scholarly journals Tissue iron deficiency and adiposity-related inflammation in disadvantaged preschoolers from NE Brazil

2014 ◽  
Vol 68 (8) ◽  
pp. 887-891 ◽  
Author(s):  
R S Gibson ◽  
K B Bailey ◽  
S Williams ◽  
L Houghton ◽  
H C Costa-Ribeiro ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Tissue Iron ◽  
Disadvantaged Preschoolers

scholarly journals Enzyme-linked Immunosorbent Assay to Measure Serum Ferritin and the Relationship between Serum Ferritin and Nonheme Iron Stores in Cats

1994 ◽  
Vol 31 (6) ◽  
pp. 674-678 ◽  
Author(s):  
G. A. Andrews ◽  
P. S. Chavey ◽  
J. E. Smith
Keyword(s):  
Iron Deficiency ◽  
Serum Ferritin ◽  
Immunosorbent Assay ◽  
Serum Iron ◽  
Nonheme Iron ◽  
Enzyme Linked Immunosorbent Assay ◽  
Ferritin Concentration ◽  
Iron Stores ◽  
Tissue Iron ◽  
Serum Ferritin Concentration

Serum ferritin concentration correlates with tissue iron stores in humans, horses, calves, dogs, and pigs but not in rats. Because serum iron and total iron-binding capacity can be affected by disorders unrelated to iron adequacy (such as hypoproteinemia, chronic infection, hemolytic anemia, hypothyroidism, and renal disease), serum ferritin is probably the most reliable indicator of total body iron stores in larger species. To test the hypothesis that serum ferritin might be correlated with tissue iron levels in cats, we developed a quantitative enzyme-linked immunosorbent assay that uses two monoclonal antibodies in a sandwich arrangement to measure feline serum ferritin. The recovery of purified ferritin added to feline sera ranged from 94% to 104%; the within-assay coefficient of variability was 8.4%, and the assay-to-assay variability was 13.2%. Mean serum ferritin from 40 apparently healthy cats was 76 ng ml (SD = 24 ng/ml). Serum ferritin concentration was significantly correlated ( P < 0.001, n = 101, r = 0.365) with the nonheme iron in the liver and spleen (expressed as milligrams of iron per kilogram of body weight), as determined by Pearson product-moment correlation analysis. Because serum iron can decrease in diseases other than iron deficiency, the combination of serum iron and serum ferritin should provide sufficient evidence to differentiate anemia of chronic inflammation from anemia of iron deficiency in the cat.

scholarly journals Thyroid Status in Patients with Low Serum Ferritin Level

2013 ◽  
Vol 5 (1) ◽  
pp. 5-11
Author(s):  
S Akhter ◽  
ZU Nahar ◽  
S Parvin ◽  
A Alam ◽  
S Sharmin ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Iron Deficiency ◽  
Serum Ferritin ◽  
Serum Ferritin Level ◽  
Ferritin Level ◽  
Thyroid Peroxidase ◽  
Hormone Synthesis ◽  
Tissue Iron ◽  
Iron Deficient ◽  
Significant Difference

Iron deficiency is the most important but preventable nutritional problem in Bangladesh. Thyroid peroxidase, an iron containing enzyme, is essential for initial two steps of thyroid hormone synthesis which is a component of tissue iron. Tissue iron diminishes early in the course of iron deficiency. So thyroid hormone level may be altered in iron deficient patients. This case-control study was carried out in the Department of Biochemistry, Bangabandhu Sheikh Mujib Medical University (BSMMU) from July 2006 to June 2007. This study was done to find out the changes of thyroid hormonal activity in iron deficiency.In this study 72 subjects were selected from the out-patient department of the hospital. Patients with low serum ferritin level <12 mgm/L were selected as cases (n=36) and healthy persons with normal serum ferritin level were taken as controls. Serum ferritin, thyroid stimulating hormone (TSH), free thyroxine (FT4) and free triiodothyronine (FT3) were measured in all study subjects. Values were expressed as mean ± SD. Unpaired 't' test and Pearson's correlation test were performed to see the level of significance and p value <0.05 was taken as significant. Serum ferritin level in cases and controls were 6.78±4.05 mgm/L and 79.04±28.08 mgm/L respectively which showed significant difference (P<0.0001).Serum TSH concentration in cases and controls were 3.32±1.54 mIU/L and 1.89±0.86 mIU/L respectively. Serum FT4 concentration in cases and controls were 11.66±1.77 pmol/L and 13/10±1.36 pmol/L respectively and that of FT3 were 3.00±0.68 and 3.31±0.61 pmol/L respectively. All showed significant difference between groups.Serum ferritin and Serum TSH showed significant negative correlation in controls whereas in cases they showed negative correlation which was not statistically significant.Both serum FT4 and FT3 revealed positive correlation with serum ferritin but that too was not significant statistically.Though the study failed to show any significant positive correlation between serum ferritin and thyroid hormones, lower level of thyroid status in iron deficient patients suggest that it could be a reflection of disturbed activities of iron dependent enzymes such as thyroid peroxidase that impairs thyroid hormone synthesis. However, a large scale study is recommeded to establish the fact.This study showed that there was significant difference in thyroid hormonal status between iron deficient patients and normal healthy persons. Therefore it can be concluded that iron deficiency may impair normal thyroid hormone status. DOI: http://dx.doi.org/10.3329/bjmb.v5i1.13424 Bangladesh J Med Biochem 2012; 5(1): 5-11

scholarly journals An Experimental Model for Iron Deficiency Anemia in Sows and Offspring Induced by Blood Removal during Gestation

Animals ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 2848
Author(s):  
Martin Peter Rydal ◽  
Sheeva Bhattarai ◽  
Jens Peter Nielsen
Keyword(s):  
Iron Deficiency ◽  
Experimental Model ◽  
Iron Deficiency Anemia ◽  
Iron Content ◽  
Deficiency Anemia ◽  
Control Group ◽  
Liver Iron ◽  
Liver Iron Content ◽  
Tissue Iron ◽  
Removal Group

Anemia is a common condition in sow herds. We aimed to study the effects of severe iron deficiency during gestation on sow and piglet health outcomes with an experimental model for blood-removal-induced iron deficiency anemia. In total, 18 multiparous sows (8 in trial I and 10 in trial II) were allocated to either a blood removal group or a control group. Hematologic parameters were monitored at regular intervals and the tissue iron concentrations were measured for the sows and newborn piglets after farrowing. In trial I, the mean liver iron content was reduced to 46.7 µg/g in the blood removal sows compared to 252.6 µg/g in the controls (p < 0.001). In trial II, sows in the blood removal group had lower iron content in the liver (147.8 µg/g), kidney (46.3 µg/g) and spleen (326.5 µg/g) compared to the control sows (323.2 µg/g, 81.3 µg/g and 728.9 µg/g, respectively; p = 0.009, 0.016, 0.01, respectively). In trial I, piglets from sows in the blood removal group had significantly decreased hematocrit (Hct), red blood cells (RBC) and a tendency for reduced hemoglobin (Hb) compared to the control piglets. We established a blood removal model that resulted in mild- to severe degrees of sow anemia and reduced tissue iron stores at farrowing.

scholarly journals Serum transferrin receptor: a quantitative measure of tissue iron deficiency

Blood ◽  
1990 ◽  
Vol 75 (9) ◽  
pp. 1870-1876 ◽  
Author(s):  
BS Skikne ◽  
CH Flowers ◽  
JD Cook
Keyword(s):  
Iron Deficiency ◽  
Serum Ferritin ◽  
Transferrin Receptor ◽  
Iron Status ◽  
Serum Transferrin ◽  
Mean Cell Volume ◽  
Functional Iron Deficiency ◽  
Iron Stores ◽  
Serum Transferrin Receptor ◽  
Tissue Iron

Abstract This study was undertaken to evaluate the role of serum transferrin receptor measurements in the assessment of iron status. Repeated phlebotomies were performed in 14 normal volunteer subjects to obtain varying degrees of iron deficiency. Serial measurements of serum iron, total iron-binding capacity, mean cell volume (MCV), free erythrocyte protoporphyrin (FEP), red cell mean index, serum ferritin, and serum transferrin receptor were performed throughout the phlebotomy program. There was no change in receptor levels during the phase of storage iron depletion. When the serum ferritin level reached subnormal values there was an increase in serum receptor levels, which continued throughout the phlebotomy program. Functional iron deficiency was defined as a reduction in body iron beyond the point of depleted iron stores. The serum receptor level was a more sensitive and reliable guide to the degree of functional iron deficiency than either the FEP or MCV. Our studies indicate that the serum receptor measurement is of particular value in identifying mild iron deficiency of recent onset. The iron status of a population can be fully assessed by using serum ferritin as a measure of iron stores, serum receptor as a measure of mild tissue iron deficiency, and hemoglobin concentration as a measure of advanced iron deficiency.

Effect of iron-deficiency anemia on hormone levels and thermoregulation during cold exposure

1984 ◽  
Vol 247 (1) ◽  
pp. R114-R119
Author(s):  
J. Beard ◽  
W. Green ◽  
L. Miller ◽  
C. Finch
Keyword(s):  
Iron Deficiency ◽  
Cold Exposure ◽  
Hormonal Regulation ◽  
Thyroid Stimulating Hormone ◽  
Cold Sensitivity ◽  
Deficiency Anemia ◽  
Tissue Iron ◽  
Iron Deficient ◽  
Hormone Responses ◽  
O2 Delivery

When exposed to an ambient temperature of 4 degrees C, iron-deficient anemic rats become hypothermic. This lesion is related more to anemia than to tissue iron deficiency, since exchange transfusion to hematocrits over 25 restored normal thermoregulatory performance. Likewise poor cold responses were induced in control rats by transfusion to low hematocrits. Cold sensitivity in all anemic animals was paralleled by poor thyroid responses: there was a significant positive correlation between hematocrit and percent rise in triiodothyronine (r = 0.63) and thyroxine (r = 0.53) during 6 h at 4 degrees C. Basal levels of thyroid-stimulating hormone (TSH) were similar in control and iron-deficient animals: after cold exposure, TSH rose to higher levels in those animals with hematocrits over 25 than in those with lower hematocrits. Diminished O2 delivery to tissues responsible for heat production is probably a major component of the cold sensitivity of anemic rats. The novel finding that thyroid hormone responses are compromised by anemia implies effects on hormonal regulation that may also contribute to this functional lesion.

scholarly journals Dietary-induced gestational iron deficiency inhibits postnatal tissue iron delivery and postpones the cessation of active nephrogenesis in rats

2017 ◽  
Vol 29 (5) ◽  
pp. 855 ◽  
Author(s):  
Mary Y. Sun ◽  
Joseph C. Woolley ◽  
Sharon E. Blohowiak ◽  
Zachary R. Smith ◽  
Ashajyothi M. Siddappa ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Surface Area ◽  
Iron Status ◽  
Weight Ratio ◽  
Planar Surface ◽  
Tissue Iron ◽  
Glomerular Size ◽  
Kidney Maturation ◽  
Iron Delivery ◽  
Nephrogenic Zone

Gestational iron deficiency (ID) can alter developmental programming through impaired nephron endowment, leading to adult hypertension, but nephrogenesis is unstudied. Iron status and renal development during dietary-induced gestational ID (<6 mg Fe kg–1 diet from Gestational Day 2 to Postnatal Day (PND) 7) were compared with control rats (198 mg Fe kg–1 diet). On PND2–PND10, PND15, PND30 and PND45, blood and tissue iron status were assessed. Nephrogenic zone maturation (PND2–PND10), radial glomerular counts (RGCs), glomerular size density and total planar surface area (PND15 and PND30) were also assessed. Blood pressure (BP) was measured in offspring. ID rats were smaller, exhibiting lower erythrocyte and tissue iron than control rats (PND2–PND10), but these parameters returned to control values by PND30–PND45. Relative kidney iron (µg g–1 wet weight) at PND2-PND10 was directly related to transport iron measures. In ID rats, the maturation of the active nephrogenic zone was later than control. RGCs, glomerular size, glomerular density, and glomerular planar surface area were lower than control at PND15, but returned to control by PND30. After weaning, the kidney weight/rat weight ratio (mg g–1) was heavier in ID than control rats. BP readings at PND45 were lower in ID than control rats. Altered kidney maturation and renal adaptations may contribute to glomerular size, early hyperfiltration and long-term renal function.

Chromosomal localization, hematologic characterization, and iron metabolism of the hereditary erythroblastic anemia (hea) mutant mouse

Blood ◽  
2004 ◽  
Vol 104 (5) ◽  
pp. 1511-1518 ◽  
Author(s):  
Robert A. White ◽  
Steven G. McNulty ◽  
Shelly Roman ◽  
Uttam Garg ◽  
Eric Wirtz ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Iron Metabolism ◽  
Serum Iron ◽  
Elevated Serum ◽  
Cell Number ◽  
Chromosome 17 ◽  
Hematopoietic Stem ◽  
Mouse Mutants ◽  
Tissue Iron ◽  
Blood Smears

Abstract Understanding iron metabolism has been enhanced by identification of genes for iron deficiency mouse mutants. We characterized the genetics and iron metabolism of the severe anemia mutant hea (hereditary erythroblastic anemia), which is lethal at 5 to 7 days. The hea mutation results in reduced red blood cell number, hematocrit, and hemoglobin. The hea mice also have elevated Zn protoporphyrin and serum iron. Blood smears from hea mice are abnormal with elevated numbers of smudge cells. Aspects of the hea anemia can be transferred by hematopoietic stem cell transplantation. Neonatal hea mice show a similar hematologic phenotype to the flaky skin (fsn) mutant. We mapped the hea gene near the fsn locus on mouse chromosome 17 and show that the mutants are allelic. Both tissue iron overloading and elevated serum iron are also found in hea and fsn neonates. There is a shift from iron overloading to iron deficiency as fsn mice age. The fsn anemia is cured by an iron-supplemented diet, suggesting an iron utilization defect. When this diet is removed there is reversion to anemia with concomitant loss of overloaded iron stores. We speculate that the hea/fsn gene is required for iron uptake into erythropoietic cells and for kidney iron reabsorption.

scholarly journals Is iron deficiency involved in the pathogenesis of chronic inflammatory skin disorders?

2019 ◽  
Vol 73 ◽  
pp. 359-363
Author(s):  
Małgorzata Ponikowska ◽  
Jacek C. Szepietowski
Keyword(s):  
Iron Deficiency ◽  
Iron Metabolism ◽  
Reticuloendothelial System ◽  
The Body ◽  
Iron Stores ◽  
Iron Supply ◽  
Tissue Iron ◽  
Bowel Disorders ◽  
Dermatological Disorders ◽  
Dermatologic Disease

Iron is an essential microelement in the human body due to its role in hematopoiesis, involvement in energetic processes, synthesis and decomposition of lipids, proteins and nuclear acids. Iron deficiency (ID) is common in healthy populations and also frequently coincides with natural course of chronic diseases. The former is typically present when the overall iron body storages are exhausted (absolute ID), most often due to insufficient iron supply, malabsorption or increased blood loss and coincides with anemia. The latter is a result of defected iron metabolism and reflects a condition, when despite adequate iron stores in the body, iron itself is trapped in the reticuloendothelial system, becoming unavailable for the metabolic processes. It typically occurs in the presence proinflammtory activation in chronic conditions such as chronic kidney disease, inflammatory bowel disorders, malignancies and heart failure. To date there are very few publications concerning the potential role of ID in chronic dermatological disorders. We have recently found that patients with psoriasis demonstrate pattern of ID which can be characterized by negative tissue iron balance with depleted iron stores in the body. Interestingly, presence of ID was not related to the severity of psoriasis, but rather determined by patients low body mass index. We are currently investigating the hypothesis that derangements in iron metabolism resulting in ID can be also present in hidradenitis suppurativa – the other chronic dermatologic disease associated with inflammatory and autoimmune activation.

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