scholarly journals Prognostic aspects of modeling hemogram parameters dynamics at iron-deficient erythropoiesis correction

2009 ◽  
Vol 8 (2) ◽  
pp. 17-22
Author(s):  
I. B. Baranovskaya ◽  
S. A. Onishchuk

Application of mathematical modelling in practical hematology allows to receive new data on process of treatment under the analysis of changes of variable and mathematical parameters. By means of S-functions dynamics of the some erythrocytic and reticulocytic parameters gemogram at 5 patients on a background of treatment iron-deficiency anemias has been investigated Expression of functional dependences in the form of approximated curves has allowed to execute processes interpolation and extrapolation, that is important for the decision of the questions connected with forecasting of change of parameters gemogram and results of treatment.

2017 ◽  
Vol 147 (12) ◽  
pp. 2297-2308 ◽  
Author(s):  
Michael J Wenger ◽  
Laura E Murray-Kolb ◽  
Julie EH Nevins ◽  
Sudha Venkatramanan ◽  
Gregory A Reinhart ◽  
...  

Abstract Background: Iron deficiency and iron deficiency anemia have been shown to have negative effects on aspects of perception, attention, and memory. Objective: The purpose of this investigation was to assess the extent to which increases in dietary iron consumption are related to improvements in behavioral measures of perceptual, attentional, and mnemonic function. Methods: Women were selected from a randomized, double-blind, controlled food-fortification trial involving ad libitum consumption of either a double-fortified salt (DFS) containing 47 mg potassium iodate/kg and 3.3 mg microencapsulated ferrous fumarate/g (1.1 mg elemental Fe/g) or a control iodized salt. Participants' blood iron status (primary outcomes) and cognitive functioning (secondary outcomes) were assessed at baseline and after 10 mo at endline. The study was performed on a tea plantation in the Darjeeling district of India. Participants (n = 126; 66% iron deficient and 49% anemic at baseline) were otherwise healthy women of reproductive age, 18–55 y. Results: Significant improvements were documented for iron status and for perceptual, attentional, and mnemonic function in the DFS group (percentage of variance accounted for: 16.5%) compared with the control group. In addition, the amount of change in perceptual and cognitive performance was significantly (P < 0.05) related to the amount of change in blood iron markers (mean percentage of variance accounted for: 16.0%) and baseline concentrations of blood iron markers (mean percentage of variance accounted for: 25.0%). Overall, there was evidence that the strongest effects of change in iron status were obtained for perceptual and low-level attentional function. Conclusion: DFS produced measurable and significant improvements in the perceptual, attentional, and mnemonic performance of Indian female tea pickers of reproductive age. This trial was registered at clinicaltrials.gov as NCT01032005.


1980 ◽  
Vol 239 (5) ◽  
pp. R377-R381 ◽  
Author(s):  
E. Dillman ◽  
C. Gale ◽  
W. Green ◽  
D. G. Johnson ◽  
B. Mackler ◽  
...  

Iron-deficient rats become hypothermic and have an excessive catecholamine response when exposed to an ambient temperature of 4 degrees C. This is not due to changes in body insulation, since thickness is unaltered, since differences persist after removal of hair, and since cutaneous vasoconstriction is intact. On the other hand, oxygen consumption of iron-deficient animals at 4 degrees C is reduced, 39 +/- 3 ml . kg-1 . min-1 compared to 63 +/- 2 in control animals. Thyroxine (T4) values at 4 degrees C were 4.34 +/- 0.20 microgram/dl sera as compared to control values of 3.6 +/- 0.32. Triiodothyronine (T3) values of iron-deficient animals in the cold were 48 +/- 6.8 ng/dl as compared to 72 +/- 5.6 in control animals. Treatment of iron-deficient animals with iron was shown to normalize the plasma T3 response at 4 degrees C within 6 days. Thyroidectomized iron-deficient animals injected with T3 did not show hypothermia at 4 degrees C, whereas thyroidectomized iron-deficient animals injected with T4 showed hypothermia, increased catecholamines, and decreased T3 levels as compared to non-iron-deficient animals similarly treated. It is proposed that iron deficiency impairs conversion of T4 to T3 and that this is primarily responsible for the hypothermia observed.


2021 ◽  
pp. 1-8
Author(s):  
Kriti Puri ◽  
Joseph A. Spinner ◽  
Jacquelyn M. Powers ◽  
Susan W. Denfield ◽  
Hari P. Tunuguntla ◽  
...  

Abstract Introduction: Iron deficiency is associated with worse outcomes in children and adults with systolic heart failure. While oral iron replacement has been shown to be ineffective in adults with heart failure, its efficacy in children with heart failure is unknown. We hypothesised that oral iron would be ineffective in replenishing iron stores in ≥50% of children with heart failure. Methods: We performed a single-centre retrospective cohort study of patients aged ≤21 years with systolic heart failure and iron deficiency who received oral iron between 01/2013 and 04/2019. Iron deficiency was defined as ≥2 of the following: serum iron <50 mcg/dL, serum ferritin <20 ng/mL, transferrin >300 ng/mL, transferrin saturation <15%. Iron studies and haematologic indices pre- and post-iron therapy were compared using paired-samples Wilcoxon test. Results: Fifty-one children with systolic heart failure and iron deficiency (median age 11 years, 49% female) met inclusion criteria. Heart failure aetiologies included cardiomyopathy (51%), congenital heart disease (37%), and history of heart transplantation with graft dysfunction (12%). Median dose of oral iron therapy was 2.9 mg/kg/day of elemental iron, prescribed for a median duration of 96 days. Follow-up iron testing was available for 20 patients, of whom 55% (11/20) remained iron deficient despite oral iron therapy. Conclusions: This is the first report on the efficacy of oral iron therapy in children with heart failure. Over half of the children with heart failure did not respond to oral iron and remained iron deficient.


2022 ◽  
Author(s):  
Amanda K. Barks ◽  
Montana M. Beeson ◽  
Timothy C. Hallstrom ◽  
Michael K. Georgieff ◽  
Phu V. Tran

Iron deficiency (ID) during neurodevelopment is associated with lasting cognitive and socioemotional deficits, and increased risk for neuropsychiatric disease throughout the lifespan. These neurophenotypical changes are underlain by gene dysregulation in the brain that outlasts the period of ID; however, the mechanisms by which ID establishes and maintains gene expression changes are incompletely understood. The epigenetic modification 5-hydroxymethylcytosine (5hmC), or DNA hydroxymethylation, is one candidate mechanism because of its dependence on iron-containing TET enzymes. The aim of the present study was to determine the effect of fetal-neonatal ID on regional brain TET activity, Tet expression, and 5hmC in the developing rat hippocampus and cerebellum, and to determine whether changes are reversible with dietary iron treatment. Timed pregnant Sprague-Dawley rats were fed iron deficient diet (ID; 4 mg/kg Fe) from gestational day (G)2 to generate iron deficient anemic (IDA) offspring. Control dams were fed iron sufficient diet (IS; 200 mg/kg Fe). At postnatal day (P)7, a subset of ID-fed litters was randomized to IS diet, generating treated IDA (TIDA) offspring. At P15, hippocampus and cerebellum were isolated for subsequent analysis. TET activity was quantified by ELISA from nuclear proteins. Expression of Tet1, Tet2, and Tet3 was quantified by qPCR from total RNA. Global %5hmC was quantified by ELISA from genomic DNA. ID increased DNA hydroxymethylation (p=0.0105), with a corresponding increase in TET activity (p<0.0001) and Tet3 expression (p<0.0001) in the P15 hippocampus. In contrast, ID reduced TET activity (p=0.0016) in the P15 cerebellum, with minimal effect on DNA hydroxymethylation. Neonatal dietary iron treatment resulted in partial normalization of these changes in both brain regions. These results demonstrate that the TET/DNA hydroxymethylation system is disrupted by developmental ID in a brain region-specific manner. Differential regional disruption of this epigenetic system may contribute to the lasting neural circuit dysfunction and neurobehavioral dysfunction associated with developmental ID.


1993 ◽  
Vol 264 (4) ◽  
pp. E662-E667 ◽  
Author(s):  
J. K. Linderman ◽  
P. R. Dallman ◽  
R. E. Rodriguez ◽  
G. A. Brooks

To evaluate the hypothesis that lactate supply is essential to maintain euglycemia during iron deficiency, female Sprague-Dawley rats were assigned to iron-sufficient (50 mg Fe2+/kg diet, +Fe), or iron-deficient (15 mg Fe2+/kg diet, -Fe) dietary groups and were injected with a specific beta 2-adrenergic inhibitor, ICI 118,551 (1.0 mg/kg body wt). Rats were studied at rest or after 30 min of running at 13.4 m/min 0% grade. Dietary iron deficiency decreased hemoglobin concentration 38%, but resting arterial concentrations of glucose ([Glc]), lactate ([La]), or alanine ([Ala]) were unaffected. Administration of ICI 118,551 (beta 2-blockade) decreased [La] and [Glc] 52 and 32% in resting -Fe rats, respectively. beta 2-Blockade attenuated the exercise-induced rise in [La] and decreased [Glc] 31% in exercising -Fe rats. [Ala] were unaffected by iron deficiency or exercise but decreased 24 and 18% because of beta 2-blockade in resting and exercising +Fe rats. Iron deficiency depleted resting liver glycogen concentration 45%, with no additional effect of exercise or beta 2-blockade. beta-Blockade decreased arterial insulin and increased arterial glucagon concentrations in resting -Fe and +Fe rats. During exercise glucagon concentration increased significantly more in -Fe than +Fe rats. Decreased arterial [La] with a corresponding decrease in arterial [Glc] in response to beta 2-blockade support the contention that lactate supply is critical to maintenance of euglycemia in -Fe rats at rest and during exercise.


2016 ◽  
pp. 22-28
Author(s):  
Svitlana Gaidukova ◽  
Stanislav Vydyborets

Modern views of epidemiology, etiology and pathogenesis of iron deficiency anemia (IDA) are considered. This review deals with up-to-date methods of the laboratory diagnostics of IDA. Some ideas of iron methabolism in an organism and pathogenetic mechanisms of clinical and laboratory symptomps are briefly presented. The diagnostic value of laboratory methods for diagnosing IDA is interpreted. A conclusion is drawn about the integrated approach to the diagnostics of IDA diagnostics. Causes of low treatment efficiency are discussed and the ways to address this problem are proposed based on the published results of clinical research. Present article devoted to the steps for implementation unified clinical protocol of the primary, secondary (specialized) medical care “Iron deficiency” to the practical activities.


2000 ◽  
pp. 217-223 ◽  
Author(s):  
M Zimmermann ◽  
P Adou ◽  
T Torresani ◽  
C Zeder ◽  
R Hurrell

OBJECTIVE: In developing countries, many children are at high risk for both goiter and iron-deficiency anemia. Because iron deficiency may impair thyroid metabolism, the aim of this study was to determine if iron supplementation improves the response to oral iodine in goitrous, iron-deficient anemic children. DESIGN: A trial of oral iodized oil followed by oral iron supplementation in an area of endemic goiter in the western Ivory Coast. METHODS: Goitrous, iodine-deficient children (aged 6-12 years; n=109) were divided into two groups: Group 1 consisted of goitrous children who were not anemic; Group 2 consisted of goitrous children who were iron-deficient anemic. Both groups were given 200mg oral iodine as iodized oil. Thyroid gland volume using ultrasound, urinary iodine concentration (UI), serum thyroxine (T(4)) and whole blood TSH were measured at baseline, and at 1, 5, 10, 15 and 30 weeks post intervention. Beginning at 30 weeks, the anemic group was given 60mg oral iron as ferrous sulfate four times/week for 12 weeks. At 50 and 65 weeks after oral iodine (8 and 23 weeks after completing iron supplementation), UI, TSH, T(4) and thyroid volume were remeasured. RESULTS: The prevalence of goiter at 30 weeks after oral iodine in Groups 1 and 2 was 12% and 64% respectively. Mean percent change in thyroid volume compared with baseline at 30 weeks in Groups 1 and 2 was -45.1% and -21.8% respectively (P<0.001 between groups). After iron supplementation in Group 2, there was a further decrease in mean thyroid volume from baseline in the anemic children (-34.8% and -38.4% at 50 and 65 weeks) and goiter prevalence fell to 31% and 20% at 50 and 65 weeks. CONCLUSION: Iron supplementation may improve the efficacy of oral iodized oil in goitrous children with iron-deficiency anemia.


PEDIATRICS ◽  
1983 ◽  
Vol 71 (6) ◽  
pp. 877-880 ◽  
Author(s):  
Frank A. Oski ◽  
Alice S. Honig ◽  
Brenda Helu ◽  
Peter Howanitz

In an effort to determine whether iron deficiency, in the absence of anemia (hemoglobin &gt;11.0 g/dL), might produce alterations in behavioral development, four groups of nonanemic infants, 9 to 12 months of age, with varying degrees of iron deficiency were studied. Infants were classified as iron sufficient, iron depleted, or iron deficient based on measurements of serum ferritin concentration, erythrocyte protoporphyrin values, and the mean cell volume of erythrocytes. Subjects in each group were tested with the Bayley Mental Development Index, treated with parenteral iron, and retested seven days later. The administration of iron produced a significant increase in the Mental Development Index scores (+21.6 points) in the infants with iron deficiency but no significant change in the scores of infants with iron sufficiency (+6.2 points) or only iron depletion (+5.6 points). It is concluded that iron deficiency, even in the absence of anemia, results in biochemical alterations that impair behavior in infants.


PEDIATRICS ◽  
1958 ◽  
Vol 22 (2) ◽  
pp. 258-258

These papers contain much fundamental information concerning the prevention and treatment of iron deficiency anemia in infants and children. Normal children absorb an average of about 10% of the iron in natural foods and commercially-prepared infant cereals supplemented with iron. Daily intake of iron by an infant receiving a diet which includes optimal amounts of iron-containing foods may be sufficient to meet the iron requirements of the first 18 months of life unless the infant is born with suboptimal stores of iron, suffers blood loss or is born prematurely. Such a hypothetical infant is probably not representative of a large segment of the population. The authors suggest that more data is needed on the results of giving adequate supplemental iron during infancy to determine whether the hematologic values in infancy may be made to correspond more closely to adult values. Based on the finding of the previous paper that iron supplementation of the diets of many infants may be desirable, studies were undertaken to evaluate the absorption of iron salts by normal and anemic children. Twelve to fifteen percent of a 30 mg dose of ferrous iron given once or twice a day was absorbed by normal children. Iron deficient infants absorb more ferrous iron than do normal infants. The variability between individuals in absorption of food iron and supplemental iron are discussed along with consideration of the dosage of iron salts to be employed in treatment. The authors state that as no investigations have established the desirability of increasing the normal hematologic values of infants beyond their customary levels of 11 to 13 gm/100 ml, indiscriminate supplementation of normal infants' diets is not recommended. Therapetmtic iron is indicated only if specific evidence of iron deficiency exists and the widespread use of mixtures containing several hematopoietic agents is deplored.


Endocrinology ◽  
2021 ◽  
Author(s):  
Hannah Roberts ◽  
Andrew G Woodman ◽  
Kelly J Baines ◽  
Mariyan J Jeyarajah ◽  
Stephane L Bourque ◽  
...  

Abstract Iron deficiency occurs when iron demands chronically exceed intake, and is prevalent in pregnant women. Iron deficiency during pregnancy poses major risks for the baby, including fetal growth restriction and long-term health complications. The placenta serves as the interface between a pregnant mother and her baby, and ensures adequate nutrient provisions for the fetus. Thus, maternal iron deficiency may impact fetal growth and development by altering placental function. We used a rat model of diet-induced iron deficiency to investigate changes in placental growth and development. Pregnant Sprague-Dawley rats were fed either a low-iron or iron-replete diet starting two weeks before mating. Compared to controls, both maternal and fetal hemoglobin were reduced in dams fed low-iron diets. Iron deficiency decreased fetal liver and body weight, but not brain, heart or kidney weight. Placental weight was increased in iron deficiency, due primarily to expansion of the placental junctional zone. The stimulatory effect of iron deficiency on junctional zone development was recapitulated in vitro, as exposure of rat trophoblast stem cells to the iron chelator deferoxamine increased differentiation toward junctional zone trophoblast subtypes. Gene expression analysis revealed 464 transcripts changed at least 1.5-fold (P&lt;0.05) in placentas from iron-deficient dams, including altered expression of genes associated with oxygen transport and lipoprotein metabolism. Expression of genes associated with iron homeostasis was unchanged despite differences in levels of their encoded proteins. Our findings reveal robust changes in placentation during maternal iron deficiency, which could contribute to the increased risk of fetal distress in these pregnancies.


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