron Iron is a component of a number of proteins including hemoglobin, which is essential for transporting oxygen to tissues throughout the body for use in metabolic processes. The most well-known consequence of iron deficiency is anemia. A full-term infant normally has a high hemoglobin... 

In addition to the role of flavoproteins in iron metabolism, it is possible that the anemia associated with riboflavin deficiency is a consequence of the impairment of vitamin Be metabolism in riboflavin deficiency. Pyridoxine oxidase is a flavoprotein and, like glutathione reductase, is very sensitive to riboflavin depletion (McCormick, 1989). Vitamin Be deficiency can result in hypochromic anemia as a result of impaired porphyrin synthesis. Although riboflavin depletion decreases the oxidation of dietary vitamin Be to pyridoxal (Section 9.2), it is not clear to what extent there is secondary vitamin Be deficiency in riboflavin deficiency This is partly because vitamin Be nutritional status is commonly... 

Defective erythropoiesis (dyserythropoiesis) impaired hemoglobin synthesis leading to lack of utilization and consequent accumulation of iron in mitochondria, e.g., from inhibition of ALA synthase activity by dietary vitamin 85 deficiency inhibition of heme synthesis by lead impairment of pyridoxine metabolism in alcoholic patients familial sideroblastic anemias and Cooley s anemia. 

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