Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anaemia in elderly patients should never be regarded as a normal physiological response to aging. Underlying causes must be investigated and treated in a similar manner to that used in younger adults. In addition to a thorough history and physical examination, basic investigations such as red cell indices and morphology, reticulocyte count, haematinic assays and occasionally bone marrow examination, will detect the underlying pathology in most cases. Anaemia may be classified, according to red blood cell mean corpuscular volume, into microcytic, macrocytic and normocytic types. Anaemia with an absolute reticulocytosis is due either to acute blood loss or haemolysis. Other anaemias, more frequently encountered in elderly patients, are hypoproliferative, and reflect depressed marrow production or impaired erythroid maturation. Examples include anaemia of chronic disease and iron deficiency and, less commonly, megaloblastic anaemia and anaemia due to primary bone marrow failure. The treatment of anaemia should aim to correct the underlying cause of the disorder and/or to improve the quality of the blood, e.g. by haematinic replacement therapy. Recombinant human erythropoietin has revolutionised the treatment of anaemia associated with chronic renal failure, while its role in other anaemias is currently under investigation. Regular blood transfusion may be required for some elderly patients with chronic anaemia. However, the attendant risks of this procedure, such as iron overload and viral hepatitis transmission, must be considered.
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PMID:Identification and treatment of anaemia in older patients. 818 39

Iron is universally abundant and no life can exist without it. However, iron levels should be maintained within a narrow range. Iron deficiency causes anaemia, whereas excessive iron increases cancer risk, presumably by free radical generation. Several pathological conditions such as genetic haemochromatosis, chronic viral hepatitis B and C, conditions related to asbestos fibre exposure and ovarian endometriosis have been recognized as iron overload-associated conditions that also increase human cancer risks. Iron's carcinogenicity has been documented in animal experiments. Surprisingly, these studies have revealed that the homozygous deletion of CDKN2A/2B is a major hallmark of iron-induced carcinogenesis. Recently, the hormonal regulation of iron metabolism has been elucidated. A commonly hypothesized mechanism may be the lack of any iron disposal pathway other than for bleeding and a mechanism of iron re-uptake as catechol chelate has been discovered. Iron overload in neurons via the ferroportin block may play a role in Alzheimer's disease. Furthermore, a recent epidemiological study reported that iron reduction by phlebotomy was associated with decreased cancer risks in a general population. Given that the required amounts of iron decrease during ageing, the fine control of body iron stores would be a wise strategy for chemoprevention of several diseases.
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PMID:Iron as a target of chemoprevention for longevity in humans. 2161 76

Loss of blood associated with hemodialysis procedures and laboratory testing, together with impaired iron absorption due to elevation of hepcidin, invariably cause iron deficiency in end-stage renal disease patients. For this reason, nearly all ESRD patients require intravenous iron to replete iron stores. Unfortunately, intravenously administered iron is often used routinely with inadequate attention to the body iron stores or severity of systemic inflammation. This has led to an epidemic of iron overload in the ESRD population. Only a minute amount (3-4 mg) of the total body iron (3-4 g in an adult man) resides in the plasma bound to transferrin, which serves as a safe vehicle for iron transport in the circulation. IV iron products are generally administered as bolus injections of 100 to 1000 mg, which far exceeds the available pool of free transferrin and represents a huge quantity compared to the intestinal iron absorption of 1 to 2 mg/day in the course of 3 to 4 meals. Administration of these products results in an increased plasma level of catalytically active non-transferrin bound iron and the rise in the biomarkers of oxidative stress and inflammation. IV iron bypasses the biological safeguards for the transport and handling of iron and helps to intensify chronic kidney disease-associated oxidative stress and inflammation. As briefly described in this review, indiscriminate use of IV iron can accelerate cardiovascular disease, promote microbial infections, aggravate viral hepatitis, and worsen diabetes and diabetic complications in such patients. For these reasons IV iron should be used judiciously in this vulnerable population.
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PMID:Toxic effects of IV iron preparations in CKD patients. 2464 44