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

Iron-deficient rats have an impaired work performance, even when their anemia is corrected by exchange transfusion. Muscle activity is associated with a higher blood lactate concentration than is observed in iron-replete animals. The accumulation of lactate is a result of excessive production as lactate clearance from the blood was shown to be unaffected. By adjusting the work load to a lower level, it was possible to divide iron-deficient animals into two groups, one capable of continued treadmill running and another in which animals stopped before 20 min. In the former, blood lactate concentration reached a plateau at moderate levels, whereas it continued to increase in the latter until the animal stopped running. Levels of alpha-glycerophosphate oxidase in skeletal muscle mitochondria were found to be much lower in the second group (P < 0.001). Lactate infusion into normal animals was shown to interfere with work performance, and maintenance of a normal pH in iron-deficient and iron-replete animals did not prevent the impairment in work associated with high blood lactate concentrations. Additional evidence was obtained that energy substrate (blood glucose and free fatty acids, muscle glycogen) was adequate in irondeficient animals. Oxygen tension in their vena caval blood was higher than in controls. Furthermore, the in situ behavior of electrically stimulated gastroenemius and soleus muscles appeared similar to that of control animals. Because the stimulation of the single muscle in the iron-deficient animal did not result in appreciable elevation of blood lactate and did not show impaired contractility further supported the hypothesis that the elevation of blood lactate caused the decreased work performance. It is concluded that iron deficiency by a depletion in the iron-containing mitochondrial enzyme, alpha-glycerophosphate oxidase, impairs glycolysis, resulting in excess lactate formation, which at high levels leads to cessation of physical activity.
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PMID:Lactic acidosis as a result of iron deficiency. 44 49

Serum ferritin was assayed by an immunoradiometric method in 82 people above 60 years of age. For comparison purposes, the same assay was performed in 71 younger normal adults. The serum ferritin distribution in the elderly had a larger variance than in the younger adults and in addition, there was a clear shift to higher values in the elderly. The latter was more notable in females than in males but there was still a statistically lower mean in elderly females than in elderly males. Ten out of 55 elderly subjects with evidence of iron deficiency (response to oral iron therapy) had a normal or high serum ferritin which suggests that variables unrelated to iron status may operate in determining serum ferritin levels in the elderly. The shift to higher values appears to occur upon reaching grossly 70 years of age. Whether the shift is a physiologically normal event is at present an open question.
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PMID:Serum ferritin in an elderly population. 44 43

Studies on 85 mothers with term infants and 32 mothers with preterm infants revealed that the cord serum and placental tissue iron levels were significantly reduced (P less than 0.001) in the mothers with hypoferremia (serum iron less than or equal to 50 microgram/100 ml). These levels were found to have linear correlations with the maternal serum iron levels, suggesting that the fetus and the placenta extracted iron in amounts proportional to the levels available in the mother. The high serum iron values in cord blood compared to the maternal blood even in the mothers with hypoferremia suggested that the process of active transfer of iron from mother to the fetus was maintained in maternal iron deficiency.
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PMID:Cord serum and placental tissue iron status in maternal hypoferremia. 45 61

Ochratoxin A at 8 micrograms per g of diet, but not at lower doses, fed to chickens from 1 day to 3 weeks of age resulted in significantly (P less than 0.05) decreased packed blood cell volume and hemoglobin concentration without altering the number of circulating erythrocytes. Serum iron and percentage of transferrin saturation were lowered at 4 and 8 micrograms/g. Therefore, anemia was characteristic of severe ochratoxicosis of young chickens, and the anemia was categorized as a hypochromic-microcytic anemia of the iron deficiency type. These data indicate that ochratoxin A by itself does not cause hemorrhagic anemia syndrome of chickens and that an anemia caused by a nutritional deficiency can be elicited by a mycotoxin.
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PMID:Ochratoxin A-induced iron deficiency anemia. 45 31

We performed quantitative fecal examinations, hemograms, and serum iron determinations on 103 first-grade children from Vieques Island, Puerto Rico, to determine whether trichuriasis was associated with iron deficiency and anemia. Although hemoglobin values tended to be slightly lower in Trichuris-infected children, there was no association between trichuriasis and serum iron or transferrin saturation values. These data demonstrate that in lightly infected children such as the population studied trichuriasis is not associated with iron deficiency anemia.
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PMID:Is trichuriasis associated with iron deficiency anemia? 46 98

Free iron in the circulation in contrast to iron complexed with protein or carbohyrdate, is intensely toxic. The annual morbidity and mortality from accidental overdose with iron salts is significant and has directed attention to the evaluation of safer forms of therapy. Comparative studies between oral ferrous sulphate and iron polymaltose in rats established an LD100 of 350 mg/kg for the salt, whereas neither morbidity nor mortality could be produced in doses exceeding 1 000 mg/kg for the complex. Bio-availability of iron from salt and complex for haemoglobin synthesis was then compared both in rats and in man with a twin-isotope technique. In experimental animals and in the human studies, venesected individuals were used to reproduce the iron deficiency state where treatment would be indicated. It was concluded that bioavailability is comparable for therapeutic doses of ferrous sulphate and iron polymaltose in iron-deficient subjects. The marginally lower absorption of complex was offset by a greater degree of gastrointestinal tract tolerance; the wide margin of safety may be of importance in reducing the danger of accidental iron overdose.
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PMID:Absorption of iron polymaltose and ferrous sulphate in rats and humans. A comparative study. 47 64

The anaemia resulting from iron deficiency is described as hypochromic in the medical literature. In the veterinary literature, anaemia of veal calves is usually regraded as normochromic. In order to examine the correctness of this view, the present authors studied the Hb and haematocrit (Hc) levels of the blood of veal calves in a comparative feeding trial for sixteen weeks. Three groups of male Dutch-Friesian calves, each group consisting of approximately thirty animals, were fed a milk replacer which contained 5, 10 or 25 ppm of iron respectively. The calculated mean Hb-concentration in the erythrocytes of the animals given 5 and 10 ppm of iron dropped during the trial period to below levels occurring at the age of two weeks. In the group given 25 ppm of iron, the erythrocyte Hb showed a rapid increase from the age of ten weeks and continuing throughout the rest of the trial period. At the age of sixteen weeks, the groups showed significant differences (P less than 0.01) in their mean erythrocyte Hb-concentrations. In veal calves, fed milkreplacers having an iron content below 25 ppm of Fe, the anaemia therefore is hypochromic.
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PMID:[Is anaemia of veal calves normochromic or hypochromic? (author's transl)]. 47 44

Gastrointestinal iron absorption was measured by whole body counting in 18 patients on regular peritoneal dialysis. Ten patients received regular oral iron treatment prior to the study (iron treated group), 8 patients did not receive iron treatment (non-iron treated group). Whole body retention 14 days after oral administration of 10 microCi 59Fe together with a carrier dose of 10 mg Fe2+ was used as an estimate of absorption. The erythrocyte iron incorporation, i.e. the percentage of administered 59Fe incorporated into the total erythrocyte mass, was measured. Geometric mean iron absorption in the non-iron treated groups was 7.4+/-3.3 (S.D.) % and in the iron treated group 2.8+/-2.5% (p less than 0.01). Absorption in the non-iron treated group did not differ significantly from the value in a normal control group (p greater than 0.3). Absorption in the iron treated group was distinctly lower than in the controls (p less than 0.01), due to the high iron supplementation. Several patients in the non-iron treated group had latent or overt iron deficiency, while patients in the iron treated group had satisfactory iron status. The correlation between iron absorption and erythrocyte iron incorporation was highly significant (r=0.95, p less than 0.001). Peritoneal dialysis patients on the whole have a normally functioning iron absorption. However, due to increased iron losses and insufficient dietary iron intake, the maintenance of a satisfactory iron balance implies an adequate oral iron supplementation.
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PMID:Iron absorption and iron status in patients with chronic uremia on regular peritoneal dialysis. 47 93

The aim of this investigation was to establish the relationship of cadmium-induced fetal growth retardation in the mouse to iron deficiency. Pregnant mice were either fed a low iron diet or given 40 ppm cadmium in their drinking water. The effects of these factors on fetal weight and hematological values of the fetuses and dams were established and compared, both with each other and with appropriate controls. Both treatments caused maternal and fetal anemia, the fetuses being more severely affected. The anemic fetuses were also severely growth retarded. These changes, when caused by the iron deficient diet, could be completely prevented by either parenterally or orally administered iron supplements. When the changes were caused by cadmium in the drinking water they were only partially prevented by oral supplements. From these results it was concluded that iron deficiency in pregnancy causes not only anemia but also fetal growth retardation. Cadmium exposure in pregnancy, presumably by blocking intestinal absorption of iron, also causes anemia and hence fetal growth retardation.
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PMID:Iron deficiency and its role in cadmium-induced fetal growth retardation. 47 57

Reliable methods for assessing the iron status of a population are essential for developing effective public health measures to combat iron deficiency. The hemoglobin concentration, transferrin saturation, free erythrocyte protoporphyrin, and serum ferritin are all useful but they vary widely in their specificity and sensitivity for detecting iron deficiency. In applying these laboratory parameters, the usual approach in nutritional surveys is to determine the percentage of values outside the normal range. As an alternative, a model is presented here that uses these measurements to estimate the distribution of iron stores in a population. This approach may be particularly useful for evaluating the effectiveness of iron supplementation and fortification programs.
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PMID:Assessing iron status of a population. 48 29


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