Anemia infants

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. 

More copper is found in the brain and heart than in any other tissue except for liver, where it is stored as copper thionein and released as ceruloplasmin or in the form of a complex with serum albumin. The high metabolic rate of the heart and brain requires relatively large amounts of copper metalloenzymes including tyrosinase, cytochrome c oxidase, dopamine-/3-hydroxylase, pyridoxal-requiring monamine oxidases, and Cu-Zn superoxide dismutase. Copper deficiency, which can occur for reasons analogous to those discussed above for Fe and Zn, leads to brain disease in infants, anemia (since cytochrome oxidase is required for blood formation), and heart disease. Few details are known about the molecular basis for copper uptake from foods. 

Anemia during infancy, a frequent occurrence, is closely related to the body iron stores at birth. Pregnant women may have an insufficient intake of iron thus, the newborn infant may develop anemia early in the first year of life. Also, infants (1) born prematurely, (2) of low birth weight, (3) of multiple births, or (4) whose mothers have had several pregnancies are most likely to have inadequate iron reserves at birth. Furthermore, infants are apt to develop iron deficiency anemia because milk has a low iron content and babies are just not born with sufficient iron to meet their needs beyond 6 months. Infant anemia may also be caused... 

Also see ANEMIA, section headed "Groups of Persons Susceptible to Nutritional Anemias" ANEMIA, MEGALOBLASTIC FOLIC ACID INFANT ANEMIA IRON and PREGNANCY AND LACTATION NUTRITION.)... 

The symptoms of vitamin E deficiency in animals are numerous and vary from species to species (13). Although the deficiency of the vitamin can affect different tissue types such as reproductive, gastrointestinal, vascular, neural, hepatic, and optic in a variety of species such as pigs, rats, mice, dogs, cats, chickens, turkeys, monkeys, and sheep, it is generally found that necrotizing myopathy is relatively common to most species. In humans, vitamin E deficiency can result from poor fat absorption in adults and children. Infants, especially those with low birth weights, typically have a vitamin E deficiency which can easily be corrected by supplements. This deficiency can lead to symptoms such as hemolytic anemia, reduction in red blood cell lifetimes, retinopathy, and neuromuscular disorders. 

As the above mentioned studies with high supplementation dosages exemplarily show, there is no known toxicity for phylloquinone (vitamin Kl), although allergic reactions are possible. This is NOT true for menadione (vitamin K3) that can interfere with glutathione, a natural antioxidant, resulting in oxidative stress and cell membrane damage. Injections of menadione in infants led to jaundice and hemolytic anemia and therefore should not be used for the treatment of vitamin K deficiency. 

In experimental animals, vitamin E deficiency results in resorption of femses and testicular atrophy. Dietary deficiency of vitamin E in humans is unknown, though patients with severe fat malabsorption, cystic fibrosis, and some forms of chronic fiver disease suffer deficiency because they are unable to absorb the vitamin or transport it, exhibiting nerve and muscle membrane damage. Premamre infants are born with inadequate reserves of the vitamin. Their erythrocyte membranes are abnormally fragile as a result of peroxidation, which leads to hemolytic anemia. 

However, the pregnancies of 67 percent of all mothers were complicated by a variety of medical problems including anemia, hepatitis B, syphilis, and psychiatric emergencies. At the time of delivery, 57 percent of mothers of full-term infants and 80 percent of mothers of preterm infants were noted to have had one or more medical problems during the pregnancy. Seventy-five percent of... 

Clinical features Acute exacerbation of anemia due to sequestration of large blood volume by the spleen. More commonly seen in patients with functioning spleens (e.g., infants and adults with HbSC disease) onset often is associated with viral or bacterial infections recurrences are common and can be fatal. 

Feature presentations of SCD are hemolytic anemia and vasoocclusion. Symptoms are delayed until 4 to 6 months of age when HbS replaces fetal hemoglobin (HbF). Common findings include pain with fever, pneumonia, splenomegaly and, in infants, pain and swelling of the hands and feet (e.g., hand-and-foot syndrome or dactylitis). 

Epileptiform fits associated with degenerative changes in the myelin sheath of peripheral nerves and spinal cord occur in B6-deficient animals. Lesions in the arteries, resembling those of human atherosclerosis, have been observed in Be-deficient monkeys. Recently, a state of Be deficiency in human infants, characterized by loss of ability to convert tryptophan to nicotinic acid, by impaired growth, convulsions, and hypochromic anemia, has been described, following omission of vitamin B6 from the diet. 

Dl. Dawson, J. P., Thayer, W. W., and Desforges, J. F., Acute hemolytic anemia in the newborn infant due to naphthalene poisoning Report of two cases with investigations into the mechanism of the disease. Blood 13, 1113-1125 (1958). 

The fact that certain human adults or infants develop types of anemia which respond to small doses of folic acid can be interpreted to mean that, for reasons which doubtless have some genetic basis, these individuals have unusually high demands for this vitamin. Presumably they develop the disease when consuming diets that do not induce the disease in others. Folic acid needs are (for one reason or another) highly variable from individual to individual among patients as is shown by the fact that many patients will respond to as little as 0.5 mg. folic acid per day, whereas others will not respond at all... 

Vitamin E may be indicated in some rare forms of anemia such as macrocytic, megaloblastic anemia observed in children with severe malnutrition and the hemolytic anemia seen in premature infants on a diet rich in polyunsaturated fatty acids. Also anemia s in malabsorption syndromes have shown to be responsive to vitamin E treatment. Finally, hemolysis in patients with the acanthocytosis syndrome, a rare genetic disorder where there is a lack of plasma jS-lipoprotein and consequently no circulating alpha tocopherol, responds to vitamin E treatment. In neonates requiring oxygen therapy vitamin E has been used for its antioxidant properties to prevent the development retrolental fibroplasia. It should be noted that high dose vitamin E supplements are associated with an increased risk in allcause mortality. 

Intrahepatic cholestasis and hepatitis similar to that seen in chronic active hepatitis can rarely occur fatalities have been reported. Nitrofurantoin can interfere with immature red blood cell enzyme systems found in babies less than 1 month of age and in nursing infants. This leads to cellular damage and anemia. Nitro-... 

Most adverse effects associated with aerosol ribavirin are local. Pulmonary function may decline if aerosol ribavirin is used in adults with chronic obstructive lung disease or asthma. Deterioration of pulmonary and cardiovascular function has also been seen in severely ill infants given this preparation. Rash, conjunctivitis, and rare cases of anemia have been reported. Health care workers exposed to aerosol ribavirin during its adminis-... 

Deficiency of vitamin E is characterized by low serum tocopherol levels and a positive hydrogen peroxide hemolysis test. This deficiency is believed to occur in patients with biliary, pancreatic, or intestinal disease that is characterized by excessive steatorrhea. Premature infants with a high intake of fatty acids exhibit a deficiency syndrome characterized by edema, anemia, and low tocopherol levels. This condition is reversed by giving vitamin E. 

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. 

H. Other considerations Epoetin alfa has been designated an orphan product for use in the treatment of anemia of end-stage renal disease, HIV infection, or prematurity in preterm infants, or treatment of myelodysplastic syndrome. 

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