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

The ultrastructure of intestinal mucosa in two geophagia patients with growth retardation, hypogonadism, hepatosplenomegaly, zinc deficiency, iron deficiency, and anemia was studied with an electron microscope. Alterations in the ultrastructure of intestinal mucosa, especially in Paneth's cells, possibly due to zinc deficiency were observed.
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PMID:Ultrastructural changes in the mucosa of the small intestine in patients with geophagia (Prasad's syndrome). 239 69

Seven different metals (iron, copper, zinc, calcium, manganese, lead, and cadmium) were studied in eight different brain regions (cerebral cortex, cerebellum, corpus striatum, hypothalamus, hippocampus, midbrain, medulla oblongata, and pons) of weaned rats (21-d-old) maintained on an iron-deficient (18-20 mg iron/kg) diet for 8 wk. Iron was found to decrease in all the brain regions, except medulla oblongata and pons, in comparison to their respective levels in control rats, receiving an iron-sufficient (390 mg iron/kg) diet. Brain regions showed different susceptibility toward iron deficiency-induced alterations in the levels of various metals, such as zinc, was found to increase in hippocampus (19%, p less than 0.05) and midbrain (16%, p less than 0.05), copper in cerebral cortex (18%, p less than 0.05) and corpus striatum (16% p less than 0.05), calcium in corpus striatum (22%, p less than 0.01) and hypothalamus (17%, p less than 0.02), and manganese in hypothalamus (18%, p less than 0.05) only. Toxic metals lead and cadmium also increased in cerebellum (19%, p less than 0.05) and hippocampus (17%, p less than 0.05) regions, respectively. Apart from these changes, liver (64%, p less than 0.001) and brain (19%, p less than 0.01) nonheme iron contents were found to decrease significantly, but body, liver, and brain weights, packed cell volume, and hemoglobin content remained unaltered in these experimental rats. Rehabilitation of iron-deficient rats with an iron-sufficient diet for 2 wk recovered the values of zinc in both the hippocampus and mid-brain regions and calcium in the hypothalamus region only. Liver nonheme iron improved significantly; however, no remarkable effect was noticed in brain nonheme iron following rehabilitation. It may be concluded that latent iron deficiency produced alterations in various metal levels in different brain regions, and corpus striatum was found to be the most vulnerable region for such changes. It is also evident that brain regions were resistant for any recovery in their altered metallic levels in response to rehabilitation for 2 wk.
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PMID:Effect of latent iron deficiency on metal levels of rat brain regions. 248 35

The interaction of dietary iron and zinc was studied in chicks. Zinc was found to be more toxic in iron-deficient animals than iron-supplemented animals as measured by hemoglobin concentrations and growth. Analyses of the kidney and liver for iron and zinc were carried out. As the level of iron was increased from 0-1000 ppm supplementation, the concentration of liver zinc increased. The organ levels of iron were decreased as the dietary zinc levels were increased from 0-5000 ppm. Radioisotope studies using 65Zn revealed that the iron content of the diet did not affect absorption of zinc. Administration of the isotope, either in an intestinal segment or intravenously, resulted in more zinc being taken up by the liver in the iron supplemented animals. This was especially noted when the ratio of the isotope in liver to that in the blood was compared. Gel chromatography of kidney and liver homogenates revealed that iron deficiency resulted in less zinc being eluted in a volume characteristic of metallothionein compared to homogenates of organs from iron supplemented animals. The results indicate that iron-supplemented animals have a greater capacity for sequestering zinc on metallothionein than do iron-deficient animals. Conversely, iron-deficient chicks were more susceptible to the effects of zinc toxicity than are iron-adequate chicks.
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PMID:Studies on the role of iron in zinc toxicity in chicks. 248 56

The influence of lead exposure, iron deficiency, or their combination on certain biochemical parameters in blood, plasma, and urine of rats was investigated in an attempt to identify the specific diagnostic tests of the two conditions and to draw a possible interrelationship between the two factors. The decrease in blood-glutathione peroxidase activity, -packed cell volume, plasma-ceruloplasmin, and-Fe levels and increase in urinary excretion of delta-aminolevulinic acid, plasma-cholesterol, and-total Fe binding capacity occur under Fe deficiency as well as Pb intoxication. However, increase in the activity of blood delta-aminolevulinic acid dehydratase (ALAD) without any change in blood zinc protoporphyrin (ZPP) level appears to be a specific effect of Fe deficiency that could be distinguished from Pb intoxication, a condition characterized by the inhibition in blood ALAD activity accompanied by an increase in blood ZPP level. The linear regression analysis of the data showed that the blood Pb and plasma free cholesterol levels increase with the decrease in plasma Fe level.
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PMID:Interrelationship between iron deficiency and lead intoxication (Part 1). 248 14

The influence of dietary iron deficiency, lead exposure or their combination on certain enzymes, and the accumulation of Pb and essential metal levels in vital organs of rats was investigated. Iron deficiency caused alterations in the activity of muscle, hepatic and renal succinate dehydrogenase, and hepatic mitochondrial succinate cytochrome c reductase, whereas Pb exposure had no influence on these enzymes. There was no synergistic effect of the two factors on the activity of the enzymes. However, feeding of a Fe-deficient diet during Pb exposure enhanced the accumulation of Pb in soft tissues and flat bones. The hepatic copper and zinc levels were lowered upon either feeding a Fe-deficient diet or Pb exposure. However, the synergistic effect of the two factors was evident in hepatic Cu, but not in hepatic Zn. The feeding of a Fe-deficient diet decreased liver, kidney, and spleen levels of Fe, whereas Pb exposure decreased kidney and spleen Fe. The synergistic influence of the two factors could be observed only in liver and kidney.
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PMID:Interrelationship between iron deficiency and lead intoxication (Part 2). 248 15

Seventy-three patients with hereditary spherocytosis (HS) (58 nonsplenectomized, 15 splenectomized) were studied to evaluate iron status and the adequacy of iron availability for erythropoiesis. Splenectomized patients, who had hemoglobin levels in the normal or upper normal range, had higher levels of serum iron, transferrin saturation, and serum ferritin than normal matched controls and normal zinc protoporphyrin (ZnPP) levels. On the contrary, nonsplenectomized patients presenting with mild to severe anemia had higher red cell ZnPP concentrations than both splenectomized subjects and matched normal controls. ZnPP in nonsplenectomized patients correlated inversely with Hb concentration, mean corpuscular volume (MCV), mean red cell hemoglobin concentration (MCHC), transferrin saturation, and serum iron, and directly with reticulocyte count. At multiple regression analysis only Hb concentration was a significant explanatory variable for high ZnPP. The authors conclude that a number of nonsplenectomized HS patients have relative iron deficiency primarily because of expansion of erythropoiesis caused by anemia.
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PMID:Relative iron deficiency in hereditary spherocytosis. 273 20

This paper on confounding factors in the relationship between iron deficiency and brain function is mainly limited to nutritional factors, primarily factors that can contribute to the development of iron deficiency and that may have an independent direct action on brain function. Three theoretically possible confounders were found in a systematic search for dietary factors: 1) low intake of ascorbic acid, 2) excess of phytates, and 3) increased absorption of lead. Ascorbic acid has a marked effect on the bioavailability of dietary iron and is also known to directly influence various metabolic processes in the brain. Phytates inhibit the absorption not only of iron but also of zinc. An iron deficiency may thus be accompanied by a zinc deficiency which may affect mental performance. A state of iron deficiency may increase the absorption of lead from the diet, which in turn may affect brain function.
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PMID:Search for nutritional confounding factors in the relationship between iron deficiency and brain function. 277 39

The 1970s saw a revolution in the nutritional welfare of the suckling but half way through the 1980s we have yet to achieve the same success with the weanling. In the developing world the malnutrition/diarrhoea complex is a major threat to the weanling's life. Throughout the world rickets and iron deficiency are common problems. These three, protein-energy malnutrition/diarrhoea, rickets and iron deficiency anaemia are the major nutritional problems of the weanling but there are others e.g. zinc deficiency, allergy, obesity. As the weanling crosses the bridge from suckling to schoolchild he will eat the suckling's food, specially prepared weaning foods, and eventually "sensible" family foods. Beneath this bridge we need to erect a safety net of fortified foods ensuring an adequate supply of such nutrients as iron and vitamin D.
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PMID:Food for the weanling: the next priority in infant nutrition. 309 66

Protein-calorie malnutrition is associated with impaired immunocompetence and increased susceptibility to infection. Clinically evident nutritional deficiency syndromes, however, are composite of deficits of many essential nutrients, each of which may exert an important regulating effect on immunity. Among other nutrients, several trace elements have been shown to regulate immune responses, particularly cell-mediated immunity. Zinc undernutrition results in lymphoid atrophy and reduced capacity to respond to many T-cell-dependent antigens. Plaque forming cell response to heterologous erythrocytes is decreased, as is the function of B cells. In zinc deficient rodents, the generation of cytotoxic lymphocytes in the spleen is reduced. Antibody-dependent cell-mediated cytotoxicity is largely unchanged. In acrodermatitis enteropathica, lymphocyte proliferation response to mitogens is decreased and there are significant changes in delayed hypersensitivity responses and in the proportion of various T cell subsets. Neutrophil function is not changed by zinc deficiency. Iron deficiency results in a slight decrease in the number of rosette-forming T cells and a significant impairment of lymphocyte response to mitogens and antigens. Polymorphonuclear leukocytes are unable to kill ingested bacteria and fungi in an efficient manner. Copper deficiency impairs cell-mediated immunity, as does selenium deficiency when it is associated with vitamin E lack. Several pathogenetic mechanisms may underlie such alterations in immunity. Many heavy metals impair immune responses. These effects of trace elements on immunity may have important fundamental and practical implications.
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PMID:Grace A. Goldsmith Award lecture. Trace element regulation of immunity and infection. 315 39

Microcytic anemia, long considered an effect of lead poisoning, may in fact result from coexisting iron deficiency. In this study, how RBC size, hemoglobin, and zinc protoporphyrin vary as a function of iron status in a group of children with high lead levels was examined. Charts of all children (N = 51) admitted to Cook County Hospital for treatment of lead poisoning in 1981 to 1983 were reviewed for data on age, blood lead level, hemoglobin concentration, MCV, transferrin saturation and zinc protoporphyrin level. The mean lead level was 86 micrograms/dL and the range was 63 to 190 micrograms/dL. Children with transferrin saturation values less than 7% had a mean MCV of 56 microL, hemoglobin of 8.9 g/dL, and zinc protoporphyrin of 693 micrograms/dL; for those with saturations of 7% to 16%, the values were 61 microL, 10.1 g/dL, and 581 micrograms/dL, respectively; the children with saturations greater than 16% had normal mean MCVs and hemoglobin concentrations (74 microL and 11.4 g/dL) and a mean zinc protoporphyrin value of 240 micrograms/dL (P less than .0005). Multiple linear regression was used to correct for effect of age, and transferrin saturation remained the most important predictor of MCV, hemoglobin, and zinc protoporphyrin levels; the addition of lead did not improve the models. Results of this study suggest that iron deficiency is strongly associated with some of the observed toxicities of lead. Also, lead poisoning can exist without producing microcytosis or anemia, and zinc protoporphyrin concentration may not be a sensitive indicator of lead level in the absence of iron deficiency.
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PMID:Interaction of iron deficiency and lead and the hematologic findings in children with severe lead poisoning. 327 57


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