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

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 developmental changes in red blood cell counts and indices were determined in infants after mild iron deficiency was excluded. The normal values were obtained from a selected group of healthy, term infants who were receiving continuous iron supplementation during a period of one year while normal values for transferrin saturation and serum ferritin were being maintained. The data indicated marked developmental changes in red blood cell counts and indices during the first year of life that are independent of iron intake. Serial analysis of individual infant's values indicated that the red cell measurement at 4 months of age are, to some extent, predictive of the level of subsequent values within the normal range.
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PMID:Developmental changes in red blood cell counts and indices of infants after exclusion of iron deficiency by laboratory criteria and continuous iron supplementation. 63 80

A direct radioimmunoassay for ferritin in serum is described in which Bolton and Hunter reagent is used to label ferritin. The detection limit of the assay is 150 pg; 95% reference ranges were found to be 12-200 microgram/l for men and 5-76 microgram/l for women. Ferritin concentrations in patients with iron deficiency anaemia were found to be uniformly low in subjects with uncomplicated iron deficiency but were normal or even raised in subjects with iron deficiency anaemia associated with malignant or inflammatory conditions.
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PMID:Measurement of serum ferritin by radioimmunoassay. 63 7

In mice fed a low iron diet, the addition of low levels of cadmium chloride (10 micrometer) to the drinking water impaired growth and accentuated the development of anemia. Cadmium had no effect on mice given a similar diet supplemented with iron. Iron deficiency increased the concentration of cadmium in the duodenal mucosa, the transfer of cadmium to the body from the intestinal tract, and the deposition of absorbed cadmium in the kidneys. In human subjects, the average absorption of 25 microgram of cadmium, labeled with 115mCd, from a test meal was 8.9 +/- 2.0% (mean +/- SE) in 10 people with low body iron stores (serum ferritin less than 20 ng per ml) and 2.3 +/- 0.3% in 12 subjects with normal iron stores (serum ferritin greater than 23 ng per ml). The biological half-time of the radiocadmium in 3 of the subjects ranged from 90 to 202 days. Thus, the intestinal adaptive response to iron deficiency in both experimental animals and human subjects leads to the increased absorption of cadmium, a potentially toxic element.
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PMID:Increased dietary cadmium absorption in mice and human subjects with iron deficiency. 64 Mar 39

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

The relationship between serum ferritin and duodenal ferritin was examined in normal subjects and in patients with iron deficiency, secondary iron overload, or idiopathic hemochromatosis (IHC). A positive correlation between serum ferritin and duodenal ferritin concentrations was found in all groups. In the iron-overload conditions, duodenal ferritin concentration was lower at all levels of serum ferritin in comparison with normal and iron-deficient subjects. Patients with secondary iron overload did not differ from those with IHC, which indicates that any decrease in duodenal ferritin concentration was secondary to the excess body iron stores. Purified duodenal ferritin from normal subjects and patients with iron-overload conditions showed the same two distinct isoferritins by isoelectric focusing. After the oral administration of iron, two additional isoferritins were detected. These resembled the major isoferritins of liver.
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PMID:Duodenal ferritin content and structure: relationship with body iron stores in man. 66 70

1. A state of protein deficiency has been produced in rats by feeding a low protein diet, thereafter a period of rehabilitation with a normal protein but a low iron supply followed. 2. For characterization of the iron metabolism during both periods haemoglobin, total iron binding capacity, liver non-haemin iron, intestinal iron absorption and the uptake of 59Fe in the liver was determined. 3. Under these conditions the amount of 59Fe incorporated into the mucosal transferrin and the ferritin fractions has been measured. Both fractions were obtained from the supernatant of a mucosal homogenate after chromatography on sepharose 6B. 4. In anemia due to protein deficiency the typical increase of 59Fe incorporation into the fraction of mucosal transferrin--usually occuring in iron deficiency--could not be observed. This coincides with the absence of an increased iron absorption. Moreover a decrease of iron absorption is observed, which is associated with a decreased 59Fe ratio of transferrin/ferritin-fraction. 5. After normalization of the protein supply the ratio of 59Fe incorporated into the mucosal transferrin and ferritin fractions was changed remarkably in favor to transferrin together with a several fold increase of the intestinal iron absorption. 6. The conclusion is drawn that mucosal transferrin and ferritin enable the body not only to adapt the absorption to a higher but also to a lower requirement as it is the case in protein deficiency.
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PMID:The role of mucosal iron binding proteins in adaptation of iron absorption during protein deficiency and rehabilitation. 68 93

The control of hepatic iron uptake was studied in the perfused liver isolated from rats subjected to nutritional iron deficiency. The total hepatic iron uptake and incorporation into ferritin was found to be higher in iron deficiency and during the 48 h of oral refeeding with iron than in the normal state. Specific incorporation of iron into feritin from a perfusate of normal transferrin iron saturation was enhanced in nutritional iron deficiency as compared to controls after 5 h of perfusion but not after 1 h, suggesting that increased uptake of iron from the perfusate may play a role in stimulating hepatic ferritin synthesis and assembly. This promotion of uptake into ferritin was inhibited by cycloheximide suggesting that enhanced incorporation of iron is dependent upon de novo synthesis of apoferritin. In control, nutritionally iron deficient and iron-refed rats there was a significant, direct correlation between the transferrin-iron saturation of the perfusate at physiological transferrin concentrations and total hepatic iron uptake after 5 h perfusion. A significant positive correlation was found between the hepatic total and ferritin iron uptake and the transferrin synthetic rate measured in the same liver. It is proposed that in the liver the negative feedback of iron supply on transferrin synthesis may be linked with a positive feedback on ferritin synthesis. The time-course of these reciprocal responses suggests a role for hepatic ferritin and/or a component of the non-haem, non-ferritin iron pool in the regulation of transferrin synthesis.
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PMID:The control of hepatic iron uptake: correlation with transferring synthesis. 69 24

We followed up 238 infants on 7 occasions during their first year of life. The diets of the infants were systematically either supplemented or not supplemented with iron. Developmental changes in serum ferritin were determined from a group with adequate intake of iron and without evidence of iron deficiency by three laboratory criteria: hemoglobin, mean corpuscular volume and transferrin saturation. The data indicate that the average level of serum ferritin correlates well with iron nutrition within groups of infants since the developmental changes are in accordance with the known changes in storage iron, the level of serum ferritin correlates with iron intake, and low ferritin levels are associated with lower transferrin saturation. The usefulness of serum ferritin as the sole criterion of iron deficiency in individual infants is limited, suggesting the use of more than one indicator to refine the diagnosis of iron deficiency without anemia.
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PMID:Serum ferritin in assessment of iron nutrition in healthy infants. 71 74


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