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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, the most common cause of anemia, is prevalent in 10 percent to 30 percent of the world's population. Inadequate intake of iron may be an important causative factor, particularly when the body requires more iron than usual (e.g., during infancy, early childhood, adolescence, pregnancy and periods of blood loss). The popular increase of fiber in diets may increase the incidence of iron-deficiency anemia because too much fiber in the diet renders available iron unabsorbable. Symptoms in children include skin or conjunctival pallor, excessive sleepiness, learning disabilities, diminished attention span, tiredness, irritability or inappropriate behavior, and pica. Adults may have shortness of breath, decrease in exercise tolerance, palpitations, tachycardia, angina, congestive heart failure, orthopnea and edema. Iron deficiency occurs in sequential states and is measured by many laboratory tests. The levels of hemoglobin and hematocrit are both decreased, while the red blood cell count may be normal initially, but will decrease as the iron-deficiency state continues. The steps of treatment include correction of the underlying disorder, administration of the amount of iron needed and observation of the response to treatment.
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PMID:A guide to primary care of iron-deficiency anemia. 143 77

In recent years several cases of anemia (iron deficiency) have been reported in adults who participate in long-distance running although its etiology has not been entirely explained. We report the case of a 16-year-old girl who had participated in middle-distance running at a competitive level for about three years and who had been admitted to hospital because of a progressive weakness and a reduction in her sporting performance. Evaluation revealed that the patient had a balanced diet, normal menstrual cycles and slight abdominal pain. The objective examination were negative except for the presence of a pronounced pallor of the skin and the mucous membranes. The blood count revealed Hb 7.5 g%, Ht 26%, GV 63 mu 3, the reticulocyte count was 10%, serum iron 9 micrograms/dl, serum transferrin 450 micrograms/dl and serum ferritin 4 ng/ml. All tests for constitutional anemia proved negative. Stool Hemoccult tests proved negative (these tests were carried out some weeks after the patient had stopped running). Her symptoms resolved after the beginning of iron treatment and her blood test results returned to normal. This case has been reported to draw attention to the existence of this problem in adolescents who practice sport. The knowledge of the problem night lead to a preventive scanning of young athletes and the presence of clinical manifestations would reduce the need for invasive tests.
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PMID:[Severe sideropenic anemia in a young middle-distance runner]. 158 99

The clinical efficacy and tolerability of gastroprotected ferritin were assessed in children affected by iron deficiency and/or sideropenic anemia. Forty-seven children with iron-deficiency and/or sideropenic anemia were included in the study and were treated with gastroprotected ferritin at a dose of 4-5 mg/kg/day per os for 4 months. Only 33 children correctly completed the entire treatment cycle, achieving a marked improvement of blood parameters (increased Hb, accompanied by higher levels of sideremia and in particular ferritin, with a contemporary decrease in erythrocytic protoporphyrin and transferrinemia) and clinical symptoms, especially pallor, anorexia, debility, somnolence, hyperactivity, disturbed sleep and excessive sweating. Of the remaining 14 children, 9 failed to present for the planned control after the 4 months of therapy, 3 abandoned therapy due to difficulties of assumption and 2 because of intolerance phenomena, such as nausea and diarrhoea. In conclusion, gastroprotected proteoferrin is efficacious and well tolerated in the treatment of iron deficiency in children.
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PMID:[Evaluation of the effectiveness of gastro-protected proteoferrin in the therapy of sideropenic anemia in childhood]. 228 21

Aim of this multicentric clinical trial was to evaluate the efficacy and tolerability of a new iron compound: iron proteinsuccinylate. 3,200 patients affected with iron deficiency due to obstetric or gynecologic etiology were treated with iron proteinsuccinylate, at a daily dose of 80 mg Fe3+, for at least 30 days. Iron proteinsuccinylate induced a statistically significant improvement (p less than 0.01) in mean values of hemoglobin and serum iron. The compound also caused a disappearance or improvement of subjective symptomatology (asthenia, anorexia) and of clinical conditions deriving from iron deficiency state (polypnea, cutaneous and mucous pallor). The treatment was well tolerated and caused a few slight side effects (diarrhea, epigastralgia, nausea) in 2.4% of patients.
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PMID:[Ferroprotein succinylate: treatment of iron deficiency in obstetrics and gynecology]. 237 53

169 hospital inpatients were studied to assess the association of blue sclerae with iron-deficiency anaemia. Three observers independently graded the signs of blue sclerae and mucosal pallor as absent, equivocal, definite, or striking. Blue sclerae were seen more often in patients with iron-deficiency anaemia (40/46, 87%) than in those with other anaemias (2/28, 7%; p less than 0.001) or without anaemia (5/95, 5.3%; p less than 0.001). The specificity of blue sclerae in iron-deficiency anaemia was 0.94 with a sensitivity of 0.87. By comparison, mucosal pallor was noted in only 30% of patients with iron-deficiency anaemia, with a specificity of 0.96 and a sensitivity of only 0.20 (p less than 0.001). The presence of blue sclerae was unaffected by age, sex, or colour of iris. Blue sclerae appear to be a good indicator of iron deficiency and should become a regular part of clinical examination.
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PMID:Blue sclerae: a common sign of iron deficiency? 287 43

Anaemia was detected in housed lambs by clinical and haematological investigation. Conjunctival pallor was used as a clinical test for anaemia and the results indicate that this has high specificity (91 per cent to 95 per cent) and low sensitivity (53 per cent to 55 per cent). The haematological results indicated a non-regenerative anaemia with low packed cell volume, red blood cell count and haemoglobin. In a subset of lambs examined biochemically, anaemia was associated with low serum iron concentration and low serum iron binding: cobalt levels were within normal ranges and blood copper levels were slightly raised. At present it is unclear whether this is a primary or secondary iron deficiency.
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PMID:Anaemia in housed lambs. 833 79

Iron deficiency is the most common nutritional deficiency in late infancy. In healthy term infants iron stores are depleted at the age of four to six months and the infant becomes increasingly dependent on exogenous sources of iron. Furthermore, the iron content and bioavailability in a traditional weaning diet are low. The consequences of iron deficiency in late infancy span from pallor to risk of impaired psychomotor development. Approaches to prevent iron deficiency and problems associated with these approaches are reviewed, and general guidelines for a weaning diet as well as guidelines with special emphasis on preventing iron deficiency are given. The present article identifies infants at high risk of developing iron deficiency including: immigrants, infants from a deprived background, infants to whom cows' milk is introduced early and/or given in large quantities, and infants from families with unusual eating habits. Finally, the commonly employed clinical practice for treating iron deficiency is mentioned.
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PMID:[Iron deficiency during the first year of age]. 969 16

We recently reported the hemochromatosis-like phenotype observed in our Usf2 knockout mice. In these mice, as in murine models of hemochromatosis and patients with hereditary hemochromatosis, iron accumulates in parenchymal cells (in particular, liver and pancreas), whereas the reticuloendothelial system is spared from this iron loading. We suggested that this phenotypic trait could be attributed to the absence, in the Usf2 knockout mice, of a secreted liver-specific peptide, hepcidin. We conjectured that the reverse situation, namely overexpression of hepcidin, might result in phenotypic traits of iron deficiency. This question was addressed by generating transgenic mice expressing hepcidin under the control of the liver-specific transthyretin promoter. We found that the majority of the transgenic mice were born with a pale skin and died within a few hours after birth. These transgenic animals had decreased body iron levels and presented severe microcytic hypochromic anemia. So far, three mosaic transgenic animals have survived. They were unequivocally identified by physical features, including reduced body size, pallor, hairless and crumpled skin. These pleiotropic effects were found to be associated with erythrocyte abnormalities, with marked anisocytosis, poikylocytosis and hypochromia, which are features characteristic of iron-deficiency anemia. These results strongly support the proposed role of hepcidin as a putative iron-regulatory hormone. The animal models devoid of hepcidin (the Usf2 knockout mice) or overexpressing the peptide (the transgenic mice presented in this paper) represent valuable tools for investigating iron homeostasis in vivo and for deciphering the molecular mechanisms of hepcidin action.
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PMID:Severe iron deficiency anemia in transgenic mice expressing liver hepcidin. 1193 10

Chlorosis or 'green sickness' was frequently seen in languid girls and young women in the 19th century but disappeared completely in the first part of the 20th century. The clinical picture comprised menstrual disorders such as ameonrrhoea, pallor and many vague symptoms including apathy and hypochondria. At a later stage anaemia and iron deficiency became prominent characteristics. The skin was reported to take on a greenish hue, but this is disputable. Related diseases were hysteria and anorexia. In the middle of the 19th century hydrotherapy was treatment of choice, and later on iron therapy came to the fore. In 1898 Catharine van Tussenbroek, the first female Dutch gynaecologist, pointed to the social factors at the root of the disease: the lack of perspective for young girls in society at that time. The disappearance of the disease can be partially attributed to improved diagnostics but more so to changes in the social position of women around the turn of the century.
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PMID:[Chlorosis, the lost disease of languid young women]. 1473 54

Plummer-Vinson or Paterson-Kelly syndrome presents as a classical triad of dysphagia, iron-deficiency anemia and esophageal webs. Exact data about epidemiology of the syndrome are not available; the syndrome is extremely rare. Most of the patients are white middle-aged women, in the fourth to seventh decade of life but the syndrome has also been described in children and adolescents. The dysphagia is usually painless and intermittent or progressive over years, limited to solids and sometimes associated with weight loss. Symptoms resulting from anemia (weakness, pallor, fatigue, tachycardia) may dominate the clinical picture. Additional features are glossitis, angular cheilitis and koilonychia. Enlargement of the spleen and thyroid may also be observed. One of the most important clinical aspects of Plummer-Vinson syndrome is the association with upper alimentary tract cancers. Etiopathogenesis of Plummer-Vinson syndrome is unknown. The most important possible etiological factor is iron deficiency. Other possible factors include malnutrition, genetic predisposition or autoimmune processes. Plummer-Vinson syndrome can be treated effectively with iron supplementation and mechanical dilation. In case of significant obstruction of the esophageal lumen by esophageal web and persistent dysphagia despite iron supplementation, rupture and dilation of the web are necessary. Since Plummer-Vinson syndrome is associated with an increased risk of squamous cell carcinoma of the pharynx and the esophagus, the patients should be followed closely.
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PMID:Plummer-Vinson syndrome. 1697 5


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