• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.9 no.2
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• pp.129-138
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• 2006

Lots of cases relating Helicobacter pylori infection to iron-deficiency anemia have been described in the literature and H. pylori infection has emerged as a cause of refractory iron-deficiency anemia which is unresponsive to oral iron therapy. H. pylori-associated iron-deficiency anemia can be treated by H. pylori eradication. It is not thought to be attributable to gastrointestinal blood loss, such as duodenal ulcer. The mechanism by which H. pylori infection contributes to iron-deficiency anemia remains unclear. However, four possible explanations can be posited for this relationship; occult blood loss secondary to chronic gastritis, reduced iron absorption due to hypo- or achlorhydria, increased iron consumption by H. pylori, and iron sequestration in gastric mucosa. H. pylori-associated iron-deficiency anemia seems to develop in populations at increased risk for iron depletion. When pubescent girls, including athletes, are found to have iron-deficiency anemia refractory to iron administration, they should be evaluated for H. pylori infection.

• Clinical and Experimental Pediatrics
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• v.57 no.8
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• pp.345-350
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• 2014

Iron deficiency affects approximately one-third of the world's population, occurring most frequently in children aged 6 months to 3 years. Mechanisms of iron absorption are similar to those of other divalent metals, particularly manganese, lead, and cadmium, and a diet deficient in iron can lead to excess absorption of manganese, lead, and cadmium. Iron deficiency may lead to cognitive impairments resulting from the deficiency itself or from increased metal concentrations caused by the deficiency. Iron deficiency combined with increased manganese or lead concentrations may further affect neurodevelopment. We recently showed that blood manganese and lead concentrations are elevated among iron-deficient infants. Increased blood manganese and lead levels are likely associated with prolonged breast-feeding, which is also a risk factor for iron deficiency. Thus, babies who are breast-fed for prolonged periods should be given plain, iron-fortified cereals or other good sources of dietary iron.

• Journal of the East Asian Society of Dietary Life
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• v.16 no.1
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• pp.93-98
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• 2006

This study examined whether or not the iron that is accumulated in the recombinant microbes that produce ferritin is bioavailable to rats with iron deficiency. Rats induced with iron deficiency were treated with iron preparations of $Fe(NH_4)_2(SO_4)_2$, horse spleen ferritin, control yeast, and ferritin-producing recombinant yeast for 14 days. The bioavailability of iron was examined by measuring hemoglobin concentration, hematocrit value, and tissue iron stores. Differences between dietary groups were determined by one-way ANOVA, at the level of significance p<0.05. Based on hemoglobin concentration and hematocrit value, iron in $Fe(NH_4)_2(SO_4)_2$, horse spleen ferritin, and ferritin-producing yeast were bioavailable in rats and cured iron deficiency. The efficacy of ferritin and ferritin-producing yeast was confirmed in establishing tissue iron stores after the induction of iron deficiency. The iron sources of ferritin and the ferritin-producing yeast seemed to be as effective for the recovery from iron deficiency as the iron compounds of ferric citrate and ferrous ammonium sulfate. The results suggest that the iron stored in ferritin of the recombinant yeast is bioavailable, and that the recombinant yeast may contribute widely as a source of iron to resolve the global problem of iron deficiency.

• The Korean Journal of Nuclear Medicine
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• v.10 no.1
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• pp.21-34
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• 1976

The diagnosis of iron deficiency rests upon the correct evaluation of body iron stores. Morphological interpretation of blood film and the red cell indices are not reliable and often absent in mild iron deficiency. Serum iron levels and iron-binding capacity are more sensitive indices of iron deficiency, but they are often normal in iron depletion and mild iron deficiency anemia. They are also subject to many variables which may introduce substantial errors and influenced by many pathologic and physiologic states. Examination of the bone marrow aspirate for stainable iron has been regarded as one of the most sensitive and reliable diagnostic method for detecting iron deficiency, but this also has limitations. Thus, there is still need for a more practical, but sensitive and reliable substitute as a screening test of iron deficiency. Pollack et al. (1965) observed that the intestinal absorption of cobalt was raised in iron-deficient rats and Valberg et al. (1969) found that cobalt absorption was elevated in patients with iron deficiency. A direct correlation was demonstrated between the amounts of radioiron and radiocobalt absorbed. Unlike iron, excess cobalt was excreted by the kidney, the percentage of radioactivity in the urine being directly related to the percentage absorbed from the gastrointestinal tract. Recently a test based on the urinary excretion of an oral dose of $^{57}Co$ has been proposed as a method for detecting iron deficiency. To assess the diagnostic value of urinary cobalt excretion test cobaltous chloride labelled with $1{\mu}Ci\;of\;^{58}Co$ was given by mouth and the percentage of the test dose excreted in the urine was measured by a gamma counter. The mean 24 hour urinary cobalt excretion in control subjects with normal iron stores was 6.1% ($1.9{\sim}15.2%$). Cobalt excretion was markedly increased in patients with iron deficiency and excreted more than 29% of the dose. In contrast, patients with anemia due to causes other than iron deficiency excreted less than 27%. Hence, 24 hour urinary cobalt excretion of 27% or less in a patient with anemia suggets that the primary cause of the anemia is not iron deficiency. A value greater than 27% in an anemic subject suggests that the anemia is caused by iron deficiency. The cobalt excretion test is a simple, sensitive and accurate method for the assessment of body iron stores. It may be particularly valuable in the epidemiological studies of iron deficiency and repeated evaluations of the body iron stores.

• Journal of Sport and Applied Science
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• v.6 no.4
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• pp.11-23
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• 2022

New insights into the aetiology of anaemia in athletes have been discovered in recent years. From hemodilution and redistribution, which are thought to commit to so-called "sports anaemia," to iron deficiency triggered by higher requirements, dietary requirements, decreased uptake, enhanced losses, hemolysis, and sequester, to genetic factors of different types of anaemia (some related to sport), anaemia in athletes necessitates a careful and multisystem methodology. Dietary factors that hinder iron absorption and enhance iron bioavailability (e.g., phytate, polyphenols) should be considered. Celiac disease, which is more common in female athletes, may be the consequence of an iron deficiency anaemia that is unidentified. Sweating, hematuria, gastrointestinal bleeding, inflammation, and intravascular and extravascular hemolysis are all ways iron is lost during strength training. In training, evaluating the iron status, particularly in athletes at risk of iron deficiency, may work on improving iron balance and possibly effectiveness. Iron status is influenced by a healthy gut microbiome. To eliminate hemolysis, athletes at risk of iron deficiency should engage in non-weight-bearing, low-intensity sporting activities.

• The Journal of Internal Korean Medicine
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• v.30 no.1
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• pp.228-232
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• 2009

Objective : To expend the oriental medicine-based strategies or therapeutics for anemia, including iron deficiency anemia. Methods : A 23 year-old man suffering from severe and chronic iron deficiency anemia was believed to have disorder of iron absorption. He had neither specific medical cause nor positive response to western treatments. Blood and biochemical parameters such as levels of hemoglobin, ferritin, transferrin and serum iron were serially chased during treatments. Result : Bojungicki-tang was given to the patient based on diagnosis as a deficiency of spleen qi. The hemoglobin level was normalized along with administration of Bojungicki-tang. Also, the distortions of biochemical indicators (ferritin, transferrin and serum iron) reached a normal range within three months. Conclusion : Bojungicki-tang could be a curing remedy for iron deficiency anemia caused by problems in iron absorption if symptom-differentiation has deficiency of spleen qi.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.5 no.2
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• pp.129-135
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• 2002

Purpose: The purpose of this study was to investigate the relationship between Helicobacter pylori (H. pylori) infection and iron-deficiency anemia in pubescent children, susceptible to iron deficiency due to the high iron requirements for growth. Methods: Hemoglobin, serum iron, total iron-binding capacity, serum ferritin, and serum IgG antibodies to H. pylori were measured in 937 children (475 boys and 462 girls). Their ages ranged from 10 to 18 years. The prevalences of H. pylori infection were compared between groups, based on the presence or absence of anemia, hypoferritinemia, iron deficiency, and iron-deficiency anemia. The levels of hemoglobin, serum iron, total iron-binding capacity, transferrin saturation, and serum ferritin were obtained according to the presence or absence of H. pylori infection. Results: The prevalences of anemia, iron deficiency, iron-deficiency anemia, and H. pylori infection were 8.1%, 9.1%, 3.1%, and 20.8%, respectively. The H. pylori-positive rates in anemia, hypoferritinemia, and iron-deficiency group were 34.2%, 29.5%, and 35.3%, respectively, compared to 19.6% in the non-anemia group, 19.2% in the non-hypoferritinemia group, and 19.4% in the non-iron deficiency group. The H. pylori-positive rate in the iron-deficiency anemia group was 44.8% in comparison with 20.0% in the non-iron-deficiency anemia group. Hemoglobin and iron levels did not show any significant differences between the H. pylori-positive and -negative groups, whereas the serum ferritin level decreased significantly in the H. pylori-infected group. Conclusion: H. pylori infection is thought to be associated with iron deficiency in pubescent children.

• Nutrition Research and Practice
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• v.9 no.6
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• pp.613-618
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• 2015

BACKGROUND/OBJECTIVES: Iron deficiency in early life is associated with developmental problems, which may persist until later in life. The question of whether iron repletion after developmental iron deficiency could restore iron homeostasis is not well characterized. In the present study, we investigated the changes of iron transporters after iron depletion during the gestational-neonatal period and iron repletion during the post-weaning period. MATERIALS/METHODS: Pregnant rats were provided iron-deficient (< 6 ppm Fe) or control (36 ppm Fe) diets from gestational day 2. At weaning, pups from iron-deficient dams were fed either iron-deficient (ID group) or control (IDR group) diets for 4 week. Pups from control dams were continued to be fed with the control diet throughout the study period (CON). RESULTS: Compared to the CON, ID rats had significantly lower hemoglobin and hematocrits in the blood and significantly lower tissue iron in the liver and spleen. Hepatic hepcidin and BMP6 mRNA levels were also strongly down-regulated in the ID group. Developmental iron deficiency significantly increased iron transporters divalent metal transporter 1 (DMT1) and ferroportin (FPN) in the duodenum, but decreased DMT1 in the liver. Dietary iron repletion restored the levels of hemoglobin and hematocrit to a normal range, but the tissue iron levels and hepatic hepcidin mRNA levels were significantly lower than those in the CON group. Both FPN and DMT1 protein levels in the liver and in the duodenum were not different between the IDR and the CON. By contrast, DMT1 in the spleen was significantly lower in the IDR, compared to the CON. The splenic FPN was also decreased in the IDR more than in the CON, although the difference did not reach statistical significance. CONCLUSIONS: Our findings demonstrate that iron transporter proteins in the duodenum, liver and spleen are differentially regulated during developmental iron deficiency. Also, post-weaning iron repletion efficiently restores iron transporters in the duodenum and the liver but not in the spleen, which suggests that early-life iron deficiency may cause long term abnormalities in iron recycling from the spleen.

• Journal of Yeungnam Medical Science
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• v.20 no.2
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• pp.206-211
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• 2003

Simultaneous deficiency of Vitamin $B_{12}$ and iron induces that the bone marrow erythroid megaloblastosis and peripheral blood macroovalocytosis are masked because of countervailing the tendency of iron deficiency to produce hypochromic microcytic erythrocytes. We report two cases of Vitamin $B_{12}$ deficiency anemia with low mean corpuscular volume (MCV) due to combined iron deficiency anemia with review of literature.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.12 no.sup1
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• pp.46-52
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• 2009

As the most common nutrition deficiency, iron deficiency not only causes anemia but also influences the central nervous system development. Its pathogenesis is supposed to be the alteration of neurometabolism and neurotransmission in major brain structures, and the disruption of myelination. The first two years after birth is a crucial period for cognitive, behavior, and emotional development with fast brain growth. If iron deficiency occurs in this period, cognitive and psychomotor function cannot be restored in spite of adequate iron supplementation. Thus, iron deficiency in infancy should be considered as a serious disease.