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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 a common medical problem that may present in a variety of ways to the general practitioner or the specialist. An understanding of iron physiology is relevant to diagnosis and treatment of iron deficiency. Human iron metabolism is a system based on conservation. For this reason, the most common cause of iron deficiency is loss of the normal conservation of iron and this usually means blood loss. The important implication is that the search for the cause of iron deficiency will usually focus on the gastrointestinal tract in males and non-pregnant, non-menstruating females. Iron deficiency is commonly misdiagnosed. The usual error is misinterpretation of the laboratory features of the anaemia of chronic disease. The serum iron is low, but the iron binding capacity is normal and ferritin is normal or high. There are problems and exceptions involved in interpretation of iron indices. Treatment of iron deficiency requires an understanding of iron absorption and the ability of the marrow to respond. In most circumstances, iron deficiency will respond to adequate doses of oral iron; however, there are a few situations when oral iron is unsuitable and parenteral iron is required. An inadequate response to iron may indicate inadequate supply of iron to the bone marrow (e.g. malabsorption, non-compliance) or failure of the marrow to respond (e.g. concomitant folate deficiency). Pregnancy is a special situation in which conservation of iron is overcome by fetal iron requirements and in which application of the knowledge of iron physiology should be applied to prevent and treat iron deficiency.
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PMID:Iron deficiency. Misunderstood, misdiagnosed and mistreated. 310 99

A dual isotope vitamin B12 absorption test in which vitamin B12 is given both in aqueous solution and bound to protein (chicken serum), was evaluated in 26 controls and 68 patients with subnormal serum vitamin B12 concentrations (19 with pernicious anaemia, 13 with iron deficiency, seven after partial gastrectomy, seven with malabsorptive states, five with folate deficiency, four with chronic alcoholism and 13 in whom no cause was apparent). In control patients protein bound absorption decreased with age; isotope excretion was 1.0% or over in those aged under 60 and 0.5% or over in those aged 60 and above. Malabsorption of protein bound vitamin B12 with normal aqueous absorption occurred in five patients with iron deficiency, three with alcoholism, two after partial gastrectomy, two with folate deficiency and in one with a malabsorptive state. In alcoholics abstinence produced an improvement in protein bound absorption. All patients in the group for whom no cause could be found for the subnormal serum vitamin B12 concentration had normal aqueous absorption but four had malabsorption of protein bound vitamin. Although the dual isotope test gave reproducible results and was consistent with the standard Schilling test some anomalies were detected; nine patients had reduced aqueous absorption with normal protein bound absorption. Despite this the dual test may prove useful in determining the importance of a subnormal vitamin B12 concentration where the cause is not clinically apparent. Further development is needed before it can be considered for routine use.
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PMID:Experiences with dual protein bound aqueous vitamin B12 absorption test in subjects with low serum vitamin B12 concentrations. 361 94

When iron deficiency occurs in the elderly, it is usually due to bleeding and not to nutritional lack or malabsorption. Iron deficiency early in life may lead to irreversible changes (for example, gastric achlorhydria) that are troublesome in later life. The nonhematologic effects of iron deficiency still need to be studied in the elderly. In particular, the role of iron in brain metabolism would seem important in geriatrics. Although it is important to prevent iron deficiency, indiscriminate use of iron could conceivably lead to iron overload. As with many beneficial compounds, patients must be cautioned against the prolonged ingestion of large amounts of iron salts.
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PMID:Clinical disorders of iron metabolism in the elderly. 391 18

Among 10 children with giardiasis, eight had iron deficiency; iron deficiency anemia was the main complaint in three. Evaluation of iron absorption by the oral iron load test demonstrated a subnormal response (i.e., increase in serum iron levels of less than 100 micrograms/dl) in all eight patients with iron deficiency. In contrast, in two iron-sufficient patients with giardiasis the response to an oral iron load was normal. Xylose absorption was abnormal in five of the 10 patients. After metronidazole dosing, iron absorption became normal in seven patients but remained abnormal in one patient, who also had IgA deficiency. Xylose absorption became normal in all five patients who underwent a second test, but remained abnormal in the patient with IgA deficiency. Concomitant morphologic-studies of jejunal biopsy material from these patients revealed moderate changes in the intestinal mucosa of two patients. We conclude that malabsorption of iron is a complication of giardiasis.
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PMID:Iron malabsorption in giardiasis. 400 42

The iron status in children with sickle cell anaemia has been studied in 45 patients. The mean haemoglobin level was 7.4 g/dl (s.d. 1.7) and the white cell count more than 11 X 10(9)/l in 35 (78%). Bone marrow examination showed depletion of iron stores of 21 (47%). The total iron binding capacity was elevated in most of the children and serum iron was below the normal mean level for age in 14 (31%) children. The possible causes of iron deficiency in some of these children include dietary deficiency, infections, malabsorption, blood loss through hookworm infestation and growth spurt. In the management of a child with sickle cell disease, iron administration is not recommended unless there is evidence of coexisting iron deficiency.
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PMID:Iron deficiency in sickle cell anaemia in Nigerian children. 618 85

Therapy of the malabsorption syndrome centers on adequate diagnosis of the underlying pathology, with vigorous therapeutic efforts directed at correcting this and thereby preventing ongoing losses of nutrients. Dietary therapy includes a high-protein, high-calorie, low-fat diet often supplemented with MCTs in an effort to minimize steatorrhea. Water-soluble vitamin deficiency is rare, but supplementation with small daily doses is innocuous and probably should be prescribed. Significant fat-soluble vitamin deficiencies are seen more commonly and can be monitored by physical examination and the prothrombin time. Calcium, magnesium, and vitamin D deficiencies are more common than originally suspected. Adequate therapy requires monitoring of the serum calcium, magnesium, parathyroid hormone levels, and, optimally, 24-hour urinary collections for calcium. Supplementation of these mineral deficiencies requires ongoing close observation to prevent hypercalcemia. Iron deficiency can be easily diagnosed by available serum iron determination, and replacement with oral supplements is curative. Trace metal deficiencies occur, but our capabilities of detecting and treating them is still in its infancy. Figure 3 outlines our approach to the evaluation and treatment of the patients suspected of having the malabsorption syndrome.
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PMID:Nutritional aspects of malabsorption syndromes. 641 33

Iron deficiency and iron deficiency anemias are very common disturbances of the hematopoiesis. Although symptomatology and therapeutic possibilities are well known, one should keep in mind that iron deficiency is a symptom and not a diagnosis. The causes of iron deficiency are iron loss, malabsorption and insufficient supply. The best therapy is peroral treatment with well absorbable preparations, whereby the bioavailability has to be taken into consideration. Only in few cases a parenteral therapy which has more side effects is necessary. A overview about the possible therapy is given.
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PMID:[Clinical aspects and therapy of iron deficiency]. 671 Oct 5

A mesenteric mass, histologically characterized as giant lymph node hyperplasia was found in an 18-yr-old man with at least 11 yr of growth retardation and anemia. The anemia was characterized by iron deficiency from selective malabsorption of iron, and by features of the anemia of chronic disorders. In contrast with a previous report, no inhibitor of erythropoietin was found and there was no abnormality of erythropoietin secretion. Resection of the mass was followed by rapid correction of the anemia and catch-up growth. The mass had histologic features of the hyaline vascular and plasma cell types of Castleman's disease with multinucleate giant cells probably of macrophage origin. Immunologic studies of the mass showed that the B lymphocytes were polyclonal and the T lymphocyte helper/suppressor cell ratio was normal, suggesting that giant lymph node hyperplasia is a local inflammatory reaction.
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PMID:Giant lymph node hyperplasia (Castleman's disease) of the mesentery. Observations on the associated anemia. 672 65

An increase in hemoglobin concentration characterizes the normal compensatory response to chronic tissue hypoxia. We observed no such increase in 42 chronically hypoxic patients with cystic fibrosis, in whom the mean concentration was 12.6 gm/dl; one third of the patients were anemic. Compared with patients with cyanotic heart disease, patients with cystic fibrosis did not have a compensatory increase in P50 or 2,3-diphosphoglycerate. Despite anemia, erythropoietin levels in patients with cystic fibrosis were not significantly different from normal control values. The growth of colony-forming units-erythroid in patients with cystic fibrosis was similar to that in control subjects, and there was no inhibition of growth with the addition of autologous serum. Erythropoietin sensitivity, determined by measuring the CFUe dose response curve, was normal in both patients and controls. Results of iron studies were consistent with iron deficiency in the majority of patients. Impaired absorption of iron was observed in six of 13 iron-deficient patients with cystic fibrosis. An inverse correlation between erythrocyte sedimentation rate and peak serum iron was obtained during the iron absorption study. Eight patients who underwent a therapeutic trial of iron demonstrated a 1.8 gm/dl rise in hemoglobin concentration. Two patients with previously documented iron malabsorption responded to parenteral iron therapy after failure to respond to oral supplementation. These studies demonstrate that patients with cystic fibrosis not only have an impaired erythroid response to hypoxia, but are frequently anemic. Their inadequate erythroid response to hypoxia results in part from disturbances in erythropoietin regulation and iron availability.
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PMID:Inadequate erythroid response to hypoxia in cystic fibrosis. 673 32

We conducted studies using intravenous (IV) iron dextran injection in 14 hospitalized infants and children with iron deficiency who required total parenteral nutrition. A single, total dose of IV iron dextran was administered during a two-hour period (preceded by a test dose of 25 mg). Doses administered ranged from 50 to 782 mg, with an average dose of 15.2 mg/kg body weight. No adverse reactions were noted during the test dose or infusion. The IV administration of iron dextran appears to be a safe method of treatment for iron repletion in children who are unable to tolerate feedings as a result of malabsorption, inflammatory bowel disease, or chronic debilitating diseases.
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PMID:Use of intravenous iron dextran injection in children receiving total parenteral nutrition. 679 6


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