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

Of 125 pregnant women, of whom 81 were treated and 44 not treated, 14 (12,5%) were found to be suffering from anemia, with a hemoglobin count to be diminished. In 31 cases iron deficiency was established and in 8 women vitamin B12 in serum was reduced. Iron and vitamin deficiencies were found more frequently in the non-treated group than in the treated group.
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PMID:[Serum folic acid, vitamin b12 and iron values during pregnancy (author's transl)]. 60 35

The influence of oral doses of iron on the hemoglobin regeneration of pregnancy anemias and postpartum anemias was examined. The examinations were carried out in 45 pregnant women and in 70 puerperae. Other hematologic parameters besides hemoglobin were determined before, and 4 and 6 weeks during treatment with 110 mg iron sulfate daily. In pregnancy anemias, hemoglobin regeneration took place at a much slower rate under the iron therapy than was the case in postpartum anemias. Postpartum anemias of medium severity require for elevating the hemoglobin values to 12.0 g% at iron absorption rate of 22%, a treatment period of 35 days with a total amount of 3.8 g ferrous sulfate. In milder forms of anemia iron absorption diminished to 15% as hemoglobin conditions improved. An iron treatment course of 6 weeks will not be sufficient to cover the maternal iron deficiency during pregnancy and lyingin. To achieve optimum iron compensation, the daily supply of 100 mg iron will be necessary during pregnancy from the 16th week until delivery. In mild to medium anemias, postpartum iron treatment of 10 to 18 weeks' duration will be necessary until the exhausted iron deposits have been replenished.
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PMID:[Iron therapy and hemoglobin regeneration in pregnancy anemias and postpartum anemias (author's transl)]. 60 46

Two experiments are reported which show that rats are capable of forming an association between the presence of iron in a solution when it is not specifically needed and a subsequent state of iron deficiency. Specifically, rats were trained to lever press for water while thirsty. One group received ferrous ions in addition to the water. When these rats were subsequently rendered iron deficient, they lever pressed more under extinction conditions as a graded function of lower hemoglobin levels. Controls that either did not receive ferrous ions during training or received solutions other than ferrous solutions during training did not respond this way under extinction conditions. This is therefore a type of latent learning previously demonstrated only for sodium appetite.
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PMID:Iron appetite and latent learning in rats. 61 94

The present studies were conducted to determine the relationships between iron status and ferritin levels in plasma, liver, and spleen of rats. Rats were fed either iron-adequate or iron-deficient purified diets, and measurements of hemoglobin and plasma and tissue ferritin levels were made at various times during iron depletion and iron repletion. Although mean plasma ferritin concentrations of iron-deficient rats were directionally less than those of iron-adequate rats, these differences were not statistically significant due to high variability among similarly treated animals. During iron repletion plasma ferritin concentrations again were so variable that no significant effect of iron repletion on plasma ferritin concentrations was observed. On the other hand, liver and spleen ferritin concentrations of similarly treated rats were much less variable. Ferritin liver and spleen stores decreased more rapidly than hemoglobin during iron deficiency and were restored more slowly than hemoglobin during iron repletion. There was no evidence of correlation between liver and plasma ferritin concentration. Because of the variable responses of plasma ferritin concentration to iron depletion and repletion and the lack of relationship between plasma and liver ferritin concentrations, it is concluded that plasma ferritin concentration is not a good indicator of iron status in rats.
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PMID:Variable effects of iron status on the concentration of ferritin in rat plasma, liver, and spleen. 62 22

The concentration of hemoglobin in blacks was found to be 0.5 to 1.0 g/dl lower than that of income-matched whites in several large surveys. This difference could be a racial characteristic of blacks, or it might be due to a higher frequency of genetic traits such as thalassemia minor and hemoglobinopathies, or to environmental factors such as iron deficiency. To help in making this distinction, we analyzed the data from multiphasic examinations (1973 to 1975) on 1718 white, 741 black, and 315 Oriental healthy, nonindigent children between 5 and 14 years of age. In the entire population, the median hemoglobin concentration averaged 0.5 g/dl lower in blacks than in whites of both sexes (t test, P less than 0.001). The differences still averaged 0.5 g/dl (P less than 0.001) after exclusion of all those with abnormal hemoglobin by electrophoresis (Hgb S and C) and those whose mean corpuscular volume was more than 5% below the normal mean for age (to exclude iron deficiency or thalassemia minor). The data strengthen the impression that blacks normally have a concentration of hemoglobin averaging about 0.5 g/dl less than in whites. If this is the case, about 10% of normal blacks will be mistakenly designated anemic, if the same norms are applied.
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PMID:Hemoglobin concentration in white, black, and Oriental children: is there a need for separate criteria in screening for anemia? 62 13

Five American black patients, ages 1 to 16 years, with the sickle cell anemia-alpha-thalassemia syndrome are described. Each patient had persistent microcytosis not explained by iron deficiency, and in each family the presence of alpha-thalassemia in combination with sickle cell trait was demonstrated in one of the parents. In one patient, in whom the diagnosis of sickle cell anemia was established at birth, an elevated level of Barts (gamma4) hemoglobin was also found. In these patients levels of alkali-resistant hemoglobin and reticulocyte counts were similar to those of sickle cell anemia patients of comparable age; however, stained smears of their peripheral blood rarely showed the presence of irreversibly sickled cells. No major ameliorative effect of the alpha-thalassemia on the clinical expression of the sickle cell disease of these patients was evident.
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PMID:Sickle cell syndromes. II. The sickle cell anemia-alpha-thalassemia syndrome. 63 12

A fluorimeter has recently been developed to detect lead poisoning and iron deficiency by measuring erythrocyte ZPP directly from whole blood. Plasma bilirubin fluorescence has been found to influence this technique. ZPP levels determined by the fluorimeter were elevated by artificially increasing the plasma bilirubin concentration, both within and above the normal range, in whole blood samples. A rise in ZPP levels were also observed when the hemoglobin concentration was lowered by dilution with native plasma. When blood samples of patients with hyperbilirubinemia were analyzed, direct measurement of ZPP by this fluorimeter yielded significantly higher levels than did an alternate extraction method. Photodegradation of bilirubin in whole blood samples did not decrease fluorescent interference. Although the bilirubin measurably decreased, fluorescence increased following a 5 hr exposure to light.
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PMID:The influence of plasma bilirubin on zinc protoporphyrin measurement by a hematofluorimeter. 64 95

Using customary hematological and biochemical criteria, peripheral iron deficiency was observed, depending on age, in 12-51% and anemia in up to 6%, in a sample of 337 children (age: 4 4 months to 10 years). The majority of children were well nourished. Since iron deficiency occurs even in these children, it appears to be important to study this situation in underpriviledged German children as well. Even after peripheral iron deficiency was excluded, hemoglobin concentration varied significantly with age. This has to be considered in order to avoid unnecessary iron medication, that, according to recent findings, could cause adverse effects. The data presented here, do not as yet justify a general iron fortification program for all infants in Germany. Iron research should be directed toward the relationship of iron nutrition and iron-related blood chemistry of children on the one hand, and general criteria of functional capacity, morbidity, and longivity on the other. It will only be possible to give rational definitions of what are normal iron and hemoglobin concentrations in childhood, when we know more about these relationships.
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PMID:[Incidence of iron deficiency in a sample-population of Frankfurt children (author's transl)]. 65 93

Free erythrocyte protoporphyrin (FEP) and serum ferritin have been determined in 57 healthy children and in 25 children with varying degrees of iron deficiency. FEP was found to be inversely correlated to the concentration of hemoglobin (r = -0.80) as well as to serum ferritin (r=-0.64). Elevated FEP was found in children with hemoglobin less than 12.5 g/dl, or serum ferritin less than 8 microgram/l. In a group of apparently hematologically normal children between the age of 10--14 years (hemoglobin greater than 12.5 g/dl), a 2-month-trial of iron medication resulted in an increase in hemoglobin and ferritin, and a decrease in FEP, indicating suboptimal supply of iron for hemoglobin synthesis before iron medication. In a patient with iron deficiency (FEP 15.3 mumole/l, hemoglobin 5.2 g/dl), iron therapy was followed by a rapid fall in FEP before any changes in hemoglobin, serum iron transferrin saturation and ferritin could be detected. The rapid fall in FEP during start of treatment in iron deficiency makes FEP a sensitive biochemical parameter on iron homeostasis in iron deficiency anemia.
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PMID:The diagnosis of iron deficiency by erythrocyte protoporphyrin and serum ferritin analyses. 65 13

Patients with juvenile rheumatoid arthritis may have an anemia attributable to the chronic disease, to iron deficiency, or to a combination of the two. The contribution of iron deficiency is often difficult to determine by routine laboratory studies. We studied 51 patients with pauciarticular and polyarticular juvenile rheumatoid arthritis with red blood cell counts, indices, free erythrocyte protoporphyrin, and serum ferritin. Fifteen of the 18 who were anemic were restudied after a 3 to 6-month period of iron therapy. Thirteen of the 15 responded by these criteria: a rise in hemoglobin of 1.0 gm/dl or more and an increase in mean corpuscular volume of 3 fl or more; in 11 of these 13, hemoglobin values returned to the normal range for age. These findings indicate that iron deficiency can be a major component of the anemia that is commonly found in patients with active juvenile rheumatoid arthritis.
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PMID:Anemia in patients with juvenile rheumatoid arthritis. 66 Mar 58


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