Infants iron deficiency

The answer is d. (Hardman, pp 1331-1333.) Iron-deficiency anemia usually occurs in infants undergoing rapid growth. In adults in a late stage, it may result in a bowel syndrome associated with gastritis and hypochlo-rhydria (Plummer-Vinson syndrome). Characteristically, all iron-deficiency anemias are associated with a hypochromic microcytic blood profile. Infestation with the tapeworm D. latum is accompanied by a hyperchromic macrocytic anemia, which is treatable with vitamin B12. Bleeding syndromes are treated with iron. 

Nutritional iron deficiency anaemia other causes in which iron deficiency can occur are pregnancy, lactation, infants, children. In patients with malabsorption syndrome, patients who are taking NSAIDs for long period, patients with chronic inflammatory disease and in patients of gastrectomy. 

Anon. 1974, Fresh cows milk and iron deficiency in infants. Nutr. Rev. 31, 318-320. 

Wilson, J. F., Lahey, M. E. and Heiner, D. C. 1974. Studies on iron metabolism. V. Further observations on cow s milk-induced gastrointestinal bleeding in infants with iron-deficiency anemia. J. Pediatr. 84, 335-344. 

Infants with Iron Deficiency. B. l.o/off (Case Western Reserve University) and associates repotted that "Several consistent results have emerged from five studies of the behavior and development of infant with iron-deliciency anemia, a condition that affects at least 21) to 25 percent of the world s babies." All live studies used careful de lin it ions of iron status and included comparison groups without anemia All showed that infants with anemia scored lower on tests of mental development administered before treatment than infants without anemia did. 

Iron is normally absorbed in the duodenum and proximal jejunum, though the more distal small intestine can absorb iron if necessary. The average diet in the USA contains 10-15 mg of elemental iron daily. A normal individual without iron deficiency absorbs 5-10% of this iron, or about 0.5-1 mg daily. Iron absorption increases in response to low iron stores or increased iron requirements. Total iron absorption increases to 1-2 mg/d in normal menstruating women and may be as high as 3-4 mg/d in pregnant women. Infants and adolescents also have increased iron requirements during rapid growth periods. 

There is a possibility that some milk constituents regulate the absorption of ions in the intestine. In studying manganese metabolism we turned to the low iron content in milk. Iron has received great attention in pediatric nutrition. The concern has been to prevent the anemia caused by iron deficiency earlier often found in childhood. Wide milk consumption by infants and young children makes this food an attractive vehicle for iron fortification. Iron-enriched proprietary milk substitutes can adequately prevent the anemia common to infants who subsist largely on low-iron mother s or cow s milk (53). 

Those at risk for iron deficiency Include infants and children bctw cen the ages of 0.5 and 4.0 years, because of the rapid rate of growth at this time and because the... 

In one other instance, plasma ferritin levels may be elevated even when the body s iron stores are low. Plasma ferritin may be elevated in the first few days of iron therapy in anemia, particularly where the doses of iron are high. Anemia in infants, for example, can be treated with 6 mg of iron/kg body weight per day. The iron can be supplied as oral ferrous sulfate. Iron deficiency anernia in adults can be treated with 50 mg of iron three times a day. The iron can be supplied as ferrous sulfate. Early rises in serum ferritin may not occur at these doses, but can occur at higher doses. With the use of standard doses, scrum ferritin may rise into the ronraJ range only after the anemia has been corrected. 

Ercterm infants may be at a risk for iron deficiency because of their relatively rapid rate of growth and low iron stores. The marginal supply of breast milk iron dictates that preterm infants be supplemented with iron at an early age. Dallman el ai (1980) recommend that preterm infants receive supplements beginning at 2 months. 

Iron deficiency is a common adverse effect (30%) in children with chronic renal insufficiency treated with epoetin, even with iron supplementation (62). In premature infants given enteral epoetin, there was a significant fall in ferritin concentrations despite iron supplementation (81), and there were increased numbers of hjrpochro-mic erythrocytes and soluble transferrin receptors (14). This implies that active erjdhropoiesis in premature infants causes increased iron requirements. 

Iron deficiency anemia occurs mainly in infants, children, and fertile women. For this reason, a variety of foods, including infant formula and infant cereals, is fortified with iron. Ferrous sulfate is a form of iron that is most readily absorbed by the gut, but when added to dry cereals it can promote their spoilage and rancidity. For this reason, dry cereals are fortified with elemental iron particles, ferric pyrophosphate, or ferrous fumarate (Davidsson et ah, 1997). Ascorbic add may also be added to the cereal to enhance iron absorption. To view some of the numbers, infant cereals may contain 75 mg iron/kg cereal (1.3 mmol iron/kg), 1 mmol phytic acid/kg, and 2.6 mmol ascorbic acid/kg (Davidsson et cd., 1997). Although phytic acid impairs iron absorption, the added ascorbate serves to prevent this effect. An alternate method for preventing phytate from impairing iron absorption is to treat the food with the enzyme phytase. A parent interested in enhancing a child s iron absorption can easily feed a child some orange juice, but it would not be practical to pretreat the child s cereal with phytase. A typical availability of ferrous sulfate in infants is about 3-5% (with no ascorbate), and 6-10% (with ascorbate). Ascorbate is effective when present in a twofold molar excess over the iron. 

Iron deficiency in infancy remains a common nutritional problem. In infants, milk feeding represents the basis of nutrition and an essential source of iron during infancy. It is felt that iron deficiency becomes a problem after the first four mounths of life. 

Copper was also shown to be essential in the early 1900s. Copper is needed for the absorption and mobilization of iron, so a deficiency of copper causes a type of anemia that is difficult to distinguish from iron deficiency anemia. Copper is also needed for the cardiovascular system, bone, brain, and nervous system. Premature and malnourished infants are particularly susceptible to developing copper deficiency, in part because milk is a poor source of copper. Whole grains, legumes, and nuts are the major dietary sources of copper. 

Since iron is involved in many central nervous system processes that could affect infant behaviour and development, iron deficiency has adverse effects on brain development, both pre- and post-natal. In various epidemiological studies, it is reported that children with iron-deficiency anaemia have poorer performances on tests of some specific cognitive function. Animal experiments have identified some of the defects of reduced iron availability on brain function, which include post-translational changes (which result in a failure of iron incorporation into protein structures which are subsequently degraded), vulnerability of the developing hippocampus (with loss of the neuronal metabolic marker cytochrome c oxidase), and altered dendritic stmcture. Iron deficiency will also have a direct effect on myelin, including a decrease in myelin lipids and proteins, as well as neurotransmitter systems, since iron... 

Sturgeon, P., and Brubacker, C., Copper deficiency in infants. A syndrome characterized by hypocupremia, iron deficiency anaemia and hypoproteinaemia.A.Af.A. J. Diseases Children 92, 254-265 (1956). 

IDA is a leading cause of infant morbidity and mortality in the world. In the United States, the prevalence of IDA among children is declining due to improved iron supplementation. Data from the third NHANES indicated that 9% of children ages 12 to 36 months in the United States had iron deficiency and 3% had IDA. Another... 

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