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Query: UMLS:C0162316 (iron deficiency anemia)
3,806 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

Plasma ferritin was measured in 420 apparently healthy active elderly subjects living in the community. Mean values were comparable to other published results for elderly subjects. Higher values were obtained in men and in diabetic subjects. Mean values for men and women after exclusion of subjects with diabetes and other diseases were not significantly lower. It is concluded that a) the age-related rise in plasma ferritin observed in other studies represents a physiologic change, with pathologic processes only playing a small part in contributing to the increase, b) reference intervals appropriate to the elderly should be used, and c) plasma ferritin may not be a useful screening test for iron deficiency anemia or hemochromatosis in the elderly.
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PMID:Plasma ferritin in an elderly population living in the community. 276 82

Iron absorption is under delicate control and the level of absorption is adjusted to comply with the body's need for iron. To measure the intestinal setting for iron absorption, and thereby indirectly assess body iron requirements, cobaltous chloride labelled with (57)Co or (60)Co was given by mouth and the percentage of the test dose excreted in the urine in 24 hours was measured in a gamma counter. Seventeen control subjects with normal iron stores excreted 18% (9-23%) of the dose. Increased excretion, 31% (23-42%), was found in 10 patients with iron deficiency anemia and in 15 patients with depleted iron stores in the absence of anemia. In contrast, 12 patients with anemia due to causes other than iron deficiency excreted amounts of radiocobalt within the normal control range. In patients with iron deficiency, replenishment of iron stores by either oral or parenteral iron caused the previously high results to return to normal.Excretion of the test dose was normal in portal cirrhosis with normal iron stores but it was markedly increased in patients with cirrhosis complicated by either iron deficiency or endogenous iron overload. It was also raised in primary hemochromatosis. Excretion of the dose was reduced in gluten-sensitive enteropathy. Gastrointestinal surgery and inflammatory disease of the lower small intestine had no effect on the results except that some patients with steatorrhea had diminished excretion.The cobalt excretion test provides the clinician with a tool for the assessment of iron absorption, the detection of a reduction in body iron stores below the level that is normal for the subject in question, the differentiation of iron deficiency anemia from anemia due to other causes, and the investigation of patients with iron-loading disorders.
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PMID:Cobalt excretion test for the assessment of body iron stores. 557 25

The authors used the 57 Co urinary excretion test to assess the intestinal absorption of iron in anemia associated with hypoferrinemia and in iron overload states. Among the anemia associated with hypoferrinemia, a high elimination of 57 Co had been found in all patients (15) with post-haemorrhagic iron deficiency anemia. Conversely, this elimination was very low in all 10 patients with anemia due to chronic inflammatory diseases. Moreover the test detected few iron deficiency anemia due to a decreased intestinal absorption of iron. In the iron overload states, the test had been performed in 2 subgroups of patients : chronic anemic patients with transfusional iron overload and hemochromatosis without anemia. In the transfusional iron overload group, 19 patients with thalassemia major who are routinely transfused have a moderate decrease of the 57 Co excretion. This finding probably reflects a continuing intestinal absorption of iron. On the other hand, 6 patients with acquired idiopathic sideroblastic anemia have a very low excretion. In the non anemic hemochromatosis, a high urinary level of 57 Co was present in 5 patients with idiopathic hemochromatosis when it was lower and variable in 6 patients with alcoholic siderosis. Using Wilcoxon, Mann and Whitney's non parametric test, there is a significant difference between the results of both groups. So, in idiopathic hemochromatosis, the high urinary level of 57 Co reflects an inappropriately high absorption of iron in spite of the iron overload and the test may be of value in detecting asymptomatic carriers of the disease.
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PMID:[The urinary elimination of cobalt 57 in iron-deficiency anemia and in iron-overload states]. 626 88

Basic ferritin (liver-type) was measured in erythrocytes of subjects with alpha- and beta-thalassemia trait, thalassemia intermedia and Cooley's disease, and compared with normals and patients with abnormal iron metabolism without erythrocyte metabolic defect (iron deficiency anemia and idiopathic hemochromatosis). In all the thalassemic syndromes considered, erythrocyte ferritin was significantly higher than in normals (p less than 0.001) and increased progressively with the increasing 'severity' of the thalassemic disorder. In both thalassemic and non-thalassemic subjects, erythrocyte ferritin levels were related to body iron status, but in the thalassemic group, the increased erythrocyte ferritin values seemed also to be closely related to the intracellular metabolic abnormality. The severity of the defect in globin chain synthesis seemed to play an important role in determining ferritin accumulation in red cells of thalassemic subjects.
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PMID:Erythrocyte ferritin in thalassemia syndromes. 642 38

In healthy persons the plasma ferritin concentration is a sensitive index of the size of body iron stores. It has been successfully applied to large-scale surveys of the iron status of populations. It has also proved useful in the assessment of clinical disorders of iron metabolism. A low plasma ferritin level has a high predictive value for the diagnosis of uncomplicated iron deficiency anemia. It is of less value, however, in anemia associated with infection, chronic inflammatory disorders, liver disease and malignant hematologic diseases, for which a low level indicates iron deficiency and a high level excludes it, but intermediate levels are not diagnostic. Measuring the plasma ferritin concentration is also useful for the detection of excess body iron, particularly in idiopathic hemochromatosis, but again it lacks specificity in the presence of active hepatocellular disease. If iron overload is suspected in these circumstances determination of the iron content of a percutaneous liver biopsy specimen is required. In families with idiopathic hemochromatosis the combined determination of the plasma ferritin concentration and the transferrin saturation is a sufficient screen to identify affected relatives; however, estimation of the hepatic iron concentration is required to establish the diagnosis.
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PMID:Plasma ferritin concentrations: their clinical significance and relevance to patient care. 699 66

We describe a 31 year old male patient who presented with severe cardiomyopathy caused by primary hemochromatosis. After a stormy course, complicated by heart failure and severe ventricular arrythmias, improvement in clinical status and myocardial function occurred. Depletion of myocardial iron was documented by the technique of serial endomyocardial biopsy. Myocardial iron stores were not yet depleted when hypoferremia and iron deficiency anemia occurred. This is the first reported study of myocardial morphology in a successfully treated patient with hemochromatotic cardiomyopathy.
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PMID:Myocardial involvement in idiopathic hemochromatosis. Morphologic and clinical improvement following venesection. 723 94

Iron deficiency severe enough to cause anemia is associated with significant morbidity while uncontrolled iron absorption which occurs in disorders such as hereditary hemochromatosis causes multiorgan failure and early death. Preliminary data from the Third National Health and Nutrition Examination Survey demonstrate that the prevalence of iron deficiency anemia in the United States is now very low. This implies that the current iron consumption is adequate for most individuals. An important unresolved question relates to the necessity for further reducing the prevalence of iron deficiency without anemia. More information is required to determine whether this lesser degree of iron deficiency is harmful. Recent survey data indicate that concomitantly with the reduced prevalence of iron deficiency there has been a rise in serum ferritin concentrations in American men and postmenopausal women. These findings have led to concern about the effectiveness of the physiological mechanisms for limiting storage accumulation in normal individuals and carriers of the hemochromatosis gene when dietary iron content is high. Furthermore, recent epidemiological observations suggest that a modest increase in iron stores (in a range previously considered safe) is a possible risk factor for ischemic heart disease and cancer; however, a causal relationship remains to be proven. Nonetheless, because there is no known benefit of high iron storage status, it seems prudent to avoid further increases in and possibly to reduce the dietary iron intake of men and postmenopausal women. Mean intake in these groups exceeds the current RDA by a significant margin. Therefore, the sources of dietary iron as well as other factors contributing to high serum ferritin values have to be defined. Also, efforts should be made to increase the awareness of professionals and the public about the possible risks of excessive dietary iron. The complexity of the Western diet and an incomplete understanding of all of the factors affecting serum ferritin concentrations make it very difficult to specify a safe upper range for daily iron intake at the present time.
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PMID:Deliberations and evaluations of the approaches, endpoints and paradigms for iron dietary recommendations. 881 5

A patient with diabetes mellitus caused by secondary hemochromatosis was treated using recombinant human erythropoietin and phlebotomy. A total of 12 g of iron had been infused in the patient because of iron deficiency anemia. Blood glucose level was 17.3 mmol/L, and hemoglobin A1c level was 9.0% at admission. He was treated using phlebotomy (400 mL per week), along with subcutaneous injection of 3,000 U of recombinant human erythropoietin three times a week. After approximately 100 days, a total of 5,500 mL of blood (2.75 g iron) could be removed. Serum ferritin level decreased from 10,000 micrograms/L to 4,807 micrograms/L. Fasting and maximum serum C-peptide immunoreactivity values during 100-g oral glucose tolerance tests were improved from 0.14 nmol/L to 0.42 nmol/L and from 1.84 nmol/L to 2.61 nmol/L, respectively. This case suggests that pancreatic beta-cell recovers in diabetes caused by hemochromatosis by reducing iron overload during a short period.
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PMID:Recovery of pancreatic beta-cell function in hemochromatosis: combined treatment with recombinant human erythropoietin and phlebotomy. 941 46

Carbohydrate-deficient transferrin (CDT), a microheterogeneous form of serum transferrin (Tf), has been proposed as the most reliable marker of chronic alcohol consumption, although unexplained false-positive and -negative results have been reported. We investigated whether body iron influenced CDT serum levels by studying alcohol abusers with or without iron overload and nonabusers with iron deficiency or iron overload caused by genetic hemochromatosis (GH). In alcohol abusers, CDT was significantly lower in the presence of iron overload than in the absence (24.6 +/- 16.5 U/L vs. 33.3 +/- 11.7 U/L; P <.01), with false-negative results almost exclusively in patients with iron overload. Similarly, in nonabusers with GH, CDT was lower than in normal controls (9.6 +/- 2. 2 U/L vs. 15.7 +/- 3.3 U/L; P <.0001), whereas, patients with iron deficiency anemia had significantly higher levels than controls (28. 1 +/- 5.8 U/L vs. 15.7 +/- 3.3 U/L; P <.0001). In nonabusers, iron supplementation therapy significantly decreased CDT levels in patients with iron deficiency anemia (33.7 +/- 6.6 U/L vs. 21.7 +/- 5.2 U/L; P =.0007), while iron-depletion treatment significantly increased CDT levels in patients with GH (9.7 +/- 2.0 U/L vs. 14.7 +/- 4.0 U/L; P =.001). Alcohol abusers had a significant relationship between liver iron concentration (LIC) and the reciprocal of CDT (r =.65; P <.0001), while in nonabusers, there was a significant correlation between Tf and CDT (r =.72; P <.0001). In conclusion, CDT serum levels are markedly affected by the patient's iron status, with iron overload reducing its sensitivity in alcohol abusers and iron deficiency its specificity in nonabusers. CDT can be considered a reliable marker of alcohol abuse only when iron stores are normal.
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PMID:Carbohydrate-deficient transferrin, a sensitive marker of chronic alcohol abuse, is highly influenced by body iron. 1005 65


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