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

Concentration of ferritin in blood serum of dairy cows was measured by a two-site immunoradiometric assay to assess changes in the iron nutritional status during gestation, parturition, and lactation. Although anemia did not occur in pregnancy of dairy cows, there were slight decreases of red cell counts, hemoglobin, and hematocrit in the early stage of lactation. Ferritin concentration remained relatively constant in late gestation (35 ng/ml), but deviations were considerable. Ferritin rose gradually from 3 days prepartum with a sharp elevation after parturition. At 1 to 2 wk postpartum, it had increased to about twice amounts in late gestation. During the subsequent 8 wk postpartum, it fell gradually and thereafter maintained almost unchanged (40 ng/ml). Both iron in blood serum and total iron-binding capacity declined from 2 wk prepartum to the end of gestation but showed a rise beginning about 2 wk after parturition. Because changes in iron-related proteins just before and after delivery may be results of inflammatory reactions accompanying delivery, ferritin concentration is not a good index for diagnosis of iron deficiency in lactating cows just after parturition.
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PMID:Ferritin in blood serum of dairy cows. 714 30

Rheumatoid arthritis is a systemic disease in which anaemia is common. The origin of the anaemia is usually multifactorial. Iron deficiency, a defect of release of iron from the reticulo-endothelial system is discussed. Ferritin content of monocytes, lymphocytes and polymorphs is found altered and mostly elevated in monocytes affected by serum iron deficiency. In all cell types iron uptake is related to transferrin saturation. Alterations against normal subjects in iron uptake, ferritin synthesis and iron incorporation into ferritin are mostly found in patients with serum iron deficiency.
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PMID:Serum ferritin and iron uptake by peripheral blood leucocytes in patients with active rheumatoid arthritis. 718 34

Ferritin concentrations in cord blood were determined in 22 normal term and 32 preterm infants (birth weights 600-2000 g). Eight of the preterms were SGA infants. AGA preterm infants had significantly lower concentrations than term infants, and the SGA preterm newborn had even lower levels. Plasma ferritin in cord blood of the term and AGA preterm infants correlated positively with plasma iron and transferrin saturations, but not with the transferrin level, while plasma iron and transferrin concentrations correlated positively. In a longitudinal study, 17 AGA preterm infants (birth weights 850-1500 g) were followed during the early anaemia of prematurity. Iron was supplemented from 4 weeks of age. Plasma ferritin rose rapidly during the first days after birth, peak levels being reached at 1-4 weeks. Thereafter linear falls (semilog) occurred with similar slopes in different infants. Transferrin concentrations showed a slow progressive increase from 0-8 weeks. Plasma ferritin, after reaching the peak value, correlated negatively with weight gain. No infant had low ferritin values indicating iron deficiency during the early anaemia.
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PMID:Plasma ferritin concentrations in preterm infants in cord blood and during the early anaemia of prematurity. 723 84

Ferritin values for 250 selected sera were compared with values for iron, total iron-binding capacity (TIBC), and transferrin saturation, to assess the potential of the ferritin assay for the detection of latent iron deficiency. The specimens were grouped (50 in each group) according to their values for iron and TIBC. In Group 1 (low iron, high TIBC) the saturation and ferritin values both indicated iron deficiency in all but one. In the 100 specimens of Groups 2 (normal iron, high TIBC) and 4 (normal iron, high normal TIBC), the saturation values revealed 16 iron-deficient cases, the ferritin test 55. For Groups 3 (low iron, normal TIBC) and 5 (low iron, low TIBC), the ferritin test revealed fewer cases of iron deficiency than did the saturation values (37 cases vs 51 cases, in the 100 specimens). Evidently the ferritin test detects iron deficiency in many cases for whom the serum iron and TIBC tests are not positively indicative. The correlation of serum ferritin with iron, TIBC, and transferrin saturation in the five groups was good only in the case of specimens for which the TIBC was normal; if it was abnormal the correlation was very poor.
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PMID:Serum iron and total iron-binding capacity compared with serum ferritin in assessment of iron deficiency. 746 Feb 79

Ferritin and soybean meal were reevaluated as dietary treatments of iron deficiency in rats. Isotopes that had been used in the past were avoided because of contemporary knowledge of the physiological and structural complexity of ferritin protein and the solid iron mineral. Rats made anemic by iron-deficient diets were given equivalent amounts of iron as FeSO4, horse spleen ferritin, baked soybean meal, or soybean meal plus ferritin. Full recovery (89-109%) from anemia and increased tissue iron occurred after 28 d of treatment with any of the iron sources, which contrasts to past bioavailability studies using 59Fe-labeled ferritin and generally shorter periods of observation. Cultivar-specific variability was observed in soybean seed soluble iron and ferritin content (1.9-2.0 times the control cultivar, Arksoy), which was apparently heritable. The combined data suggest that manipulating ferritin expression and other soluble components of seed iron in soybeans and possibly other seeds, using Mendelian and biotechnological approaches, could contribute to a sustainable solution to global problems of iron deficiency.
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PMID:Purified ferritin and soybean meal can be sources of iron for treating iron deficiency in rats. 855 96

The regulation of expression of hepatic iron-related proteins was examined during iron deficiency caused by scurvy in guinea pigs. Previous studies showed that some effects of scurvy, such as suppression of collagen gene expression, result from events associated with weight loss. During the initial phase of scurvy when vitamin C is depleted but animals grow normally, serum iron levels decreased to 50% of normal. During the second phase of scurvy when animals lose weight, there was a further decrease in iron levels to 10-15% of normal. Serum transferrin levels increased during scurvy, but this increase was related neither to the rate of weight loss nor to hepatic transferrin mRNA expression, which decreased. Serum ferritin levels of diminished early in scurvy with a preferential loss of the L subunit. In liver, however, both ferritin animals gaining weight. Ferritin gene expression during vitamin C deficiency was correlated with serum ferritin levels in that the level of mRNA for the H subunit remained relatively constant while that of the L subunit decreased early. Transferrin receptor mRNA expression in liver was induced as soon as iron levels decreased early in scurvy, which is similar to results reported for iron-depleted cultured cells. In contrast to results in cell culture, expression of iron regulatory protein 1 mRNA was decreased to approximately 50% of normal early in scurvy with a concomitant decrease in hepatic cytosolic aconitase activity. Our data indicate that iron deficiency occurs early during vitamin C deficiency and leads to changes in expression of iron-related proteins that differ in some aspects from regulation by iron in cell culture. Other events associated with weight loss in late scurvy may play a further role in this regulation.
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PMID:Gene expression of iron-related proteins during iron deficiency caused by scurvy in guinea pigs. 856 10

We demonstrate that simple correlation between the various tests of iron status is not sufficient for examining their value in diagnosing iron deficiency (ID). Three degrees of ID are recognized: Iron depletion (ID grade I) is defined by decreased total body iron and normal iron support to erythropoiesis, as diagnosed by decreased storage iron, decreased ferritin, normal sideroblast count, normal zinc protoporphyrin (ZPP), and transferrin saturation >15%. When the iron supply to erythropoiesis becomes insufficient, as diagnosed by transferrin saturation < or = 15%, increased ZPP, and decreased sideroblast count, iron-deficient erythropoiesis (ID grade II) occurs. When finally hemoglobin is below its normal range, iron-deficiency anemia (ID grade III) results. The various tests for ID cannot be compared without taking into account the severity of the deficiency. Depending on the grade of ID examined, the correlation of markers seen in our patients' data varied considerably. We conclude that a "best" marker of ID does not exist. However, the different tests efficiently complement each other by detecting different stages and individually show the clinical extent of ID. Ferritin reflects the iron stores. ZPP indicates whether the ID in a given patient is clinically relevant or not. Finally, the extent of a clinically relevant ID can be assessed by the measured ZPP, hemoglobin concentration, and red cell indices.
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PMID:Laboratory tests of iron status: correlation or common sense? 896 57

Oligodendrocytes are the predominant iron-containing cells in the brain. Iron-containing oligodendrocytes are found near neuronal cell bodies, along blood vessels, and are particularly abundant within white matter tracts. Iron-positive cells in white matter are present from birth and eventually reside in defined patches of cells in the adult. These patches of iron-containing cells typically have a blood vessel in their center. Ferritin, the iron storage protein, is also expressed early in development in oligodendrocytes in a regional and cellular pattern similar to that seen for iron. Recently, the functionally distinct subunits of ferritin have been analyzed; only heavy (H)-chain ferritin is found in oligodendrocytes early in development. H-ferritin is associated with high iron utilization and low iron storage. Consistent with the expression of H-ferritin is the expression of transferrin receptors (for iron acquisition) on immature oligodendrocytes. Transferrin protein accumulation and mRNA expression in the brain are both dependent on a viable population of oligodendrocytes and may have an autocrine function to assist oligodendrocytes in iron acquisition. Although apparently the majority of oligodendrocytes in white matter tracts contain ferritin, transferrin, and iron, not all of them do, indicating that there is a subset of oligodendrocytes in white matter tracts. The only known function of oligodendrocytes is myelin production, and both a direct and indirect relationship exists between iron acquisition and myelin production. Iron is directly involved in myelin production as a required co-factor for cholesterol and lipid biosynthesis and indirectly because of its requirement for oxidative metabolism (which occurs in oligodendrocytes at a higher rate than other brain cells). Factors (such as cytokines) and conditions such as iron deficiency may reduce iron acquisition by oligodendrocytes and the susceptibility of oligodendrocytes to oxidative injury may be a result of their iron-rich cytoplasm. Thus, the many known phenomena that decrease oligodendrocyte survival and/or myelin production may mediate their effect through a final common pathway that involves disruptions in iron availability or intracellular management of iron.
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PMID:Relationship of iron to oligodendrocytes and myelination. 877 76

During April-May 1990 in Taiwan, health workers collected 10 ml venous blood samples from 371 school children 7-12.9 years old and from 352 adolescent students 13-19.9 years old attending primary, junior high, and senior high schools in Pingtung County and Taichung County. The researcher aimed to determine the iron status and prevalence of anemia in these children. Ferritin levels of less than 12 mcg/l defined iron deficiency. In both counties, girls were more likely to suffer from iron deficiency than boys. Teenage girls had the highest rate of iron deficiency (9.38% vs. 1.22-2% in Pingtung and 26.4% vs. 0-2.17% in Taichung). Among school children 7-12.9 years old in Pingtung, 2% of the boys in Pingtung and 3.33% of girls had iron deficiency. In Taichung, 0% of boys and 2.17% of girls had iron deficiency. Among the teenagers in Pingtung, 1.22% of the boys and 9.38% of girls had iron deficiency. These rates in Taichung were 0% and 26.4%, respectively. Less than 2% of all children had iron deficiency anemia. Among school children 7-12.9 years old in Pingtung, the anemia rate was 5% for boys and 5.56% for girls. In Taichung, 3.37% of the boys and 1.09% of girls had anemia. Among teenagers 13-19.9 years old in Pingtung, 3.66% of boys and 8.33% of girls had anemia. In Taichung, the anemia rate was 3.45% and 5.75%, respectively. These findings show that teenage girls are more likely to have iron deficiency than males. Thus, health officials need to develop an effective nutritional intervention and health care for youths to improve their iron status.
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PMID:Iron deficiency and anemia in school children and adolescents. 891 58

Iron regulatory protein 1 (IRP1) and IRP2 are cytoplasmic RNA binding proteins that coordinate cellular iron homeostasis in mammals. We investigated the effect of dietary iron intake on rat liver IRP activity in relation to the abundance of two targets of IRP action, ferritin and mitochondrial aconitase (m-aconitase). Rats were fed diets containing 2, 11, 20, 37 (control), 72 or 107 mg iron/kg diet for 3 wk. RNA binding activity of IRP1 and IRP2 was enhanced one- to twofold in rats fed 11 or 2 mg iron/kg diet compared with control rats. IRP RNA binding activity was inversely correlated to blood hemoglobin levels (r = -0.787; P < 0.0001). Compared with control rats, liver ferritin levels were depressed in rats fed 20 mg iron/kg diet and were undetectable in rats ingesting diets with 11 or 2 mg iron/kg diet. Ferritin concentrations were biphasically related to IRP RNA binding activity with the regulation of IRP occurring before the onset of ferritin accumulation. Iron deficiency caused up to a 50% decline in m-aconitase abundance. IRP RNA binding activity and m-aconitase abundance were inversely correlated (r = -0.751; P < 0.0001). Our results indicate that (1) liver IRP activity is responsive to a range of dietary iron levels, (2) there appears to be a differential effect of IRPs on ferritin and m-aconitase abundance, and (3) activation of IRPs may contribute to the alterations in energy metabolism in iron deficiency through an impairment of m-aconitase synthesis.
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PMID:Dietary iron intake modulates the activity of iron regulatory proteins and the abundance of ferritin and mitochondrial aconitase in rat liver. 903 23


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