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

Anemia is common in acute critically ill patients. Although blood loss, either by trauma, surgery, phlebotomies or gastrointestinal bleeding, may play a role, the anemia in these patients bears many similarities to the anemia characteristic of chronic disease. Serum iron is low with a high concentration of ferritin and low-to-normal transferrin and serum transferrin receptor levels. Several mechanisms may be involved, with inflammation playing a crucial role. Although the exact nature of the inflammatory response and the role of various cytokines need further elucidation, it is known that inflammation blunts the responsiveness of the hormone erythropoietin and induces functional iron deficiency. Iron is trapped in cells of the mononuclear phagocytic system and its release is temporarily blocked. The bone marrow is still capable of incorporating iron and of responding to treatment with recombinant human erythropoietin (rh-EPO). The duration of the anemia is related to the persistence of the inflammation. Although the effects of anemia on morbidity and mortality in the critically ill are poorly defined, a restrictive transfusion policy, in which hemoglobin concentration is maintained between 7.0 and 9.0 g/dl, proves to be at least as effective as, if not superior to, a more liberal regimen. In individual situations, such as in cardiovascular and cancer patients, higher thresholds may be appropriate. The administration of rh-EPO is an alternative to reduce the need for red blood cell transfusions and to avoid transfusion-related complications. Although its efficacy has been shown, questions regarding cost-benefit, dose regimen and clinical outcomes need to be answered before its large-scale use can be recommended.
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PMID:Anemia in critically ill patients. 1566 82

Soluble transferrin receptor (sTfR) is a biochemical parameter used for the detection of iron deficiency in situations where ferritin has limited diagnostic value owing to the present chronic disease. The sTfR concentration was determined in 118 patients divided according to their inflammatory status and underlying disease into groups of patients with iron-deficiency anemia (IDA), anemia of chronic disease (ACD) and patients with a coexisting state of iron deficiency and anemia of chronic disease (ID+ACD). All patients with iron deficiency had elevated sTfR levels, but ferritin concentrations were normal or increased in patients with inflammatory characteristics. Diagnostic efficiencies of sTfR, sTfR/log ferritin index (sTfR/F) and ferritin were evaluated by receiver operating characteristic curve (ROC) analysis. According to the results obtained, the best diagnostic efficiency for differential diagnosis of anemic patients with iron deficiency compared to the control group had a sTfR concentration (0.884) that was significantly higher than ferritin (0.638), but not higher than the calculated ratio sTfR/F (0.820). The cut-off value of the sTfR/F index differentiating the best control group from the IDA and ID+ACD groups was 1.30, and for differentiation of ACD from IDA and ID+ACD, the value was 0.90. Soluble transferrin receptor is an additional parameter to ferritin for the diagnosis of IDA and differential diagnosis of ID+ACD, but calculation of the sTfR/F index did not improve the diagnostic value of determining sTfR alone.
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PMID:Usefulness of soluble transferrin receptor and ferritin in iron deficiency and chronic disease. 1627 88

Epidemiological studies report that a third of the cases of anaemia in older persons is unexplained. We compared erythropoietin (EPO), inflammatory markers and major comorbidities between older subjects with normal haemoglobin levels and those with different aetiologic forms of anaemia, including unexplained anaemia. Participants were a representative sample of 964 persons aged > or =65 years, with no evidence of bleeding, complete blood tests, and a complete blood count within 6 h of phlebotomy. Anaemia was defined as haemoglobin <130 g/l in men and 120 g/l in women, and classified as a result of chronic kidney disease, iron deficiency, chronic disease and B12/folate deficiency anaemia, or unexplained anaemia based on standard criteria. Of the 124 anaemic participants, 42 (36.8%) had unexplained anaemia. Participants with anaemia of chronic diseases had significantly higher interleukin-6 (IL-6) and C-reactive protein (CRP) levels, while those with unexplained anaemia had significantly lower CRP than non-anaemic controls. Iron deficiency anaemia was characterised by significantly higher EPO levels compared with other types of anaemia and normal haemoglobin, B12 and/or folate deficiency. Unexplained anaemia was characterised by unexpectedly low EPO and low lymphocyte count. Unexplained anaemia is associated with reduced kidney EPO response, low levels of pro-inflammatory markers and low lymphocyte counts.
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PMID:Unexplained anaemia in older persons is characterised by low erythropoietin and low levels of pro-inflammatory markers. 1734 Dec 72

Anemia is common in patients who have both heart failure and chronic kidney disease, and there is an association between anemia and progression of both diseases. The main causes of anemia are deficient production of erythropoietin (EPO), iron deficiency, and chronic disease with endogenous EPO resistance. EPO has been successfully used for over a decade to treat anemia in patients with chronic kidney disease. Less obvious are the safety and efficacy of EPO treatment in patients with both heart failure and renal disease. Up to 10% of patients receiving EPO are hyporesponsive to therapy and require large doses of the agent. Several mechanisms could explain resistance to endogenous and exogenous EPO. Proinflammatory cytokines antagonize the action of EPO by exerting an inhibitory effect on erythroid progenitor cells and by disrupting iron metabolism (a process in which hepcidin has a central role). EPO resistance might also be caused by inflammation, which has a negative effect on EPO receptors. Furthermore, neocytolysis could have a role. As resistance to exogenous EPO is associated with an increased risk of death, it is important to understand how cardiorenal failure affects EPO production and function.
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PMID:Mechanisms of Disease: erythropoietin resistance in patients with both heart and kidney failure. 1809 27

Iron is utilised by the body for oxygen transport and energy production, and is therefore essential to athletic performance. Commonly, athletes are diagnosed as iron deficient, however, contrasting evidence exists as to the severity of deficiency and the effect on performance. Iron losses can result from a host of mechanisms during exercise such as hemolysis, hematuria, sweating and gastrointestinal bleeding. Additionally, recent research investigating the anemia of inflammation during states of chronic disease has allowed us to draw some comparisons between unhealthy populations and athletes. The acute-phase response is a well-recognised reaction to both exercise and disease. Elevated cytokine levels from such a response have been shown to increase the liver production of the hormone Hepcidin. Hepcidin up-regulation has a negative impact on the iron transport and absorption channels within the body, and may explain a potential new mechanism behind iron deficiency in athletes. This review will attempt to explore the current literature that exits in this new area of iron metabolism and exercise.
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PMID:Athletic induced iron deficiency: new insights into the role of inflammation, cytokines and hormones. 1836 40

In 6% of 854 patients in a city general practice anemia was found. Anemia was defined by WHO criteria. An algorithm for the evaluation of the cause includes patient's history and laboratory investigations inclusive of reticulocyte count, serum ferritin with CRP, serum vitamin B12, serum or erythrocyte folate and serum creatinine, depending on clinical situation and mean corpuscular volume (MCV). Median age of the patients was 77 years. The most frequent underlying cause of anemia was chronic renal failure (in 21%). According to the high patient's age, iron deficiency, chronic disease and malignancy were frequent for anemia, too. 35% of patients had more than one cause of anemia. The results are compared with other sparse reports from general practices and are discussed regarding the particular situation in the elderly.
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PMID:[Prevalence and causes of anemia in a city general practice]. 1877 Sep 23

Curcumin is a natural product currently in human clinical trials for a variety of neoplastic, preneoplastic, and inflammatory conditions. We previously observed that, in cultured cells, curcumin exhibits properties of an iron chelator. To test whether the chelator activity of curcumin is sufficient to induce iron deficiency in vivo, mice were placed on diets containing graded concentrations of both iron and curcumin for 26 weeks. Mice receiving the lowest level of dietary iron exhibited borderline iron deficiency, with reductions in spleen and liver iron, but little effect on hemoglobin, hematocrit, transferrin saturation, or plasma iron. Against this backdrop of subclinical iron deficiency, curcumin exerted profound 2 effects on systemic iron, inducing a dose-dependent decline in hematocrit, hemoglobin, serum iron, and transferrin saturation, the appearance of microcytic anisocytotic red blood cells, and decreases in spleen and liver iron content. Curcumin repressed synthesis of hepcidin, a peptide that plays a central role in regulation of systemic iron balance. These results demonstrate that curcumin has the potential to affect systemic iron metabolism, particularly in a setting of subclinical iron deficiency. This may affect the use of curcumin in patients with marginal iron stores or those exhibiting the anemia of cancer and chronic disease.
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PMID:Curcumin, a cancer chemopreventive and chemotherapeutic agent, is a biologically active iron chelator. 1913 57

Inflammatory bowel diseases (IBD), comprising Crohn's disease (CD) and ulcerative colitis (UC), are chronic inflammatory disorders of the gut, which lead to significant morbidity and impaired quality of life (QoL) in sufferers, without generally affecting mortality. Despite CD and UC being chronic, life-long illnesses, most medical management is directed at acute flares of disease. Moreover, with more intensive medical therapy and the development of biological therapy, there is a risk that management will become even more narrowly focused on acute care, and be directed only at those with more severe disease, rather than encompassing all sufferers and addressing important non-acute issues. This imbalance of concentration of medical attention on 'high-end' care is in part driven by the need to perform and publish randomized clinical trials of newer therapies to obtain registration and licensing for these agents, which thus occupy a large proportion of the recent IBD treatment literature. This leads to less attention on relatively 'low-technology' issues including: (i) the psychosocial burden of chronic disease, QoL and specific psychological comorbidities; (ii) comorbidity with functional gastrointestinal disorders (FGIDs); (iii) maintenance therapy, monitoring and compliance; (iv) smoking (with regard to CD); (v) sexuality, fertility, family planning and pregnancy; and (vi) iron deficiency and anaemia. We propose these to be the 'Un-promoted Issues' in IBD and review the importance and treatment of each of these in the current management of IBD.
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PMID:Un-promoted issues in inflammatory bowel disease: opportunities to optimize care. 1984 44

Iron and its homeostasis are intimately tied to the inflammatory response. The adaptation to iron deficiency, which confers resistance to infection and improves the inflammatory condition, underlies what is probably the most obvious link: the anemia of inflammation or chronic disease. A large number of stimulatory inputs must be integrated to tightly control iron homeostasis during the inflammatory response. In order to understand the pathways of iron trafficking and how they are regulated, this article presents a brief overview of iron homeostasis. A major focus is on the regulation of the peptide hormone hepcidin during the inflammatory response and how its function contributes to the process of iron withdrawal. The review also summarizes new and emerging information about other iron metabolic regulators and effectors that contribute to the inflammatory response. Potential benefits of treatment to ameliorate the hypoferremic condition promoted by inflammation are also considered.
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PMID:Iron homeostasis and the inflammatory response. 2042 May 24

After iron deficiency anemia the anemia of chronic disorder is the second most frequent anemia, and in hospitalized patients and/or patients suffering from chronic disease, especially infection, cancer and autoimmune disorders it is even the most frequent anemia. Morphologically it belongs to the normochromic, normocytic, hyporegeneratoric anemias. Pathogenetically it is induced by the upregulation of hepcidin, a recently detected acute phase protein with most important regulatory function in the iron-household. As a consequence of elevated hepcidin at the same time iron absorption in the bowel as well as iron release from macrophages are reduced, resulting in sequestration of iron in the RES and therefore functional iron deficiency. The other reason is a blunted release of erythropoetin (EPO) with at the same time reduced effectiveness due to down-regulation of EPO-receptors on erythroid cells. Treatment consists first of all in the therapy of the underlying disease and possibly in the combined application of EPO and iron.
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PMID:[Anemia of chronic disorder - pathogenesis, clinical presentation and treatment]. 2050 18


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