Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “IRON”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed1999

[Storage iron decrease rates and their clinical significance in iron deficiency anemia patients following intravenous iron therapy].

A simple method was devised for determination of the storage iron decrease rate (SID) and the number of days to a recurrent state of iron deficiency. Several patients with iron deficiency anemia were given intravenous doses of iron, and their serum ferritin levels were periodically assayed. A serum ferritin decrease curve was plotted semi-logarithmically; back-extrapolation of that curve yielded the period of days (D) from the starting day of iron supplement therapy to the day by which serum ferritin had decreased to 12 ug/l. The amount of administered iron that was initially stored and eventually lost during period D was calculated by subtracting the amount of iron utilized for hemoglobin increase (R) from the total amount of iron administered (T) to each patient. R was calculated from values for patient body weight and change in hemoglobin concentration prior to and after therapy. SID values were obtained from the following formula: SID = (T-R)/mg/day. SID rates and the number of days to a state of recurrent iron deficiency were measured in 12 patients. SID rates ranged from 0.8 to 9.8 mg/day, and were larger in those patients who exhibited heavier blood loss. A correlation was observed between SID values and the half-times for serum ferritin decrease, as expressed by the equation, Y = 248.5X0.129 (r = 0.129). SID values reflected the negative iron balance of each patient. That observation suggested it should be possible to select a more appropriate intravenous iron does for individual patients if their SID values are taken into full account.

Anemia, Iron-Deficiency↗
PubMed2002

The labile iron pool of hepatocytes in chronic and acute iron overload and chelator-induced iron deprivation.

BACKGROUND: The cytosolic labile iron pool (LIP) is a transitory, catalytically active compartment that has been implicated in cell iron homeostasis and in metal-induced cytotoxicity. AIMS: We attempted to define LIP levels in living hepatocytes derived from chronic overloaded rats and from normal hepatocytes either acutely loaded with iron or depleted by chelation. METHODS: LIP levels were measured in living rat hepatocytes derived from normal and iron-fed rats. RESULTS: Steady-state LIP levels in untreated hepatocytes ( approximately 0.2 microM) were raised by 1.8-fold following iron loading and were reduced by 0.66-fold by short-term chelation treatment. Changes in LIP were accompanied by the corresponding changes in iron-responsive protein (IRP) activity and ferritin levels, that, in rat hepatocytes isolated from chronically loaded animals, raised by approximately 19-fold. CONCLUSIONS: Whereas ferritin levels provide an index of long-term or cumulative iron loading, LIP measurements provide an "instantaneous" parameter of iron availability within hepatocytes. The latter was associated with the cell chelatable pool in cells derived from normal and iron-loaded animals, both of which showed similar accessibility to iron chelators.

Acute Disease↗
PubMedDate not supplied

Anemia associated with changes in iron and iron-59 utilization in copper deficient rats fed high levels of dietary ascorbic acid and iron.

The influence of dietary copper, iron, and ascorbic acid on iron utilization was examined in a 2 x 2 x 2 factorial experiment. Male Sprague-Dawley weanling rats were fed copper-deficient (Cu-, 0.42 microgram Cu/g) or copper-adequate (Cu+, 5.74 micrograms Cu/g) diets that contained one of two levels of iron (38 or 191 micrograms Fe/g) and ascorbic acid (0 or 1% of the diet). These eight diets were fed for 20 d, and rats received an oral dose of 4 microCi iron-59 on d 15. Compared to Cu+ rats, the Cu- rats had 27% lower hemoglobin levels with 45, 59, and 65% lower cytochrome c oxidase (CCO) activities in the liver, heart, and bone marrow, respectively (p less than 0.0001). High dietary iron or ascorbic acid did not alter hemoglobin in Cu+ rats. However, hemoglobin was 23% lower in Cu- rats fed the highest, rather than the lowest levels of iron and ascorbic acid. Liver CCO was decreased (p less than 0.02) in Cu- rats fed high iron. Among Cu- rats, ascorbic acid did not influence CCO but decreased hemoglobin by 17% (p less than 0.001), reduced the percentage of absorbed iron-59 in the erythrocytes by 91% (p less than 0.05) and depressed the percentage apparent absorption of iron (p less than 0.05). These results suggest that the effects of elevated dietary iron and ascorbic acid on iron utilization are influenced by copper status.

Anemia, Hypochromic↗
PubMed1992

Iron absorption from chewable vitamins with iron versus iron tablets: implications for toxicity.

The medical literature contains few, if any, reports of severe iron (Fe) poisonings from ingestion of chewable multivitamins with iron. One possible explanation for this observation is that iron from multivitamins is more poorly absorbed than iron from iron tablets. To compare iron absorption from multivitamins with iron absorption from ferrous fumarate tablets, male adult volunteers were given 6 mg of elemental Fe/kg body weight as chewable multivitamins with iron or as crushed ferrous fumarate tablets in a crossover study. Serum Fe and total iron binding capacity (TIBC) were determined prior to administration of the tablets and one, two, four, and six hours after ingestion. Statistical analyses demonstrated increased and more rapid absorption of Fe from the multivitamin preparation. These results suggest that iron is well absorbed from chewable multivitamins with iron and should theoretically have the potential for producing serious toxicity when taken in overdose. The reasons that such toxicity is not commonly seen clinically are discussed, and a plan for further investigation of this issue is proposed.

Adult↗
PubMed1975

Iron absorption in early pregnancy - a study of the absorption of non-haeme iron and ferrous iron in early pregnancy.

The absorption of non-haeme iron in the food and from a 3 mg reference dose of ferrous iron in solution was measured in 17 healthy women before the 12th week of gestation and in 13 of the women two months after legal abortion. The absorption of ferrous iron in solution was calculated from determinations of the 55Fe activity in blood samples. The food iron absorption was measured from 59Fe-labelled test meals using a highly sensitive whole-body counter. In addition bone-marrow smears and other haematological parameters were studied. The median value of the absorption from the non-haeme food iron was 2.5% and from the ferrous iron salt 10.0 % in early pregnancy in women with storage iron. Two months after abortion the absorption increased to 12.6 and 42.6 % respectively. In early pregnancy the absorption of iron was higher in women without stainable iron in bone-marrow smears. The present results confirm previous observations that the absorption of food iron in early pregnancy is lower than the basal daily requirements. The low absorption is only partly explained by the reduced requirements of iron in early pregnancy. Some other factors related to pregnancy seem also to be involved.

Abortion, Induced↗
PubMed2001

A simple, highly sensitive and improved method for the measurement of bleomycin-detectable iron: the 'catalytic iron index' and its value in the assessment of iron status in haemochromatosis.

In the presence of ferrous ions (Fe(2+)), the anti-tumour agent bleomycin will induce DNA degradation. Degradation of DNA into substances detectable by the thiobarbituric acid test has been used previously for the detection of iron in a form that is capable of catalysing the formation of the potentially harmful hydroxyl free radical. In the present paper, we describe the application of the ethidium-binding assay of DNA damage to the measurement of bleomycin-detectable iron, comparing its performance with the conventional method in the assessment of iron standard solutions and plasma samples from haemochromatosis patients. The ethidium-binding assay proved to be more responsive than the thiobarbituric acid test in the detection of DNA damage induced by very low concentrations of iron, but became saturated at higher iron concentrations. Agreement between the two versions of the assay in the identification of plasma samples containing bleomycin-detectable iron was good, but agreement on the actual concentrations of such iron in the positive samples was poor. This discrepancy is believed to be due to interference with the thiobarbituric acid assay by plasma. Consequently, it was not possible to obtain reliable estimates of free iron concentrations in plasma when using the conventional version of the bleomycin assay. We have devised a parameter of iron status called the catalytic iron index. For healthy, non-haemochromatotic individuals, the mean value of this parameter was found to be 0.81 (range 0.78-0.84; n=20). Elevated values were observed in some plasma samples from haemochromatosis patients, but these showed no correlation with serum ferritin levels. In contrast, correlations were seen with both serum iron and transferrin saturation levels, but only when these were above the normal range.

Antimetabolites, Antineoplastic↗
PubMed1996

Effects of dietary iron loading with carbonyl iron and of iron depletion on intestinal growth, morphology, and expression of transferrin receptor in the rat.

BACKGROUND: The intestine has one of the highest cell turnovers of the body, which is characterised by cell proliferation and differentiation occurring at specified locations along the crypt to the villus axis. These processes require iron for the synthesis of iron-dependent proteins, the supply of which is mediated through the transferrin receptor. In this study, we varied dietary iron intake to determine whether this affected the pattern of transferrin receptor expression and activity on intestinal cell turnover and cell differentiation. METHODS: Variations in iron stores were produced by feeding a control diet and diets high (2% carbonyl iron) or low in iron for 8-10 weeks. Total tissue DNA and the incorporation of thymidine into DNA, and RNA and protein were used as indices of hyperplasia and hypertrophy, respectively. Transferrin receptor expression and activity in the intestinal mucosa were assessed by using in situ hybridisation and the uptake of transferrin-bound 55Fe. RESULTS: Iron loading caused mucosal hypertrophy in the small and large intestines. With all levels of dietary iron transferrin- receptor expression and activity were present within the progenitor and differentiating regions of the mucosa but ceased upon cellular maturation. CONCLUSIONS: Feeding carbonyl iron leads to mucosal hypertrophy. Expression of transferrin receptor mRNA and activity is dependent upon proliferation and differentiation of the mucosal epithelium, regardless of the cellular iron stores within these cells.

Animals↗
PubMed2002

Duodenal mRNA expression of iron related genes in response to iron loading and iron deficiency in four strains of mice.

BACKGROUND: Although much progress has been made recently in characterising the proteins involved in duodenal iron trafficking, regulation of intestinal iron transport remains poorly understood. It is not known whether the level of mRNA expression of these recently described molecules is genetically regulated. This is of particular interest however as genetic factors are likely to determine differences in iron status among mouse strains and probably also contribute to the phenotypic variability seen with disruption of the haemochromatosis gene. AIMS: To investigate this issue, we examined concomitant variations in duodenal cytochrome b (Dcytb), divalent metal transporter 1 (DMT1), ferroportin 1 (FPN1), hephaestin, stimulator of Fe transport (SFT), HFE, and transferrin receptor 1 (TfR1) transcripts in response to different dietary iron contents in the four mouse strains C57BL/6, DBA/2, CBA, and 129/Sv. SUBJECTS: Six mice of each strain were fed normal levels of dietary iron, six were subjected to the same diet supplemented with 2% carbonyl iron, and six were fed an iron deficient diet. METHODS: Quantification of mRNAs isolated from the duodenum was performed using real time reverse transcription-polymerase chain reaction. RESULTS: There was a significant increase in mRNA expression of Dcytb, DMT1, FPN1, and TfR1 when mice were fed an iron deficient diet, and a significant decrease in mRNA expression of these molecules when mice were fed an iron supplemented diet. Strain to strain differences were observed not only in serum transferrin saturations, with C57BL/6 mice having the lowest values, but also in hepatic iron stores and in duodenal mRNA expression of Dcytb, DMT1, FPN1, hephaestin, HFE, and TfR1. CONCLUSIONS: The results favour some degree of genetic control of mRNA levels of these molecules.

Animals↗
PubMed1997

[Iron requirements and iron balance during pregnancy. Is iron supplementation needed for pregnant women?].

Among fertile, nonpregnant, Danish women, 33% have absent or reduced iron stores; 22% have serum ferritin values above 70 micrograms/l, i.e., iron reserves of more than 530 mg, corresponding to the net iron losses during a normal pregnancy. During pregnancy, the demands for absorbed iron increase from 0.8 to 7.5 mg/day. Controlled studies show that iron-treated pregnant women have higher serum ferritin levels, i.e., larger iron stores, and higher haemoglobin levels than placebo-treated women. A supplement of 66 mg ferrous iron daily from the beginning of the 2nd trimester prevents iron deficiency anaemia. In Denmark, general iron prophylaxis with 60-70 mg ferrous iron daily from 20 weeks of gestation is recommended by the health authorities.

Anemia, Iron-Deficiency↗
PubMed1981

Tissue iron, copper and zinc levels in offspring of iron-sufficient and iron-deficient rats.

To study the effects of iron nutriture on tissue iron, copper and zinc contents, we fed iron-deficient or control diets to pregnant rats and their offspring. Pups were weaned to the same or opposite diet as that fed to their dams, yielding four groups: control-control (CC), control-deficient (CD), deficient-control (DC) and deficient-deficient (DD). Offspring were killed at 2, 21, 30, 60 and 90 days of age. Iron deficiency, induced by feeding a 5 ppm iron diet to the dam and/or to the weanlings, resulted in impaired body growth, lower hemoglobin and hematocrit levels and reduced iron levels in liver, spleen and kidney of the offspring. Two-day-old iron-deficient pups had hepatic copper levels 1.5- fold higher than control pups. By the end of the suckling period, hepatic copper levels in iron-deficient pups were 3-fold greater than those of control pups. Hepatic copper concentration in control-fed rats (CC and DC) declined with maturation. In deficient rats (CD and DD), this normal decrease in hepatic copper did not occur and in CD rats, there was a progressive accumulation of copper in the liver. Renal zinc concentrations were lower in CD and DD than in control-fed animals at 60 and 90 days of age. These interactions among iron, copper and zinc may assume clinical importance since iron deficiency is a common nutritional problem.

Aging↗
PubMed1991

[Iron stores, iron deficiency and iron supplementation].

In order to assess the prevalence of iron deficiency in the Danish population, a randomised cross sectional investigation was carried out one year after repealing of the order from 1939 concerning supplementing of corn products with iron. A randomised group of 198 persons divided into ten groups of 20 persons with equal numbers of men and women in the age group 20-69 years was submitted to determinations of serum-iron, serum-transferrin and serum-ferritin. The prevalence of iron deficiency as determined by serum-ferritin values of below 15 micrograms/l was 18% and 12% respectively, for women under and over 45 years while iron deficiency determined by transferrin saturation under 16% was 18% for both groups. 6% of the women under 45 years had severe iron deficiency as determined by low transferrin saturation and low ferritin. The prevalence among men was 1% and 3% as assessed by serum-ferritin levels and transferritin saturation. These results were compared with corresponding population investigations from Sweden where iron enrichment is the highest in the world and the sale of iron tablets is the greatest in the world. No significant differences in the frequency of latent iron deficiency could be demonstrated but the number of persons with severe iron depletion appears to be less in Sweden. Differences in the methodological procedures, however, cannot be excluded.

Adult↗
PubMed2003

Iron deficiency alters iron regulatory protein and iron transport protein expression in the perinatal rat brain.

Iron plays an important role in numerous vital enzyme systems in the perinatal brain. The membrane proteins that mediate iron transport [transferrin receptor (TfR) and divalent metal transporter 1 (DMT-1)] and the iron regulatory proteins (IRP-1 and IRP-2) that stabilize their mRNAs undergo regional developmental changes in the iron-sufficient rat brain between postnatal day (P) 5 and 15. Perinatal iron deficiency (ID) affects developing brain regions nonhomogeneously, suggesting potential differences in regional iron transporter and regulatory protein expression. The objective of the study was to determine the effect of perinatal ID on regional expression of IRP-1, IRP-2, TfR, and DMT-1 in the developing rat brain. Gestationally iron-deficient Sprague Dawley rat pups were compared with iron-sufficient control pups at P10. Serial 12-mu coronal sections of fixed frozen brain from pups on P10 were assessed by light microscopy for IRP-1, IRP-2, DMT-1, and TfR localization. ID did not change the percentage of cells with positive staining for the four proteins in the choroid epithelium, ependyma, vascular endothelium, or neurons of the striatum. ID increased the percentage of neurons expressing the four proteins in the hippocampus and the cerebral cortex. Increased numbers of TfR- and DMT-1-positive cells were always associated with increased IRP-positive cells. The P10 rat responds to perinatal ID by selectively increasing the number of neurons expressing IRP-regulated transporters in brain regions that are rapidly developing, without any change at transport surfaces or in regions that are quiescent. Brain iron distribution during ID seems to be locally rather than globally regulated.

Anemia, Iron-Deficiency↗
PubMed2004

Protection against iron- and hydrogen peroxide-dependent cell injuries by a novel synthetic iron catalase mimic and its precursor, the iron-free ligand.

Hydrogen peroxide is involved in many types of cell injury and exerts most of its injurious effects in conjunction with chelatable iron. We previously described a synthetic nonporphyrin iron-containing catalase mimic, TAA-1/Fe. Its ligand TAA-1 was designed for application in biological systems in which it is supposed to fulfill a dual task: it should chelate cellular labile iron and thus form the active catalase mimic, thereby decreasing levels of redox-active iron and enhancing the degradation of hydrogen peroxide. Here, we tested these novel compounds in cellular systems, i.e., in cultured hepatocytes and liver endothelial cells. Both the iron complex, i.e., the complete mimic, and the ligand, i.e., the putative precursor of this mimic, provided protection against endothelial cell injury induced by exogenous hydrogen peroxide. Furthermore, the ligand--but not (or less so) the complex--strongly protected both cell types against iron-dependent hypothermic injury and hepatocytes against iron-induced cell injury and against iron-dependent, histidine-induced injury. Together, these results demonstrate that the putative catalase mimic precursor TAA-1 is able to protect cells against iron- and/or hydrogen peroxide-dependent cell injuries and that--in line with our initial concept--it is likely to exert its protection by both iron chelation and hydrogen peroxide degradation.

Animals↗
PubMed2006

Iron and infection: effects of host iron status and the iron-regulatory genes haptoglobin and NRAMP1 (SLC11A1) on host-pathogen interactions in tuberculosis and HIV.

There are many lines of evidence illustrating that iron plays a pivotal role in modulating the battle for survival between mammalian hosts and their pathogens. Each displays considerable genetic investment in a wide range of mechanisms for acquiring and maintaining iron. These competitive mechanisms are highly complex, existing within an interacting matrix of absorption, transport, storage and detoxification systems, each of which are iron-responsive and thus able to adapt to the different phases of infection. Considerable genetic polymorphism in some of these systems, with signals of geographic selection in the hosts, and niche selection in the pathogens, indicates that they are critical for species survival. In this review we briefly summarize the role of iron in host immune function before reviewing the available evidence that iron modulates susceptibility and disease outcomes in HIV and TB (tuberculosis). We then examine the putative role of iron-related host genes by focussing on two candidate genes, haptoglobin and NRAMP1, for which there are common polymorphic variants in humans with strong evidence of functionally distinct biochemical phenotypes that would be predicted to influence the course of HIV and TB infections. Finally, we examine the limited evidence so far available that nutrient-gene interactions are likely to influence the way in which gene variants can protect against infection. We conclude that there is a wealth of evidence associating alterations in iron balance and in iron-regulatory systems with disease progression, but that many issues related to the direction of causality, mechanisms of action and sensitivity to pharmacological intervention remain to be elucidated. Since iron is probably the most widely prescribed compound throughout the world, used in both preventative and treatment regimens, a deeper understanding of the host-pathogen interactions relating to iron constitutes an important area for both basic and clinical research.

Cation Transport Proteins↗
PubMed1987

Iron transport in Mycobacterium smegmatis: occurrence of iron-regulated envelope proteins as potential receptors for iron uptake.

Cell-envelope fractions were isolated from the rapidly growing saprophyte Mycobacterium smegmatis following growth in glycerol/asparagine medium under both iron-limited (0.02 microgram Fe ml-1) and iron-sufficient (2.0 to 4.0 micrograms Fe ml-1) conditions. Examination of these preparations by SDS-PAGE demonstrated the production of at least four additional proteins when iron was limiting. These iron-regulated envelope proteins (IREPs) were ascribed apparent molecular masses of 180 kDa (protein I), 84 kDa (protein II), 29 kDa (protein III) and 25 kDa (protein IV). All four proteins were present in both cell-wall and membrane preparations but spheroplast preparations were devoid of the 29 kDa protein. Attempts at labelling the proteins with 55FeCl3 or 55Fe-exochelin, the siderophore for iron uptake, were unsuccessful, though this was attributed to the denatured state of the proteins following electrophoresis. Antibodies were raised to each of the four proteins: the one raised to protein III inhibited exochelin-mediated iron uptake into iron-deficiently grown cells by 70% but was ineffective against iron uptake into iron-sufficiently grown cells. As exochelin is taken up into both types of cells by a similar process, protein III may not be a simple receptor for iron uptake though the results imply some function connected with this process. The role of the other IREPs is less certain.

Antibodies, Bacterial↗
PubMed2003

Effects of iron(II) salts and iron(III) complexes on trace element status in children with iron-deficiency anemia.

Iron-deficiency anemia (IDA) is the most common nutritional deficiency in childhood throughout the world. Although it has been shown that IRA is associated with elevated plasma copper and depleted zinc levels in children, there are conflicting results on the effect of iron supplementation on the absorption of these elements. The aim of this study was to investigate the effects of ferrous and ferric iron supplementation on the trace element status in children (n=25, aged 8-168 mo) with IDA. Fourteen of them were treated with ferric hydroxide-polymaltose complex (Ferrum, Vifor, Switzerland) (6 mg/d in the first 3 mo for initial therapy and 3 mg/kg for 3 mo as maintenance); the others were treated with a ferrous sulfate complex (FerroSanol, Schwarz, Germany) (6 mg/d in the first 3 mo for initial therapy and 3 mg/kg for 3 mo as maintenance). Plasma copper, zinc, and ceruloplasmin levels as well as hematological parameters were determined at baseline and the first, third, and sixth month of the treatment period. The hemoglobin and iron levels of patients in both groups were higher in the first and sixth months compared to baseline. Although the ceruloplasmin levels were depleted (48.9 mg/dL vs 41.4 mg/dL, p=0.035) during ferrous iron treatment, the copper and zinc levels remained unchanged. On the other hand, ferric iron supplementation led to an increase in zinc levels in the sixth month of treatment (0.77 mg/L vs 1.0 mg/L, p=0.021). The plasma copper levels were lower in the ferrous iron-treated group at the end of the first month of treatment than in the ferric irontreated group (1.06 mg/L vs 1.29 mg/L, p=0.008). In conclusion, our data showed that copper and ceruloplasmin metabolisms were affected by ferrous iron supplementation, whereas ferric iron kept them to normal levels of zinc, possibly by affecting their absorption. We conclude that the copper and zinc status of patients with IDA should be taken into consideration before and after iron therapy.

Adolescent↗
PubMed1981

Iron absorption in relation to iron status. Model proposed to express results to food iron absorption measurements.

The absorption from a 3 mg dose of ferrous iron was measured in 250 male subjects. The absorption was related to the log concentration of serum ferritin in 186 subjects of whom 99 were regular blood donors (r = -0.76), and to bone marrow haemosiderin grading in 52 subjects with varying iron status. The purpose was to try and establish a percentage absorption from such a dose that is representative of subjects who are borderline iron deficient. This information is necessary for food iron absorption studies in order (1) to calculate the absorption of iron from the diet at a given iron status and (2) compare the absorption of iron from different meals studied in different groups of subjects by different investigators. The results suggest that an absorption of about 40% of a 3 mg reference dose of ferrous iron is given in a fasting state, roughly corresponds to the absorption in borderline-iron-deficient subjects. The results indicate that this 40% absorption value corresponds to a serum ferritin level of 30 microgram/l and that food iron absorption in a group of subjects should be expressed preferably as the absorption corresponding to a reference-dose absorption of 40%, or possibly a serum ferritin level of 30 microgram/l.

Absorption↗
PubMed2006

Effects of administration of iron, iodine and simultaneous iron-plus-iodine on the thyroid hormone profile in iron-deficient adolescent Iranian girls.

OBJECTIVE: To investigate whether iron supplementation can improve thyroid hormone function in iron-deficient adolescent girls. DESIGN: A double-blind randomized intervention study. SETTING: The study was performed from 2002 through 2003 in the Islamic Republic of Iran. SUBJECTS: 103 iron-deficient non-anaemic girls who fulfilled all inclusion criteria were included, and 94 subjects successfully completed the study. INTERVENTIONS: Patients were randomly assigned to one of four groups and treated with a single oral dose of 190 mg iodine plus 300 mg ferrous sulphate 5 times/week (n=24), 300 mg ferrous sulphate 5 times/week (n=23), a single oral dose of 190 mg iodine (n=25), or a placebo (n=22) for 12 weeks. RESULTS: All groups were comparable at baseline. After the intervention, there was a significant increase in ferritin and transferrin saturation in the iron+iodine group (17.6 vs 8.7 microg/dl, and 18.8 vs 7.2%, respectively, P<0.001 for both) and in the iron group (P<0.001 for both). Urinary iodine doubled in the iron+iodine group and in the iodine group (P<0.001 for both). Thyroid indices tT4, tT3 and T3RU increased and reverse RT3 decreased in the iron+iodine group (10 vs 8.9 microg/dl, P< 0.001; 143 vs 138 microg/dl, P<0.05; 32.3 vs 28.4%, P<0.001 and 24.8 vs 44.2 ng/dl, P<0.001, respectively) and in the iron group. These two groups did not differ for any of the four indices, but both differed significantly from the iodine and placebo groups. CONCLUSIONS: Our results indicate that improvement of iron status was accompanied by an improvement in some indices of thyroid hormones. SPONSORSHIP: This study was supported by the Dean of Research Affairs of the Tehran University of Medical Sciences.

Adolescent↗