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

The results of this trials confirmed the earlier experience that suckling piglets kept indoors, without iron supplementation, develop iron deficiency after 14 days postpartum. Piglets kept outdoors did not develop iron deficiency because of the daily iron supplementation from the ground. Principally, a single dose of iron either parenteral (injection) or oral (iron paste) would supply the iron requirements of the suckling piglets. However, iron injection provided even results than that of the oral supply where some piglets treated orally, developed anemia because oral treatment runs a greater risk of misapplication. Best results were obtained by use of an iron form which can be scattered on the ground during the whole period of suckling. The piglets would receive their iron requirement freely during this period. Another form of iron-electrolyte solution can be supplied through the drinking automate. However, the results were unfavorable and the piglets developed symptoms of anemia. This could be attributed to the fact that the piglets do not require extra fluids during the suckling period, when they receive enough dam milk.
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PMID:[Effects of different anemia prevention forms on the blood parameters of the suckling piglet]. 778 36

Low basal hemoglobin and functional iron deficiency are the limiting factors in autologous blood donation program. Treatment with recombinant human erythropoietin can increase the volume of autologous blood and makes donation of > or = 3 units possible-even in patients with low basal hemoglobin. Best results are obtained if stimulation begins already one week before first donation.
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PMID:[Autologous blood donation with preliminary erythropoietin stimulation]. 897 94

During the last decade, a considerable amount of new information has accumulated regarding therapy optimalization of renal anaemia with recombinant human erythropoietin (EPO). Key question involved is EPO hyporesponsiveness caused by absolute or functional iron deficiency. Most controversial issue in the treatment of renal anaemia in patients with chronic renal insufficiency is the definition of optimal target haemoglobin. Many questions about optimizing EPO therapy were considered at the 2nd European Epoetin Symposium which was held in April 1998 on Crete. Discussion was devoted also to revision of a draft version of the European Best Practice Guidelines for the Management of Anaemia in Patients with Chronic Renal Failure. The presented review is on summary of new insights presented at the symposium. (Ref. 85.)
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PMID:[Treatment of renal anemia with erythropoietin]. 1064 31

Recombinant human erythropoietin (rhEPO), which increases red cell mass, is one of the most abused substances in sport. Abuse is currently undetectable by the only direct routine method, immunoassay, since blood and urine rhEPO are immunologically indistinguishable from endogenous EPO. Elevated EPO levels are only detectable several days after rhEPO administration. Indirect parameters have therefore been introduced, primarily the haematocrit level, but also markers of functional iron deficiency during or after rhEPO administration (hypochromic red cells and reticulocytes, serum transferrin receptors, ferritin levels) and, in the urine, fibrin degradation products. Although iron status indices have yielded promising results, athletes are currently banned solely on the basis of their haematocrit. Yet various factors can cause false positive haematocrit results with potentially fatal consequences to athletes' careers. Until new direct assays such as liquid chromatography-mass spectrometry have been evaluated and introduced, efforts must be directed at using a battery of tests to increase the sensitivity and specificity and reduce the number of false positives and false negatives.
Baillieres Best Pract Res Clin Endocrinol Metab 2000 Mar
PMID:Erythropoietin test methods. 1093 16

The invention of recombinant human erythropoietin (rHuEpo) for the treatment of renal anaemia was a hallmark in the care of patients with renal insufficiency. Recently published guidelines (European Best Practice Guidelines, NKF-DOQI) have set the target haemoglobin to be reached by treatment with rHuEpo to >11 g/dl. Normalizing haemoglobin levels may reduce morbidity and mortality and improve quality of life in haemodialysis patients. During long-term treatment, most patients will not respond adequately to therapy with rHuEpo alone. The most important confounding factor, limiting the effectiveness of rHuEpo, is absolute or functional iron deficiency, which is now recognized and treated in many dialysis units. However, there are several other adjuvant treatment options which may help to optimize the response to treatment with rHuEpo. A weekly dose of 2-3 mg of folic acid and 100-150 mg of vitamin B6 is recommended for haemodialysis patients on rHuEpo therapy. The addition of 0.25 mg/month of vitamin B12 may be necessary in selected patients. Vitamin C (1-1.5 g/week) was shown to overcome functional iron deficiency in patients with high ferritin levels. The potential increase of oxidative stress induced by intravenous iron therapy may be blunted by concomitant administration of vitamin E (1200 IU). There is clear evidence from the literature that treatment of secondary hyperparathyroidism by vitamin D improves erythropoiesis. The most recently discovered biological effects of rHuEpo include the induction of several genes in endothelial cells as well as a role for erythropoietin in the outcome of plasmodium infection. A new erythropoietin-like molecule is novel erythropoiesis stimulating protein (NESP), which is as effective and safe as rHuEpo, with the potential advantage of less frequent dosing.
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PMID:Novel aspects of erythropoietin response in renal failure patients. 1150 83

The modern British diet contains less red meat and is lower in iron than that consumed 30 years ago. This is in spite of the fact that fortification of foods, particularly breakfast cereals, with iron has become more widespread. Although there is no clear relationship between dietary iron intake and iron status, isotope studies have identified multiple dietary factors that influence iron absorption, such as ascorbic acid, animal tissue, phytates and polyphenols. There is no evidence to suggest that current dietary changes will have a major impact on iron status in the general population; however, effects on the incidence of iron overload in individuals with HFE mutations and iron deficiency in children and premenopausal women remain to be determined.
Best Pract Res Clin Haematol 2002 Jun
PMID:Clinical implications of changes in the modern diet: iron intake, absorption and status. 1240 5

Haemochromatosis may be inherited or acquired. The commonest inherited form is HFE-related genetic haemochromatosis (GH). This is associated with homozygosity for the C282Y mutation in the HFE gene. Individuals with GH present in several ways depending upon the severity of iron overload. However, only a small proportion of genetically susceptible individuals develop disease. Diagnosis of GH is based on measurement of transferrin saturation, serum ferritin levels and mutation analysis of HFE. Liver biopsy is not necessary for diagnosis. It is used to establish the severity of liver disease in selected patients. Other complications of iron overload are identified by specific tests. Initial management of GH is by weekly venesection until borderline iron deficiency is achieved. The serum ferritin is then maintained at 50 microg/l by 3-6 monthly venesection. Specific organ damage is managed appropriately. Early diagnosis and treatment before irreversible damage has occurred gives a normal life expectancy. Non-HFE related inherited iron overload may be due to mutations in other iron related genes. Management is along the same lines as for GH, although if venesection is not tolerated, other approaches may be necessary.
Best Pract Res Clin Haematol 2002 Jun
PMID:Diagnosis and management of genetic haemochromatosis. 1240 8

Iron deficiency is the most common disorder of iron metabolism worldwide, but there is concern that iron accumulation resulting from enhanced iron absorption may also be a cause of morbidity. In patients with genetic haemochromatosis the clinical manifestations of iron overload are well-known. In northern Europe 90% of such patients are homozygous for the C282Y mutation of the HFE gene and this genotype is found in 1 in 200 of the population. Heterozygosity for C282Y occurs in 15% of the population and 25% carry another mutation, H63D. Population studies have revealed (i) the serum transferrin saturation is strongly influenced by HFE genotype, being lowest in subjects lacking mutations and highest in those homozygous for C282Y; (ii) most subjects homozygous for C282Y accumulate iron but do not present with the clinical manifestations of iron overload. Testing for HFE mutations in clinics for diabetes, liver disease and cardiovascular disease has shown that homozygosity for C282Y is not commonly found. Heterozygosity for either C282Y or H63D does not appear to be a risk factor for these common conditions.
Best Pract Res Clin Haematol 2002 Jun
PMID:HFE Mutations as risk factors in disease. 1240 9

Anaemia is typically the first clue to iron deficiency, but an isolated haemoglobin measurement has both low specificity and low sensitivity. The latter can be improved by including measures of iron-deficient erythropoiesis such as the transferrin iron saturation, mean corpuscular haemoglobin concentration, erythrocyte zinc protoporphyrin, percentage of hypochromic erythrocytes or reticulocyte haemoglobin concentration. However, the changes in these measurements with iron deficiency are indistinguishable from those seen in patients with the anaemia of chronic disease. The optimal diagnostic approach is to measure the serum ferritin as an index of iron stores and the serum transferrin receptor as a index of tissue iron deficiency. The treatment of iron deficiency should always be initiated with oral iron. When this fails because of large blood losses, iron malabsorption, or intolerance to oral iron, parenteral iron can be given using iron dextran, iron gluconate or iron sucrose.
Best Pract Res Clin Haematol 2005 Jun
PMID:Diagnosis and management of iron-deficiency anaemia. 1573 93

Iron deficiency continues to be the most prevalent nutritional deficiency disorder in the world, affecting an estimated two billion people, most of whom live in developing countries. It has far-reaching effects on the health, well-being and productivity of those affected. Iron fortification of food is regarded as the most cost-effective method for reducing the prevalence of nutritional iron deficiency. In industrialized countries this has had an important beneficial effect; however, nutritional anaemia remains very prevalent in developing countries, and iron fortification appears until recently to have had little impact. Two important reasons for the latter situation are inadequate documentation of the magnitude of the iron deficiency component of anaemia in different regions of the world, and the use of iron compounds that are poorly bioavailable in fortification programmes. Several recent interventions using innovative approaches to dietary fortification that ensure the delivery of adequate quantities of bioavailable iron have demonstrated that iron fortification of food can be an effective and implementable strategy for controlling nutritional iron deficiency in non-industrialized countries.
Best Pract Res Clin Haematol 2005 Jun
PMID:The impact of iron fortification on nutritional anaemia. 1573 94


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