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

Iron supplements are commonly administered to infants in order to prevent iron deficiency. We wished to determine whether iron administration could compromise zinc nutrition as might be suspected from previous studies. Measures of iron nutrition, serum zinc, and serum copper were measured before and after randomization of 291 healthy 1-yr-old infants to a 3 mo course of placebo or iron treatment (30 mg iron as ferrous sulfate given before a meal). There was no significant difference in serum zinc or copper in the two groups before or after treatment; thus iron administration did not result in any evidence of zinc deficiency in a healthy, well-nourished group of T-yr-old infants.
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PMID:Does iron supplementation compromise zinc nutrition in healthy infants? 405 Jul 28

Elevation of zinc protoporphyrin (ZPP) levels in the blood has served as an indicator of lead poisoning and iron deficiency anemia for many years. We have discovered that sublethal doses of whole body irradiation with x-rays also elevates ZPP 2-3-fold over normal levels. The ZPP level does not begin to increase until days 12-14 postirradiation and peaks between days 18 and 20 before returning to normal levels between days 28 and 35. Increasing the radiation dose delays the onset of the rise in ZPP, but does not affect the magnitude of the elevation. At lethal doses, ZPP elevation is not observed. Neither of the two previously described mechanisms that cause elevations of ZPP, namely iron deficiency and inhibition of ferrochelatase, are responsible for the radiation-induced elevation of ZPP. The elevation of ZPP appears to be correlated with the recovery of the hematopoietic system from radiation injury.
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PMID:The elevation of blood levels of zinc protoporphyrin in mice following whole body irradiation. 632 27

A patient with greatly increased erythrocyte protoporphyrin, but normal porphyrins in urine and feces, is described. The patient later developed a malignant lymphoma, and the reason why she accumulated protoporphyrin in her erythrocytes is not known. The protoporphyrin in the erythrocytes consisted of two types of protoporphyrin, free protoporphyrin (30%) and zinc protoporphyrin (70%). Upon irradiation of erythrocytes in the absence of albumin, protoporphyrin and zinc protoporphyrin, which were both bound to hemoglobin, were released. In contrast, when the irradiation was carried out in the presence of albumin, the photohemolysis was negligible, and there was release of free protoporphyrin, but not of zinc protoporphyrin, from the erythrocytes. In vivo albumin is present in the plasma and the results may help to explain why patients with erythropoietic protoporphyria (erythrocytes containing free protoporphyrin) are photosensitive, whereas patients with lead intoxication and iron deficiency (erythrocytes containing zinc protoporphyrin) are not.
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PMID:Light-induced release of protoporphyrin, but not of zinc protoporphyrin, from erythrocytes in a patient with greatly elevated erythrocyte protoporphyrin. 688 26

Fully crossed, factorially arranged experiments showed that, under defined conditions, interactions occur between nickel and iron, nickel and copper, arsenic and zinc, and possibly vanadium and chromium. Nickel and iron interacted when dietary iron was supplemented as ferric sulfate only. Signs of nickel deprivation were more severe when dietary iron was low; or the signs of moderate iron deficiency were more severe when dietary nickel was deficient. When iron was supplemented to the diet as a 60% ferric-40% ferrous sulfate mixture, nickel and iron apparently did not interact. The findings suggested a synergistic relationship between nickel and iron when dietary iron was in a relatively unavailable form. An antagonistic interaction between nickel and copper was found when dietary iron was supplemented as a 60% ferric-40% ferrous sulfate mixture. Signs of copper deficiency were more severe in nickel-supplemented than in nickel-deprived rats. When the rats were made severely iron deficient by feeding of low levels of ferric sulfate only, no apparent interaction between nickel and copper was found. The interaction between arsenic and zinc apparently was noncompetitive. When dietary zinc was 40 microgram/g, arsenic-deprived chicks exhibited depressed growth and elevated hematocrits. In zinc deficiency, growth was more markedly depressed and hematocrits more markedly elevated in arsenic-supplemented than in arsenic-deficient chicks. Arsenic might be necessary for the efficient utilization or metabolism of zinc. Findings indicating an interaction between vanadium and chromium were tentative. In one experiment, the addition of 500 microgram of chromium/g of diet apparently made 5 micrograms of vanadium/g of diet toxic for chicks. Thus, the interactions between essential trace and ultratrace elements might be of nutritional significance.
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PMID:Interactions between essential trace and ultratrace elements. 694 Apr 72

This article reviews selected nutrition research pertinent to adolescent health care. Protein--calorie malnutrition affects 25% of hospitalized adolescents studied, which correlates, as in adults, with increased morbidity and mortality. Some subgroups of adolescents, notably Asian immigrants, have been shown to be at high risk for developing vitamin D deficient rickets. On the other hand, excessive vitamin D intake has been linked to arteriosclerosis in animal models. Calcium supplementation is not likely to be indicated in U.S. adolescents. Iron deficiency prevalence in adolescence is not well documented, owing to the confusion between anemia and iron deficiency. Serum ferritin and free erythrocyte protoporphyrin measures should help to clarify this issue. Zinc nutrition must be assessed in high-risk groups such as those with short stature or Crohn's disease. Oral contraception effects on vitamin B6 and on serum lipids need to be considered in the risk-benefit equation when prescribing this method of birth control for adolescents.
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PMID:Nutrition and the adolescent: an update. 702 6

For several years, a 4-12-fold increase of the upper normal limit in erythrocyte protoporphyrin concentrations persisted in two men 34 and 39 years of age who were chronically exposed to lead. We are dealing with a zinc protoporphyrinemia in both cases, without lead intoxication or anemia. The 34-year-old had been a regular blood donor for 10 years and had already been treated for iron deficiency several times. Hemoglobin, red cell counts, hematocrit, and iron were at the lower normal limit. The activity of porphobilinogen synthase (PBG-S), uroporphyrinogen-synthase and -decarboxylase as well as urinary porphyrin precursors and porphyrin excretion were normal. Protoporphyrinemia was said to be due to a prelatent/latent iron deficiency. In the 39-year-old, the activity of PBG-S was lowered to 388 mumol/1 . h, as compared to the mean of controls (1,190 +/- 210, x +/- SD, n = 50), in connection with a slightly elevated excretion of delta-aminolevulinic acid and coproporphyrin in the urine and a high-normal blood lead level. In his family there was no history of either a protoporphyrinemia or a hematological disturbance. Six of eight family members in three generations showed a diminished activity of PBG-S: 600 +/- 160, P less than 0.001 compared to controls. These family members are heterozygous with regard to the PBG-S deficiency; they are clinically unobtrusive in comparison to homozygotes with an acute prophyria syndrome. Activation by zinc and reactivation by dithiothreitol were normal in contrast to PBG-S from patients with lead intoxication. The cause of biochemical symptoms of subclinical lead intoxication developed by the propositus is probably due to the hereditary PBG-S deficiency which sensitizes him to low-level lead exposure. The determination of red cell PBG-S activity can be recommended as a test detecting heterozygotes. The hereditary PBG-S deficiency is recognized as a new molecular basis for the pathogenesis of lead intoxication.
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PMID:Persistent protoporphyrinemia in hereditary porphobilinogen synthase (delta-aminolevulinic acid dehydrase) deficiency under low lead exposure. A new molecular basis for the pathogenesis of lead intoxication. 710

We determined the prevalence and optimal methods for laboratory diagnosis of iron deficiency anemia in patients with sickle cell disease. Laboratory investigations of 38 nontransfused and 32 transfused patients included transferrin saturation, serum ferritin, mean corpuscular volume (MCV), and free erythrocyte protoporphyrin (FEP). Response to iron supplementation confirmed the diagnosis of iron deficiency anemia in 16% of the nontransfused patients. None of the transfused patients were iron deficient. All iron-deficient patients (mean age 2.4 yr) had a low MCV, serum ferritin less than 25 ng/ml, transferrin saturation less than 15%, and FEP less than 90 micrograms/dl RBC. Following therapy, all parameters improved and the hemoglobin concentration increased greater than 2 g/dl. A serum ferritin below 25 ng/ml was the most reliable screening test for iron deficiency. There were 13% false positive results with transferrin saturation, 3% with MCV, and 62% with FEP. FEP values correlated strongly with reticulocyte counts. The high FEP was in part due to protoporphyrin IX and not completely due to zinc protoporphyrin, which is elevated in iron deficiency. We conclude that iron deficiency anemia is a potential problem in young nontransfused sickle cell patients. Serum ferritin below 25 ng/ml and low MCV are the most useful screening tests.
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PMID:The diagnosis of iron deficiency anemia in sickle cell disease. 729 5

The content of the microelements (ME) iron, copper and zinc was determined in healthy subjects and patients with iron deficiency anemia (IDA), aged 17 to 86, subdivided into three groups: First group--51 healthy females with iron, copper and zinc levels, close to those reported in literature, the same values used for the control groups. The second group--61 females with IDA had mean copper value higher than the control norms and those of the other authors--23,842 mumol/l (151.48 mkg%). Zinc content in serum was lower than the norm. A parallel determination of serum iron was performed according to Beta-phenantroline method and AAC method with affirmative aim. The IDA group were distributed into three subgroups, depending on the causes, leading to iron deficiency: First subgroup--28 patients with undistinguished cause of iron deficiency: Second subgroup--19 patients with diseases, causing acute and chronic blood losses. Third subgroup--14 patients with various diseases (inflammatory diseases, states after difficult operations, hemopathies, etc.) without blood loss. Low serum iron was found in the three subgroups, determined according to both methods and high ISC. Serum copper level was high in the first and second subgroups, being highest in some patients with uterine myoma and gastric polyps. Serum zinc level was decreased in the second and third subgroups. The normal values of zinc in the serum of the first subgroup were associated with the absence of blood loss. Zinc is recommended to be added to the treatment of IDA.
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PMID:[Iron, copper and zinc content in healthy persons and iron-deficiency anemia patients]. 733 2

Thirty-eight % of obese children and adolescents showed a variable impairment of cell-mediated immune responses in vivo and in vitro and reduction of intracellular bacterial killing by polymorphonuclear leukocytes. The obese group had a higher incidence of iron deficiency and moderately lower serum zinc concentrations. Levels of serum immunoglobulins, complement components C3 and C4, and numbers of T and B lymphocytes were comparable in the two groups. Serum triglycerides, cholesterol and lipoproteins were normal in all subjects. Immunologic changes correlated with the presence of subclinical deficiencies of iron and zinc. Therapy with these micronutrients for 4 weeks resulted in improvement in immunologic responses.
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PMID:Immunocompetence in obesity. 736 8

Dietary iron deficiency enhances the absorption of iron, cobalt, manganese, zinc, cadmium and lead, whereas, iron deficiency due to bleeding increases the absorption of iron, cobalt and perhaps manganese. To determine whether the response to bleeding is qualitatively different from that induced by dietary iron deficiency, metal absorption was studied in mice fed either a high-iron diet (120 ppm Fe) and bled (0.5 ml) or fed a low-iron diet (< 3 ppm Fe). Iron absorption from an intragastric dose was increased by the loss of 0.5 ml of blood; smaller losses of blood had no effect. Also, iron absorption was increased more by dietary iron deficiency than by bleeding. In perfusion experiments, bleeding increased the duodenal absorption of only iron and cobalt, whereas dietary iron deficiency enhanced the absorption of all the metals except cadmium. The patterns of absorptive inhibition of the metals by each other were similar in bled mice and in mice with dietary iron deficiency except that interactions among metals with lower affinities for the iron absorption mechanism--manganese, zinc, cadmium and lead--were more obvious in mice fed the low-iron diet. We concluded that bleeding only partially activates the iron absorptive mechanism and that the lack of a bleeding effect on the absorption of manganese, zinc, cadmium and lead results from the weaker interactions of these metals, with a partly-activated absorption process.
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PMID:Comparative effects of iron deficiency induced by bleeding and a low-iron diet on the intestinal absorptive interactions of iron, cobalt, manganese, zinc, lead and cadmium. 741 Dec 35


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