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

The world's leading nutritional problem is iron deficiency. 66% of children and women aged 15-44 years in developing countries have it. Further, 10-20% of women of childbearing age in developed countries are anemic. Iron deficiency is identified with often irreversible impairment of a child's learning ability. It is also associated with low capacity for adults to work which reduces productivity. In addition, it impairs the immune system which reduces the body's ability to fight infection. Iron deficiency also lowers the metabolic rate and the body temperature when exposed to cold. Hemoglobin contains nearly 73% of the body's iron. This iron is always being recycled as more red blood cells are made. The rest of the needed iron does important tasks for the body, such as binds to molecules that are reservoirs of oxygen for muscle cells. This iron comes from our diet, especially meat. Even though some plants, such as spinach, are high in iron, the body can only absorb 1.4-7% of the iron in plants whereas it can absorb 20% of the iron in red meat. In many developing countries, the common vegetarian diets contribute to high rates of iron deficiency. Parasitic diseases and abnormal uterine bleeding also promote iron deficiency. Iron therapy in anemic children can often, but not always, improve behavior and cognitive performance. Iron deficiency during pregnancy often contributes to maternal and perinatal mortality. Yet treatment, if given to a child in time, can lead to normal growth and hinder infections. However, excess iron can be damaging. Too much supplemental iron in a malnourished child promotes fatal infections since the excess iron is available for the pathogens use. Many countries do not have an effective system for diagnosing, treating, and preventing iron deficiency. Therefore a concerted international effort is needed to eliminate iron deficiency in the world.
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PMID:Iron deficiency. 174

During a health survey for chest disease in Ladakh, it was noted that women and a few men had marked koilonychia. It caused disfigurement, discomfort and sometimes disturbance of function. It occurred mainly in spring and summer and usually disappeared in winter. It is thought to be due to exposure to cold wet mud while repairing walls and irrigation canals. There was no evidence of iron deficiency.
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PMID:Seasonal koilonychia in Ladakh. 232 7

Iron-deficient anemic rats have previously been shown to have low plasma levels of thyroid hormone and a poor plasma thyroid hormone response to acute cold exposure. As an initial exploration, we examined thyroid hormone metabolism during iron deficiency in age-matched rats from three aspects: 1) plasma TSH (thyrotropin, thyroid stimulating hormone), T4 (thyroxine) and T3 (triiodothyronine) responses to graded doses of exogenous TRH (thyrotropin releasing hormone), 2) plasma T3 kinetics, and 3) rates of hepatic T3 production. Iron-deficient anemic rats had lower basal TSH values and blunted TSH responses to intravenous TRH injection at three different doses (10, 25 and 50 ng TRH/100 g body wt). Iron-deficient anemic rats also had a significant decrease in plasma T3 turnover (42 vs. 88 ng/h in controls), and significantly lower hepatic T4-5'-deiodinase activities than controls [26 vs. 44.0 ng T3/(mg protein.20 min)]. Thus, decreased rates of T3 production in iron-deficient anemic rats, as documented by turnover studies, may be related to decreased deiodinase activity and reduced peripheral formation of T3. The dampened TSH responses to TRH further facilitate or perpetuate this T3 deficiency. We propose that this abnormal thyroid state is partially responsible for impaired thermogenesis in iron-deficiency anemia.
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PMID:Evidence for thyroid hormone deficiency in iron-deficient anemic rats. 249 73

Most of the previous studies on the effects of iron deficiency on skeletal muscle respiratory capacity and work performance have been investigated in severe or moderate iron-deficiency anemia. We report here that even in mild iron deficiency where the hemoglobin concentration was 10 g/dl and the iron stores in livers and spleen were not completely depleted, a marked reduction in succinate dehydrogenase was observed in skeletal muscles but not in heart. Similarly, cytochrome oxidase activities were reduced. Although no significant change in glycerophosphate dehydrogenase was detected in the iron-deficient rats, exposure to cold in this group greatly reduced this enzyme activity. As cold acclimatization accelerates marrow erythropoiesis (20) which in turn, demands more iron, it seems that in the iron-insufficient state, this iron demand for marrow activity may persist at the expense of the tissue iron pool, resulting in a marked reduction in glycerophosphate dehydrogenase activities. Since succinate dehydrogenase plays a significant role in the impairment of mitochondrial function and early fatigue of iron-deficient muscle (11), the present study shows that even in mild iron deficiency, some loss of muscle functions could result as succinate dehydrogenase activities were greatly reduced.
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PMID:Biochemical effects of mild iron deficiency and cold acclimatization on rat skeletal muscle. 300 73

1. We present the results of a study of the prevalence of anemia and its causes in the population of Ecuador. The following parameters were used: blood cytology, reticulocyte count, serum iron, iron binding capacity, ferritin, folic acid and vitamin B 12 concentration. 2. The study was carried out on 4 groups: 426 individuals of both sexes and all ages from the rural population of the lowlands, with a warm and humid climate; 226 individuals from the highlands, with a cold and dry climate; 1000 individuals of the urban working group from the lowlands; and 1000 individuals of the urban working group from the highlands. All subjects were chosen randomly. 3. The prevalence of anemia was 31.4% in the rural group from the lowlands, 27.9% in the rural group from the highlands, 5.5% in the urban group from the lowlands, and 2.7% in the urban group from the highlands, with an overall estimated prevalence of 20.6% for the population of Ecuador as a whole. Iron deficiency was the most frequent cause of anemia (91.3%; 18.7% of the total population), followed by bone marrow failure (6%; 1.2% of the total population), hemolysis (2.2%; 0.5% of the total population), and finally megaloblastic anemia (0.5%; 0.1% of the total population). 4. Since iron deficiency with and without anemia is very frequent, we believe it is justified to establish mechanisms for food iron enrichment for liable groups such as children and pregnant women from marginal areas.
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PMID:Prevalence of different types of anemia in Ecuador. 326 72

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.
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PMID:Effect of iron-deficiency anemia on hormone levels and thermoregulation during cold exposure. 674 20

We have earlier shown that iron-deficient rats have increased urinary norepinephrine (NE) excretion. They also have an exaggerated rise in urinary NE when placed in the cold, a stimulus known to cause increased NE excretion in normal rats. Nonetheless, they fall to maintain body temperature. We have now examined the thyroidal response to cold in iron-deficient rats. As others have shown, control rats had a rise in plasma levels of thyroxine (T4) and triiodothyronine (T3) soon after entering the cold environment (4 degree C); they also maintained a rectal temperature above 36 degree C. In the iron-deficient rats, basal levels of T3 and T4 were normal, but there was little or no increase after 6 hr in the cold, and, as before, body temperatures fell. Injections of T3, 10 microgram/kg, 15 min before cold exposure improved the ability of iron-deficient rats to maintain body temperature, but they still did not do as well as the controls. We conclude that the inability of iron-deficient rats to increase T3 levels after cold exposure is one factor in their poor resistance to cold. The defect could involve inability to augment thyroid secretion, imparied ability to convert T4 to T3 in peripheral tissues, or both. Preliminary data suggest that anemia is an important and perhaps critical factor in the cold sensitivity of iron deficiency. Transfusing iron-deficient rats from their usual hematocrit of 15-20 to one of 30 restores cold resistance to normal. Transfusion also allows a more normal thyroid response, with a rise in T3 and T4 levels, so thyroid hormones may be a factor in the improvement produced by transfusion.
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PMID:Interactions of iron deficiency, anemia, and thyroid hormone levels in response of rats to cold exposure. 707 Feb 26

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.
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PMID:Hypothermia in iron deficiency due to altered triiodothyronine metabolism. 743 50

The effect of sucrose overfeeding and low iron diet on brown adipose tissue (BAT) thermogenesis of rats has been investigated from the view point of in vitro BAT oxygen consumption and BAT fatty acids (FA) compositions in rats. Control group was fed on a standard diet with tap water, sucrose group was on the standard diet and 32% sucrose solution, and iron deficient group on a low iron diet with tap water. In vitro interscapular BAT thermogenesis as estimated by oxygen consumption was measured in minced tissue blocks in Krebs-Ringer phosphate buffer using a Clark oxygen electrode. In sucrose overfeeding rats, caloric intake was greater than in controls, but did not differ body weight. Interscapular BAT weight and DNA content were greater. Colonic and tail skin temperatures were higher. Basal oxygen consumption was higher. Noradrenaline- and glucagon-stimulated oxygen consumptions did not differ when expressed per DNA, but significantly greater per whole tissue pad. Both BAT-triglyceride (TG) and -phospholipid (PL) levels were higher. Polyunsaturated FA were lower, while monosaturated FA were higher in both BAT-TG and -PL. In iron deficient rats, BAT weight and DNA content were higher. Colonic and tail skin temperatures did not differ. Although basal oxygen consumption did not differ, noradrenaline-stimulated oxygen consumption was less per DNA, but did not differ per whole tissue pad, while glucagon-stimulated oxygen consumption was less when expressed per DNA, as well as whole tissue pad. Cold-tolerance as assessed by the fall in colonic temperature at 0 degree C was decreased. BAT-TG and -PL levels did not differ. Polyunsaturated FA were higher in both BAT-TG and -PL. These findings indicated that sucrose-induced overfeeding enhances BAT thermogenesis mainly by tissue hyperplasia, while iron deficiency suppresses BAT thermogenic response, although it causes the compensatory tissue hyperplasia.
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PMID:[Nutritional adaptation in brown adipose tissue thermogenesis--with special reference to overfeeding and iron deficiency]. 786 52

Anemia does not correct in many kidney transplant recipients, probably due to iron deficiency or inadequate erythropoietin (Epo) production. We evaluated effects of iron (Fe) availability on correction of anemia in renal transplant recipients and sought to characterize patterns of early Epo production by transplanted kidneys as related to peritransplant factors. In a prospective randomized trial, 51 consecutive renal transplant patients were followed for 6 months. Epo was measured on days 0, 3, 14, 48 and 168 posttransplantation. Fe status was monitored on days 14, 48 and 168. Pts were randomized at day 14 based on Fe status. Iron-deficient (FeD) patients (n = 24) were randomized to receive daily Fe supplementation (FeDs, n = 12) or no supplementation (FeDns, n = 12). Those with normal Fe status (FeN, n = 27) were followed as controls. No differences were found between groups at day 0 for Hct, Cr, Epo, age, dialysis history, or type of donor. Day 3 Creatinine and Hct were similar among groups, while Epo was significantly higher in FeD groups vs FeN (p < 0.004), and continued higher at 6 months. Though each pt improved Hct, most FeDns and FeN were anemic and Fe deficient at 6 months while all FeDs patients had corrected their anemia (p < or = 0.009) and Fe status. Four FeDs patients developed polycythemia. Epo production correlated inversely to cold ischemia time in cadaver renal allografts (p < 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Factors affecting erythropoietin production and correction of anemia in kidney transplant recipients. 794 39


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