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

Iron deficiency is one of the most serious nutritional problems confronting the United States and the world today. An understanding of the mechanisms operative in the control of uptake and utilization of iron is essential to develop suitable prophylactic and therapeutic strategies. Iron excess can also be a serious health hazard. Studies on Bantu siderosis, hemochromatosis and other overload pathologies also provide insight into the intake and storage of this metal. Several models for iron transport across the mucosal membrane are developed. The most satisfactory seems to involve chelation of the iron to provide solubility diffusion passively across the gut membrane, and equilibrium binding to various storage sites within the tissue. Both ferric and ferrous forms are available. The solution chemistry of iron governs its biological behavior. Low-molecular-weight compounds present in normal dietary foodstuffs, as well as those prepared synthetically, can enhance the uptake of oral iron. Suitable application of complexes of iron with fructose, nitrilotriacetate, citrate and other molecules should be efficacious in the treatment of iron deficiency anemia. Potential dangers of food fortification with iron are acknowledged, and application of immunoassay techniques for measuring circulating ferritin suggest it as a rapid and inexpensive monitor for overload.
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PMID:Tired blood and rusty livers. 125 66

A combination of biochemical quantitation and immunohistochemistry has been used to examine in detail transferrin receptor distribution and expression in the rat small intestine and its relationship to iron absorption. Receptor numbers were quantitated by transferrin binding to preparations of basolateral or brush-border membranes. Receptors were demonstrated on the basolateral membranes of the gut cells, but not on the brush-border fraction. Apotransferrin demonstrated little binding to basolateral membranes at physiological pH. Dietary or parenteral iron loading of animals produced a significant decline in transferrin binding, whereas binding was increased in iron deficiency. These data were confirmed by immunohistochemical studies using a monoclonal antibody to the transferrin receptor. When iron absorption was increased threefold following acute hemolysis and without a decrease in body iron stores, there was no change in transferrin receptor number. These data indicate that intestinal transferrin receptors may be regulated by body iron stores but suggest that they are not directly involved in iron absorption.
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PMID:Transferrin receptor distribution and regulation in the rat small intestine. Effect of iron stores and erythropoiesis. 229 64

Rats raised on a low-iron diet were used as a model system for investigating the regulation of transferrin gene expression by iron deficiency. We quantitated transferrin mRNA in a variety of tissues from normal and iron-deficient rats and found that the level of transferrin mRNA in normal rat liver was about 6500 molecules per cell, while the level in iron-deficient animals was 2.4-fold higher. The increase of transferrin mRNA in iron deficiency was the result of a specific induction of transferrin gene transcriptional activity as measured in isolated nuclei. This increase in transferrin gene expression resulted in a corresponding increase in serum total-iron-binding capacity. Of the other tissues examined, moderate amounts of transferrin mRNA were found in brain (83 molecules per cell) and testis (114 molecules per cell), and low levels were measured in spleen and kidney. The transferrin mRNA content of brain, testis, spleen, and kidney remained unchanged in iron deficiency. The small intestine had no detectable transferrin mRNA in either normal or iron-deficient rats; however, transferrin protein was present, and its level was 2-fold higher in the iron-deficient group. We hypothesize that intestinal transferrin is synthesized in the liver and is delivered to the gut via the bile. Consistent with this idea, bile transferrin content was found to be elevated in iron deficiency and appeared to be sufficient to account for intestinal transferrin levels. In addition, treatment of plasma transferrin with bile caused an acidic shift in its isoelectric-focusing behavior so that it comigrated with intestinal transferrin.
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PMID:Rat transferrin gene expression: tissue-specific regulation by iron deficiency. 345 51

The authors executed a study on the levels of T lymphocytes and of serum Fe, Zn and Cu in 50 atopic children. The boys showed a various pathology who included the eczema, the laryngotracheobronchostenosis, the choanal obstruction and/or the adenoid's obstruction, abdominal pains, stomatitis, relapsing herpes, shock, neurosis. The T4/T8 relationship resulted lower in the 34.5% of subjects, higher in the 30.5% normal in the 35.5%. In the patients with hyper-IgE the 28.2% of children showed this relationship in the normality, but in the children with a heavy atopic syndrome and normal IgE only the 7.3% of subjects showed the T4/T8 relationship in the normality. The authors dwell on the heavy iron deficiency (72%) and of the Zn (52%) and of the Cu (33%) in the serum present in these subjects. The authors suppose that these changes come from a short absorption of these ions coming from the epithelial gut's damage caused by the daily ingestion of food allergens.
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PMID:[Immunological and trace element study in 50 children with various diseases caused by food allergens and aeroallergens]. 350 23

To evaluate the incidence of either evident anemia or a subclinical status of iron deficiency in celiac disease (CD), we studied 80 celiac children aged 6 months to 18 years. They were subdivided into various groups according to morphology of gut mucosa and diet. Only eight of 47 celiac children had an evident anemia at the time of the first peroral bowel biopsy. In addition, 51% of the patients with atrophic mucosa and 56% of the children on a gluten-containing diet had serum iron levels less than 50 micrograms/dl; 35% of patients of both groups had serum ferritin levels less than 12 micrograms/L. On the contrary, only a small number of children with normal mucosa on a gluten-free diet showed a laboratory, subclinical picture of iron deficiency. The results of our study can therefore be summarized in three major items: (a) Low levels of both serum iron and ferritin can frequently be found during active CD. (b) Regular determination of serum iron levels appears to be useful in controlling the state of iron stores in such patients, as well as in deciding whether and when to recommend temporary iron supplementation. (c) Serum ferritin tests did not offer more information than the easier and cheaper serum iron determinations.
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PMID:Iron deficiency in children with celiac disease. 369 63

Intestinal iron absorption studies, which include investigation of iron deficiency, increased erythropoiesis, low iron diet and acute bleeding, have been done, but none have reported the regulation of the balance of an iron-replete individual. We bled rats at regular time intervals, such that the experimentally induced iron losses were compensated by iron from storage and nutritional procurement without the onset of anemia. During these experimental periods the hemoglobin and plasma iron concentrations were determined along with repeated histochemical gradings of the bone marrow iron. We determined the intestinal iron absorption at regular intervals after having established its relation to the intragastric ferrous iron dose. The results obtained show that regular bleedings of 15-20% of the total blood volume every 10 days or twice a week, respectively, are compensated completely by storage and nutritional iron procurement without the onset of anemia. The intestinal iron absorption is increased 4 hours after an acute bleeding and was found high during the period that the animals were bled every 10 days. Significant changes of the plasma iron concentration, mostly within the "normal range" are invariably associated with experimental changes in bleeding regimes. The observed increases of the intestinal absorption of a ferrous iron test dose and decreases of the plasma iron concentrations that precede the depletion of the histochemically graded bone marrow iron are interpreted by a modification of a reported model, in which the process of iron release into the plasma from the reticuloendothelial system and the gut mucosa is linked closely to the actual plasma iron concentration.
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PMID:Chronic experimental iron losses in rats not leading to overt iron deficiency: a model for the regulation of the whole-body iron balance in an iron-replete condition. 672 69

The main biological sign of inflammation is an increase in erythrocyte sedimentation rate (ESR). However it can be falsely normal (polyglobulia, cryoglobulinemia, hemoglobinopathy) or spuriously high in the absence of inflammation (anemia, hypergammaglobulinemia). In cases of doubt, the acute phase reactants (APR) should be measured: C reactive protein (CRP), fibrinogen, haptoglobin, alpha 1 acid glycoprotein. They have different kinetics of variation and various degrees of increase (some--the so called "negative" proteins--actually decrease). Several pitfalls can be avoided if it is remembered that the APR themselves can be modified by causes other than inflammation: low fibrinogen in intravascular coagulation, very low haptoglobin in hemolysis, raised orosomucoide in renal insufficiency and elevated transferrin in iron deficiency. Furthermore liver insufficiency or leakage through the kidney or gut lesions can lower them. In some patients, the observed levels of APR are thus the result of opposite trends. In complex cases, these pathological mechanisms are more apparent on profiles which express the concomitant blood levels of several APR in a normalized or comparative manner. In medical practice, ESR serves first and foremost to detect an inflammatory syndrome. CRP is prominent among the APR because its changes show a great sensitivity, are independant of those of ESR and have a time course fitting closely that of the inflammatory processes. Profiles yield detailed information but rarely provide major evidence in the quest of a diagnosis or the choice of a treatment. Because of their cost they are to be used only in difficult cases.
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PMID:[From sedimentation rate to inflammation profile]. 784 87

Long-term treatment with the heme oxygenase inhibitor tin-mesoporphyrin produces an iron deficiency anemia in rats analogous to that we reported in patients with the Crigler-Najjar type I syndrome receiving prolonged treatment with the inhibitor to ameliorate severe jaundice [Pediatrics 1992; 89: 175-182]. A dose- and time-dependent inhibition of intestinal heme oxygenase is produced by tin-mesoporphyrin which is independent of iron status of the animal. Tin-mesoporphyrin inhibits the intestinal enzyme whether administered orally or parenterally. Enzyme inhibition by either route results in diminished uptake of 59Fe from radiolabelled heme in the gut. Since tin-mesoporphyrin stimulates excretion of unmetabolized heme into bile its ability to inhibit intestinal heme oxygenase and to decrease heme-iron absorption in the gut probably accounts in part for the iron deficiency produced by the agent. The availability of an orally active agent which inhibits heme oxygenase and heme-iron absorption in the intestine may prove useful for experimental and therapeutic studies in diseases of iron metabolism.
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PMID:Tin-mesoporphyrin inhibits heme oxygenase activity and heme-iron absorption in the intestine. 826 22

Iron deficiency anaemia may be due to occult bleeding into the gut. However, although clinical investigations may show a high frequency of gastrointestinal tract disease in these patients, the cause-effect relationship between the lesions detected and anaemia remain uncertain. This study aimed to establish whether lesions detected by endoscopy or imaging of the gastrointestinal tract in patients with unexplained iron deficiency anaemia are bleeding continuously. Routine clinical tests were performed in 42 patients with unexplained iron deficiency anaemia referred to this unit. Whole gut lavage and assay of haemoglobin in the gut perfusate were also performed. The main outcome measures were clinical diagnoses (by imaging and endoscopy of the upper gastrointestinal tract and colon); the concentration of haemoglobin in whole gut lavage fluid; and the calculated gastrointestinal blood loss per day. There were 73 clinical, dietary, or iatrogenic factors of possible aetiological importance in the 42 patients--poor diet (10), gross gastrointestinal abnormality (34 in 28 patients), malabsorption (14), coagulation problems (6), and NSAID use (9). The gut lavage test showed, however, that at the time the test was performed, only eight patients were losing more than 2 ml blood daily into the gut, including all four with colonic cancer, one with diffuse gastric vascular ectasia, and one with severe ulcerative oesophagitis. It is concluded that occult gastrointestinal bleeding sufficient to cause anaemia was evident in only 19% of 42 patients. There was a high frequency of other potential causes of iron deficiency in the remainder, suggesting that most of the gastrointestinal diseases and lesions detected in them were probably coincidental. Factors other than blood loss should be considered and treated in patients referred for anaemia assessment.
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PMID:Use of whole gut perfusion to investigate gastrointestinal blood loss in patients with iron deficiency anaemia. 856 38

Most governmental programs to control widespread iron deficiency in the developing world involve providing daily supplements of iron to all children and pregnant women. This approach has generally poor results due in part to dose-related undesirable gastrointestinal side effects and the lack of effective absorption and retention of iron consumed on a daily basis. However, recent evidence indicates that iron is absorbed significantly better when consumed only at intervals coinciding with gut mucosal renewals. That approach also prevents constant high iron concentrations in the gut which may cause undesirable side effects. Much lower iron doses administered intermittently are as effective in correcting iron nutrition and safer than daily doses in iron deficient anemic rats. 246 healthy 3-6 year olds and 405 pregnant women were enrolled in two studies to determine whether intermittent iron supplementation in humans is more efficient than daily iron administration. Weekly iron supplementation proved to be better than daily supplementation, producing more efficient iron absorption with fewer side effects. Serum ferritin distribution patterns indicate that intermittent iron supplementation avoids the iron overload which results from daily iron supplemented.
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PMID:The effectiveness of weekly iron supplementation regimen in improving the iron status of Chinese children and pregnant women. 888 48


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