Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Healthy term infants were given a low-fat powdered milk fortified with 15 mg/100g of iron, as ferrous sulphate, for one year, starting at three months of age. The control group received non-fortified milk. A total of 510 infants entered the study, and 314 could be studied at the age of 15 months. Consumption of the fortified formulas was monitored through iron determinations in stools. Groups had a comparable hemoglobin concentration at the age of three months. Hemoglobin was higher in the fortified group at nine months (11.7 +/- 1.0 vs 11.4 +/- 1.1 g/dl, p less than 0.02), and 15 months (12.0 +/- 1.1 vs 11.4 +/- 1.2, p less than 0.001). The percentage of subjects with anemia (Hb less than 11.0 g/dl) was lower in the fortified group: 14.8% vs 27.7% of the controls at nine months and 7.0% vs 35.3% at 15 months. Percentages of subjects with iron deficiency (Fe/TIBC less than 9%) were lower in the fortified group: 28.0% vs 49.1% of the controls at nine months, and 20.0% vs 41.8% at 15 months. Although the fortified milk markedly improved iron nutrition, deficiency of this mineral was still high in the group receiving it. This was probably due to the low bioavailability of iron when administered with non-modified milks.
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PMID:[Prevention of iron deficiency in infants by fortified milk. Field study of a low-fat milk]. 343 15

Even when simple iron deficiency is strongly suspected, the child with severe anemia deserves a careful and thorough work-up before treatment is begun. Many other possible causes of anemia need to be excluded. No one test specifically identifies iron deficiency, but the combined use of several tests of iron status can establish iron deficiency with certainty. Hemoglobin level, mean corpuscular volume, serum iron, total iron binding capacity, free erythrocyte porphyrin and serum ferritin are the important studies.
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PMID:Iron deficiency anemia in children. 357 91

A group of black adolescents stratified by age and sexual maturity (Tanner stage) had electronic blood counts determined. Hemoglobin, hematocrit, and red cell count were lower than the means reported for white or Hispanic children of the same age. The difference could not be explained by iron deficiency, but the data were insufficient to exclude alpha thalassemia as a cause.
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PMID:Hematologic changes during sexual maturation. Why do black adolescents have low hemoglobin concentrations? 361 Jul 35

A new alpha chain hemoglobin variant, Hb Hobart, alpha 20(Bl)His----Arg, was detected in a 60-year-old female of British nationality. The proposita had a history of severe rheumatoid arthritis and had been treated for many years for a refractory microcytic anemia and/or iron deficiency. A hemoglobin electrophoresis screen indicated the presence of a hemoglobin variant, with electrophoretic characteristics similar to a Hb Lepore. However, the level of the variant (17.9%) and the presence of a minor variant Hb A2 band (0.4%) suggested that further investigation was indicated. The variant hemoglobin was purified by column chromatography and the alpha chain subjected to aminoethylation and tryptic digestion. Peptide mapping and amino acid analysis indicated that the histidine residue 20 had been substituted by an arginine residue. The substitution in Hb Hobart is at the first residue in the B Helix of the alpha chain of hemoglobin. As this is an externally placed amino acid in the hemoglobin molecule, a substitution at this position of the hemoglobin molecule would not be expected to cause any functional problems. A family study has shown that at least three other relatives are heterozygous for Hb Hobart. These family members have normal hematological findings.
Hemoglobin 1987
PMID:Hemoglobin Hobart or alpha 20(Bl)His----Arg: a new alpha chain hemoglobin variant. 365 64

Effects of iron supplements and training for cross-country skiing on hematological and iron status were studied in nine men and ten women from the U. S. Nordic ski team. Four men and five women received a multiple vitamin, multiple mineral supplement containing 18 mg iron for 8 months while five men and five women received a placebo. Fasting blood samples were taken from all skiers prior to supplementation (May) and in August, November, and January. Hemoglobin, hematocrit, plasma iron, total iron binding capacity (TIBC), percentage of transferrin saturation, serum ferritin, free erythrocyte porphyrin, and haptoglobin were measured on each sample. Hemoglobin, hematocrit, and TIBC were higher in November when both men and women skiers trained at altitude than in August. In January TIBC was further increased, haptoglobin was increased, hemoglobin for the men fell below May levels, and hematocrit returned to May levels. Skiers receiving iron had lower TIBC levels in November and January than the placebo group. Six women and two men had ferritin levels below 28 ng X ml-1, which suggests prelatent iron deficiency. Free erythrocyte porphyrin levels above 100 micrograms X dl-1 RBC were found in all skiers at some point during training. The results suggest that multivitamin, multimineral supplements containing iron have little effect on the iron status of cross-country skiers.
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PMID:Training for cross-country skiing and iron status. 370 43

Hemoglobin and mean corpuscular volume values appear to be lower among black than among white children. Blood hemoglobin concentration and red cell mean corpuscular volume were measured in 4,074 black boys and girls aged 1 through 20 years who lived near sea level. This is the largest hematologic survey of healthy American black children and adolescents to date. Children with sickle cell disease and elevated hemoglobin F were excluded from the study, but children with the traits for hemoglobin S, hemoglobin C, thalassemia, and iron deficiency were not. The 3rd and 97th percentile values reported here are close to the 95 percent confidence limits, and are adjusted for age and sex.
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PMID:Hemoglobin and MCV values in 4,074 healthy black children and adolescents. 382 Mar 34

To determine whether or not adolescent female athletes were more in need of routine dietary iron supplements than their nonathlete peers, the iron status of 32 athletes and 31 nonathletes was assessed. The athletes were track-team members in the middle of their season. Hemoglobin, transferrin saturation, and serum ferritin were evaluated, as well as the amount of dietary iron intake. Athletes had significantly lower serum ferritin levels and transferrin saturation (less than 16%) than did nonathletes. Black girls were significantly lower than whites on all three values. There were also a greater number of black girls deficient in serum ferritin. We conclude that athletes may be at greater risk for iron deficiency and, therefore, for iron deficiency anemia; and black adolescents may have an increased prevalence of iron deficiency, with black female athletes being at potentially greater risk for iron deficiency and its possible consequences. We recommend a more sensitive assessment of iron status in female athletes.
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PMID:Iron status of adolescent female athletes. 404 70

Hemoglobin and myoglobin are a major source of dietary iron in man. Heme, separated from these hemoproteins by intraluminal proteolysis, is absorbed intact by the intestinal mucosa. The absorbed heme is cleaved in the mucosal cell releasing inorganic iron. Although this mucosal heme-splitting activity initially was ascribed to xanthine oxidase, we investigated the possibility that it is catalyzed by microsomal heme oxygenase, an enzyme which converts heme to bilirubin, CO, and inorganic iron. Microsomes prepared from rat intestinal mucosa contain enzymatic activity similar to that of heme oxygenase in liver and spleen. The intestinal enzyme requires NADPH; is completely inhibited by 50% CO; and produces bilirubin IX-alpha, identified spectrophotometrically and chromatographically. Moreover, duodenal heme oxygenase was shown to release inorganic (55)Fe from (55)Fe-heme. Along the intestinal tract, enzyme activity was found to be highest in the duodenum where hemoglobin iron absorption is reported to be most active. Furthermore, when rats were made iron deficient, duodenal heme oxygenase activity and hemoglobin-iron absorption rose to a comparable extent. Upon iron repletion of iron-deficient animals, duodenal enzyme activity returned towards control values. In contrast to heme oxygenase, duodenal xanthine oxidase activity fell sharply in iron deficiency and rose towards base line upon iron repletion. Our findings suggest that mucosal heme oxygenase catalyzes the cleavage of heme absorbed in the intestinal mucosa and thus plays an important role in the absorption of hemoglobin iron. The mechanisms controlling this intestinal enzyme activity and the enzyme's role in the overall regulation of hemoglobin-iron absorption remain to be defined.
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PMID:Intestinal absorption of hemoglobin iron-heme cleavage by mucosal heme oxygenase. 443 36

Hemoglobin iron absorption in patients with treated prenicious anemia (PA) and concomitant iron deficiency was low compared to absorption in patients with iron deficiency alone. Crude and purified hog intrinsic factor (IF) concentrates doubled the absorption of hemoglobin iron in these patients as did normal (neutralized depepsinized) human gastric juice. Hemoglobin iron absorption was not significantly enhanced by PA gastric juice. Absorption of heme iron, like that of hemoglobin iron, was enhanced by normal neutralized depepsinized gastric juice. No enhancement of hemoglobin iron absorption by these substances was obtained in the normal or iron-deficient non-PA control subjects. Preincubation of the hog IF concentrate with antisera to IF significantly reduced the enhancement of hemoglobin iron absorption due to the concentrate. In vitro studies suggest that heme complexes with a substance present in IF-containing materials. Whether a gastric glycoprotein similar to IF serves as an intestinal transport factor for heme, similar to transport of vitamin B(12), or whether normal gastric juice acts by another mechanism cannot be determined at this time.
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PMID:Malabsorption of hemoglobin iron in pernicious anemia: correction with intrinsic factor--containing substances. 566 12

The effects of chronic iron deficiency were studied in new born rats. Hemoglobin concentrations were significantly depressed throughout the experimental period when compared with those of control animals. At third postnatal month, there was a 56% increase of absolute heart weight and a 230% increase of relative heart weight. Heart weight increased much more than myocytes dimensions. This finding may be interpreted as characteristic of a double process of hypertrophy and hyperplasia. Both cell hypertrophy and multiplication were responsible for the observed hypertrophy of the heart. Number of capillaries/mm2 was unchanged, but both mean capillary diameter and total surface of capillary wall increased progressively during the period of anemia. The adaptation to myocardial hypoxia may be, in this experiment situation, localized at the capillary level rather than at the mitochondria. At cell level, we did not note any particular modification of the ultrastructure and particularly no degenerative change. No mitochondrial lesions were found even in severe anemics (blood hemoglobin below 3.2 g/100 ml).
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PMID:[Cardiomegaly due to iron deficiency in the rat (author's transl)]. 645 60


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