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

Aluminum (Al) is a simple trivalent cation incapable of redox changes. The toxicity of the metal has been the subject of much controversy in the past few decades. Although it has been generally believed that the metal is innocuous to human health, a causal role for Al has been established in dialysis dementia (Alfrey et al., 1976), osteomalacia (Bushinsky et al., 1995) and microcytic anemia without iron deficiency (Touam et al., 1983). Aluminum has also been implicated in Alzheimer's disease (AD) although a direct causal role has not been determined. The exact mechanism of Al toxicity is not known. However, there are several lines of evidence that show the metal's capacity to exacerbate oxidative events. The present review is intended to propose a coherent pathway linking Al-induced oxidative events to Alzheimer's disease. The preliminary segment is an introduction to reactive oxygen species and their potential involvement in the pathogenesis of AD and the generation of an inflammatory response. Evidence on the relation between AD and inflammatory processes is also presented. The epidemiological and clinical evidence of Al neurotoxicity is summarized in the second section of the review. Finally, a hypothesis indicating that aluminum can exacerbate AD by activating ROS generation and initiation of an inflammatory cascade is presented.
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PMID:Aluminum induced oxidative events and its relation to inflammation: a role for the metal in Alzheimer's disease. 1087 35

We encountered two patients who presented with hypochromic-microcytic anemia and were refractory to iron therapy. The symptoms were suggestive of anemia of chronic disease (ACD); however, there was no evidence of any such disease, either inflammatory or malignant. These patients were reminiscent of patients originally described as having primary defective iron reutilization. The hematologic picture consisted of hypochromic-microcytic anemia, low serum iron, low to normal iron binding capacity, high serum ferritin, and increased bone marrow iron in the absence of ringed sideroblasts. These patients had symptomatic anemia and received danazol (200 mg orally) three times per day to which they responded very well with an increase of approximately 3 g in the hemoglobin concentration over 1 year and amelioration of their symptoms. Danazol was well tolerated and did not cause any virilizing side effects. Doses were lowered in maintenance after 1 year to 200 mg once per week, and responses were sustained up to 36 months of follow-up duration. In the differential diagnosis of hypochromic-microcytic anemia, especially in postmenopausal women, one has to consider this type of treatable anemia when more common types such as iron deficiency, chronic inflammation, malignancy, sideroblastic anemia, or thalassemia have been ruled out.
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PMID:Treatment of primary defective iron-reutilization syndrome: revisited. 1098 70

The iron status and diet of Inuit infants living in northern Quebec who were part of a prospective cohort study was described. The prevalence of anemia (hemoglobin values > 2 SD below the reference mean) was 21.1% (23/109), 47.4% (55/116) and 37.7% (46/122) at 2, 6 and 12 months, respectively. The corresponding prevalence of microcytic anemia was 0.0%, 4.3% and 21.3%. At 2, 6 and 12 months, iron-deficiency anemia (serum ferritin < 10 micrograms/L coupled with anemia) was present in 1.3% (1/79), 24.4% (21/86) and 26.3% (25/95) of infants, respectively. Compared with breastfeeding, the odds ratio for iron deficiency (serum ferritin < 10 micrograms/L) for bottle-feeding with cows' milk or low iron formula was 3.02 (95% CI 1.25-7.27) at 6 months and 3.05 (95% CI 1.28-7.28) at 12 months. This study shows iron-deficiency anemia to be a problem in Inuit infants as young as 6 months old. Breastfed infants were better protected against iron deficiency than infants fed cow's milk or low-iron formula.
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PMID:Anemia and iron status in Inuit infants from northern Quebec. 1120 Jul 28

Iron deficiency is a common cause of microcytic anaemia. However, a high prevalence of haemoglobinopathies in the Arab population makes differential diagnosis difficult. This prospective study of anaemia in children attending a regional hospital in the Sultanate of Oman looked at the prevalence and causes of anaemia in 256 children, 153 in the age group 3-5 years (group A) and 103 in the age group 10-12 years (group B). Of the children studied, 45.1% in group A and 37.9% in group B were anaemic according to WHO criteria. All the anaemic children had low mean corpuscular haemoglobin and 75% showed microcytosis. Serum ferritin levels were normal and glucose-6-phosphate dehydrogenase deficiency did not contribute to the anaemia. The microcytosis and microcytic anaemia in the study population could be attributed to the alpha-thalassaemia trait which is highly prevalent in Oman. The information is of value in any country where there is a significant prevalence of alpha-thalassaemia genes because these can confound the diagnosis of iron deficiency.
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PMID:High prevalence of microcytic anaemia in Omani children: a prospective study. 1128 46

The urinary loss of transferrin is sufficient to reduce plasma transferrin concentrations in the nephrotic syndrome. Hypotransferrinemia may lead to iron loss and microcytic anemia. The mechanism responsible for the hypotransferrinemia in the nephrotic syndrome is, however, unknown. In the present study, synthesis rate of transferrin was measured in vivo in nephrotic patients (n = 7) compared with control subjects (n = 6) using L-[1-(13)C]-valine. Plasma transferrin and iron concentration in the patients were significantly lower than in control subjects (transferrin, 1.39 +/- 0.08 versus 2.57 +/- 0.11 g/L, P < 0.0001; iron, 10.2 +/- 0.8 versus 21.1 +/- 4.5 micromol/L, P = 0.02). Furthermore, albuminuria correlated with transferrinuria (r(2) = 0.901, P = 0.001). The absolute synthesis rate of transferrin was increased in the patients (10.0 +/- 1.1 versus 7.4 +/- 0.7 mg/kg per d, P = 0.07), although this value failed to achieve significance. C-reactive protein, plasma iron, and proteinuria did not correlate with transferrin synthesis. In contrast, transferrin synthesis correlated with albumin synthesis (r(2) = 0.648, P = 0.03; n = 7). The present study indicates that increased transferrin synthesis occurs in nephrotic patients but is insufficient to compensate for urinary losses. Because, overall, no significant relationship was found between transferrin synthesis and either C-reactive protein or iron, it is unlikely that inflammation suppresses or that iron deficiency stimulates increased transferrin synthesis in these patients. The correlation between transferrin synthesis and albumin synthesis suggests that transferrin synthesis is a component of a general response in hepatic protein synthesis in the nephrotic syndrome. This suggests that a therapeutic approach to maximize plasma transferrin concentrations in nephrotic patients should be aimed primarily at reducing urinary protein excretion.
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PMID:Transferrin synthesis is increased in nephrotic patients insufficiently to replace urinary losses. 1131 61

Anemia in children is commonly encountered by the family physician. Multiple causes exist, but with a thorough history, a physical examination and limited laboratory evaluation a specific diagnosis can usually be established. The use of the mean corpuscular volume to classify the anemia as microcytic, normocytic or macrocytic is a standard diagnostic approach. The most common form of microcytic anemia is iron deficiency caused by reduced dietary intake. It is easily treatable with supplemental iron and early intervention may prevent later loss of cognitive function. Less common causes of microcytosis are thalassemia and lead poisoning. Normocytic anemia has many causes, making the diagnosis more difficult. The reticulocyte count will help narrow the differential diagnosis; however, additional testing may be necessary to rule out hemolysis, hemoglobinopathies, membrane defects and enzymopathies. Macrocytic anemia may be caused by a deficiency of folic acid and/or vitamin B12, hypothyroidism and liver disease. This form of anemia is uncommon in children.
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PMID:Anemia in children. 1168 80

There is a significant increase in cases of malaria in Italy. The incidence among Italian citizens has remained quite stable since 1990, while the number of cases among foreigners residing in Italy has continued to increase. The clinical manifestations of plasmodium infection can be less evident in these people: they often have only mild complaints for weeks or months. The case of a Senegalese woman with Plasmodium malariae infection is presented. She had been in Italy for 13 months and was 4-month pregnant. Her only symptoms were asthenia and microcytic anemia; she was afebrile. Her anemia was initially believed to be due to iron deficiency: she was treated with iron and folic acid. The anemia worsened, and resolved only after antimalarial therapy with chloroquine.
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PMID:[Unusual case of malaria in Italy]. 1179 27

Iron transport in the plasma is carried out by transferrin, which donates iron to cells through its interaction with a specific membrane receptor, the transferrin receptor (TfR). A soluble form of the TfR (sTfR) has been identified in animal and human serum. Soluble TfR is a truncated monomer of tissue receptor, lacking its first 100 amino acids, which circulates in the form of a complex of transferrin and its receptor. The erythroblasts rather than reticulocytes are the main source of serum sTfR. Serum sTfR levels average 5.0+/-1.0 mg/l in normal subjects but the various commercial assays give disparate values because of the lack of an international standard. The most important determinant of sTfR levels appears to be marrow erythropoietic activity which can cause variations up to 8 times below and up to 20 times above average normal values. Soluble TfR levels are decreased in situations characterized by diminished erythropoietic activity, and are increased when erythropoiesis is stimulated by hemolysis or ineffective erythropoiesis. Measurements of sTfR are very helpful to investigate the pathophysiology of anemia, quantitatively evaluating the absolute rate of erythropoiesis and the adequacy of marrow proliferative capacity for any given degree of anemia, and to monitor the erythropoietic response to various forms of therapy, in particular allowing to predict response early when changes in hemoglobin are not yet apparent. Iron status also influences sTfR levels, which are considerably elevated in iron deficiency anemia but remain normal in the anemia of inflammation, and thus may be of considerable help in the differential diagnosis of microcytic anemia. This is particularly useful to identify concomitant iron deficiency in a patient with inflammation because ferritin values are then generally normal. Elevated sTfR levels are also the characteristic feature of functional iron deficiency, a situation defined by tissue iron deficiency despite adequate iron stores. The sTfR/ferritin ratio can thus describe iron availability over a wide range of iron stores. With the exception of chronic lymphocytic leukemia (CLL) and high-grade non-Hodgkin's lymphoma and possibly hepatocellular carcinoma, sTfR levels are not increased in patients with malignancies. We conclude that soluble TfR represents a valuable quantitative assay of marrow erythropoietic activity as well as a marker of tissue iron deficiency.
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PMID:Soluble transferrin receptor for the evaluation of erythropoiesis and iron status. 1258 62

Iron deficiency and heterozygous beta-thalassemia are important causes of hypochromic-microcytic anemia. Two laboratory parameters are suggested for the differentiation of such anemia. High-fluorescence reticulocyte counts and soluble transferrin receptor levels were determined in iron-deficiency anemia patients (n = 49) and heterozygous beta-thalassemia patients (n = 43). There was no significant difference in high-fluorescence reticulocyte and soluble transferrin receptor values between the two groups, but a correlation was observed between high-fluorescence reticulocytes and soluble transferrin receptors in iron-deficiency anemia, probably due to increased receptor synthesis as a response to decreased iron content in erythrocytes.
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PMID:Soluble transferrin receptor and immature reticulocytes are not useful for distinguishing iron-deficiency anemia from heterozygous beta-thalassemia. 1287 58

Idiopathic pulmonary hemosiderosis is a rare condition manifested by recurrent pulmonary hemorrhage of unknown cause, diffuse radiologic abnormalities, cough, hemoptysis and moderate to severe hypochromic anemia. Diagnosis can be confirmed by iron stains of the sputum or lung aspiration or by biopsy. Prolonged spontaneous remission may occur without the use of corticosteroid therapy. Studies here reported indicated that the anemia is hypochromic and microcytic anemia of blood loss and iron deficiency, in spite of the presence of large amounts of iron in the pulmonary tissue. Correction of the anemia by intensive iron therapy and transfusion is considered an important part of therapy.
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PMID:Idiopathic pulmonary hemosiderosis. 1378 18


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