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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence and type of nutritional anemia was investigated in 344 children aged 1 to 16 years of mixed race and living in a poor urban setting. Iron deficiency anemia was common in 1-year-old children (23%) as was biochemical evidence of iron deficiency (53%). Anemia rates were minimal in older children and the prevalence of iron deficiency decreased with age. Folate deficiency did not appear to contribute to the etiology of anemia, and nutritional vitamin B12 deficiency was not present. No-relationship could be found between a number of familial variables and hematological nutritional status. It is suggested that to identify families whose children are at risk for nutritional anemia new approaches will be needed to define their characteristics.
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PMID:Anemia in urban underprivileged children. Iron, folate, and vitamin B12 nutrition. 86 88

Tests to evaluate body iron stores were compared in patients with iron deficiency and the anemia of chronic disease. The serum ferritin assay separated these disorders in 20 of 22 patients. One discrepancy was explained by the concomitant association of both disorders. From this study and review of literature a low serum ferritin level is a good indication for iron therapy. The serum ferritin assay is a clinically useful test in lieu of bone marrow estimation of body iron stores to detect patients with iron deficiency. Total iron binding capacity levels when high-normal or elevated are sometimes helpful as a screening test in separating iron deficiency from the anemia of chronic disorders. Free erythrocyte protoporphyrin values were elevated in both conditions but were higher in iron deficiency than in the anemia of chronic disorders with considerable overlap of values. Urinary iron excretion with deferoxamine was not helpful in separating these disorders but is a useful test to establish iron overload. An elevated serum ferritin level is usually found with disease of iron overload but serum iron levels, deferoxamine iron excretion tests, and liver biopsy for estimation of iron stores are still beneficial diagnostic aids.
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PMID:Serum ferritin, free erythrocyte protoporphyrin, and urinary iron excretion in patients with iron disorders. 86 19

The kinetics of erythroblast proliferation were studied by means of quantitative 14C-autoradiography in 5 patients showing anemia due to infection or malignancy, in 7 patients suffering from iron deficiency anemia, and in two individuals with bleeding enemia. Compared with a group of 5 healthy persons a markedly reduced turnover of erythroblasts was found in the anemia due to infection, malignancy, and iron deficiency, whereas this turnover was normal or increased in the case of bleeding anemia. The reduction is caused by a progressively decreasing rate of erythroblast proliferation and maturation with advancing development into mature cells. No indications of a change in the number of cell divisions were found in the anemia of infection, malignancy, and of iron deficiency, nor was there evidence of an intramedullary death of nucleated red cell percursors. The imbalance between production and loss of red cells causing anemia shows a different pattern in the 3 groups of disease: In bleeding anemia the insufficiency of supply is not yet apparent from the rate of erythroblast turnover giving weight to the factor of blood loss. In anemia due to infection, malignancy, and iron deficiency the but moderately increased rate of red cell destruction cannot be compensated because of several impairments: The rate of erythroblast turnover is reduced, and, in addition, a moderate portion of maturing cells is destroyed, probably at the reticulocyte stage. As the most significant factor, the bone marrow is unable to compensate the anemia by an effective erythroblast hyperplasia. In iron deficiency this hyperplasia is inadequately low, in infection and malignancies, however, it is more or less missing.
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PMID:[Erythropoiesis in iron deficiency]. 88 Mar 76

The role of iron supply in the regulation of hepatic transferrin synthesis by the isolated perfused rat liver was studied using nutritional iron deficiency as the experimental model. The increased transferrin release encountered in iron deficiency could be equated with enhanced de novo synthesis as evidenced by the inhibitory effects of cycloheximide and measurements of intrahepatic protein pools before and after perfusion. Refeeding with iron, sufficient to restore plasma iron and hepatic ferritin iron but before correction of anaemia, promoted a reduction towards normal in the transferrin synthetic rate. This effect was not produced by transfusional correction of the anaemia, suggesting a specific response to iron supply. Phenobarbitone treatment, which produced a marked fall in hepatic ferritin iron concentration but no change in haemoglobin or plasma iron concentrations, promoted a specific enhancement of transferrin synthesis in both control and iron deficient livers. The concentration of liver iron stores appears to be a major regulatory factor in the control of hepatic transferrin synthesis.
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PMID:The role of iron in the regulation of hepatic transferrin synthesis. 88 9

In order to evaluate the effects of iron deficiency on the absorption of pollutant metals, an iron-deficient diet was fed to young rats until their tissue-iron stores were depleted. Prior to the development of anemia, the iron-deficient rats and littermate controls were administered an intragastric gavage of lead-210 or cadmium-109 and were killed 48 hr later. The body burden of lead was approximately 6 times greater, and that of cadmium approximately 7 times greater, in iron-deficient rats than in the controls. No consistent effects were observed on concentrations of serum total lipids or serum proteins nor on protein electrophoretic patterns in rats with a deficit in iron stores.
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PMID:Effects of iron deficiency on the absorption and distribution of lead and cadmium in rats. 90 99

A group of 359 healthy children and 49 adults were studied for the purpose of estimating the normal limits for serum iron concentration and transferrin saturation. The 144 children and seven adults who has any other laboratory evidence of iron deficiency (abnormal values of serum ferritin, free erythrocyte protoporphyrin, hemoglobin concentration, or mean corpuscular volume) were excluded. In evaluating the 215 children and 42 adults who met the criteria to be considered normal we found that serum iron concentration and transferrin saturation were significantly lower in children between the ages of 0.5 and 12 years than in adults. We conclude that in children between the ages of 0.5 and 12 years, a transferrin saturation of less than 16% constitutes good evidence of iron deficiency only in conjuction with anemia and low mean corpuscular volume.
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PMID:Serum iron concentration and transferrin saturation in the diagnosis of iron deficiency in children: normal developmental changes. 92 12

Prevention of iron deficiency in low-birth-weight infants requires iron supplementation before neonatal iron stores are exhausted. In order to accurately determine when this depletion occurs, we measured the hemoglobin, mean corpuscular volume, serum iron/iron-binding capacity, and serum ferritin in 117 low-birth-weight infants (1,000 to 2,000 gm) from 0.5 until 6 months of age. All infants received banked breast milk in the hospital and breast milk or cow milk formula later; those with odd birth dates received 2 mg iron as ferrous sulfate/kg/day starting at 0.5 months; those with even birth dates received no additional iron unless they developed anemia. The results indicate that low-birth-weight infants who receive no supplemental iron may develop iron deficiency by three months of age and that a dose of iron of 2 mg/kg/day started at two weeks of age prevents iron deficiency without providing excess.
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PMID:At what age does iron supplementation become necessary in low-birth-weight infants? 92 14

Iron deficiency is a frequent complication in chronically hemodialyzed patients because of the significant blood losses associated with this technique. Quantitating iron stores (by marrow examination or serum iron and total iron-binding capacity) on a repetitive basis had been difficult or unreliable, often resulting in failure to recognize iron deficiency superimposed on the existing anemia of chronic renal failure, or overtreating, which can lead to iron excess. Use of the serum ferritin allows easier quantitation of iron stores and, when measured serially in dialysis patients, can predict the emergence of iron deficiency. There was no correlation between serum ferritin levels and serum iron, total iron-binding capacity, or percent transferrin saturation. Iron absorption studies show that food iron absorption is physiologic, increasing when the serum ferritin is below 30 ng/ml, decreasing when more than 300 ng/ml. Treatment of iron deficiency with oral iron compounds increases serum ferritin levels and usually can maintain iron balance.
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PMID:Iron balance in hemodialysis patients. 93 Dec 7

The case of a six year and ten months old girl with an iron deficiency anemia of long duration is reported. The lack of iron was associated with folic acid deficiency, which disguished the hematologic pattern, presenting a normocromic and aniso-poiquilocytic anemia. Long duration of iron deficiency allowed for evaluation of the iron deficiency effects on weight and height growth which were diminished as well as on the functioning and morphology of the gastrointestinal system, showing malabsorption syndrome which improve with iron supply.
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PMID:[Iron deficiency anemia in childhood. A case with associated deficiency of folic acid (author's transl)]. 93 74

A chronic ileo-colic intussusception of an 8 1/2 year old boy did not cause any abdominal complaints. There was a hypochromic anaemia with iron deficiency; occult blood was found in the stoll. Radiographically the lumen within the intussusceptum was extremely narrowed. Following surgery the anaemia disappeared.
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PMID:["Chronic ileo-colic intussusception without abdominal symptoms" (authors transl)]. 94 72


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