Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present study is to evaluate in an elderly hospitalized population the diagnostic value of the serum transferrin receptor (sTfR) in distinguishing IDA (iron deficiency anemia) from ACD (anemia of chronic disease) as compared to conventional laboratory tests of iron metabolism, especially serum ferritin. In a prospective study, 34 patients with IDA and 38 patients with ACD (a chronic disorder in 23 and an acute infection in 15) were evaluated using iron status tests including serum transferrin receptor assay. The iron stores were assessed by bone marrow examination. sTfR levels were elevated (>28.1 nmol/L) in 68% of the IDA patients but also in 43% of the patients with ACD-chronic inflammation and 33% with ACD-acute infection. Serum ferritin was the best test to differentiate IDA from ACD patients. We conclude that serum ferritin is a more sensitive and specific parameter than the sTfR assay to predict the bone marrow iron status in an elderly anemic population.
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PMID:Serum transferrin receptor in the evaluation of the iron status in elderly hospitalized patients with anemia. 1183 23

Although anemia is a common finding among human immunodeficiency (HIV)-infected infants in sub-Saharan Africa, the factors contributing to the pathogenesis of anemia have not been well characterized. We sought to characterize the relative contribution of iron deficiency and chronic disease to the anemia among infants. Hemoglobin, ferritin, erythropoietin, tumor necrosis factor-alpha (TNF-alpha), neopterin, CD4(+) lymphocyte count and plasma HIV load were measured in 165 HIV-infected and 39 uninfected 9-mo-old infants seen in an outpatient pediatric clinic in Kampala, Uganda. Among HIV-infected and uninfected infants, the prevalence of anemia (hemoglobin < 110 g/L) was 90.9 and 76.9%, respectively (P = 0.015), and the prevalence of iron deficiency anemia (hemoglobin < 110 g/L and ferritin < 12 microg/L) was 44.3 and 45.4%, respectively (P = 0.92). The relatively higher prevalence of anemia among HIV-infected infants was attributed to the anemia of chronic disease. Among infants with and without iron deficiency, the fitted regression line was log(10) plasma erythropoietin = 2.86 - 0.016.hemoglobin, and log(10) plasma erythropoietin = 4.11 - 0.028.hemoglobin, respectively, with a difference in the slope of the regression lines between log(10) erythropoietin and hemoglobin among infants with and without iron deficiency (P = 0.049). Infants in Uganda have an extremely high prevalence of anemia, and nearly half of the anemia is due to iron deficiency. The erythropoietin response to anemia appears to be upregulated among infants with iron deficiency.
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PMID:Iron deficiency anemia is highly prevalent among human immunodeficiency virus-infected and uninfected infants in Uganda. 1188 May 66

Iron appears to exert self-regulatory control over erythroblast iron uptake, iron storage and its incorporation into haem. It does this via iron regulatory proteins (IRPs) which bind reversibly to the iron responsive elements (IREs) on the mRNA of transferrin receptor (TfR), erythroid 5-aminolaevulinic acid synthase (ALA-S2) and ferritin. Iron deficiency leads to the binding of IRP to IRE. This binding inhibits the translation of mRNA for ALA-S2 and ferritin but stabilizes mRNA for TfR expression. Sideroblastic erythropoiesis is highly ineffective and characterized by mitochondrial iron loading. The study of X-linked sideroblastic anaemia has shown that the entry of iron into the mitochondria is poorly controlled and able to occur when protoporphyrin production is reduced, as is seen with the ALA-S2 mutations, or when it is increased as has been seen with ABC7 transporter mutations. Sideropenia characterises both iron deficiency anaemia (IDA) and the anaemia of chronic disease (ACD). Erythroblasts in ACD seem doubly equipped to protect their iron supply with their ability to increase the efficiency of transferrin-iron uptake as well as to activate the IRP/IRE system to increase surface TfR production. This increase in efficiency restricts the need to increase surface TfR production and maintains serum soluble TfR (sTfR) values within the normal range in iron replete ACD. The coexistence of iron deficiency with chronic disease, however, is associated with an increase in both the efficiency and number and a highly significant rise in sTfR values.
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PMID:Erythroblast iron metabolism in sideroblastic and sideropenic states. 1224 84

Absolute or functional iron deficiency is a common problem in chronic disease which may lead to iron-deficient erythropoesis. Moreover, lack of available iron is the most common reason for unresponsiveness to epoetin in patients on chronic dialysis. Measurements of serum ferritin, transferrin saturation and percentage of hypochromic red blood cells allow the assessment of iron status. Lack of iron resorption and dose-dependent side-effects limit oral supplementation in a number of patients. Several iron preparations are available for intravenous substitution, especially the newly registered iron-saccharose offers safe and reliable iron supplementation and reduces the risk of anaphylaxis and iron toxicity. This review discusses new guidelines concerning diagnosis of iron status, indication for therapy and application of intravenous iron preparation.
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PMID:[Indications and practical management of parenteral iron therapy]. 1287 35

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

This study aims to report on the clinical and laboratory picture and the disease course and outcome in patients having adult onset Still's disease (AOSD), to briefly review existing literature on the subject, and to compare our findings with those previously reported. Results are reported for 28 patients with AOSD satisfying the preliminary criteria of Yamaguchi et al. seen in a teaching hospital over the last 10 years. A high percent of the patients with AOSD were women. The mean (+SD) age at disease onset was 27.8 (+8.4) years. We found fever in 100%, rash in 85%, arthritis in 64%, lymphadenopathy in 60%, splenomegaly in 57%, hepatomegaly in 35%, pleural effusion in 17.9%, and pericardial effusion in 3.6% of our patients. Leukocytosis was present in 96% of the patients, a normochromic, normocytic anemia in 54%, and an elevated erythrocyte sedimentation rate (ESR) in all. Serum ferritin levels were raised in 89% of the patients. The mean follow-up of the patients was 3.72 + 2.46 years. The mean delay in diagnosis was 7.32 + 18.0 months. The mean time to enter remission was 9.7 months. Self-limited, intermittent, and chronic disease course was seen in 14.3, 57.1, and 28.6% of patients, respectively. The outcome was good in about 89% of patients, and mortality was nil. No particular clinical or laboratory variable was found to predict the subsequent disease course and outcome in our patients. On comparing our data with important previous series, we found a higher percentage of women and of patients presenting in the age group 16-35 years, a lower frequency of arthritis and pericardial effusion, and some other notable differences. Importantly, the disease course was benign, probably as an outcome of heightened awareness and less diagnostic delay than in the past, allowing for early, aggressive, and appropriate treatment. It is concluded that AOSD is now a relatively benign disease if diagnosed early and treated appropriately.
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PMID:Ten years of clinical experience with adult onset Still's disease: is the outcome improving? 1708 84

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

Adult-onset Still disease (AOSD) is an uncommon inflammatory condition of unknown origin typically characterized by four main (cardinal) symptoms: spiking fever > or =39 degrees C, arthralgia or arthritis, skin rash and hyperleucocytosis (> or =10,000 cells/mm3) with neutrophils > or =80%. As many other manifestations are possible, diagnosis is potentially challenging. Determination of the total and glycosylated ferritin levels, although not pathognomonic, can help in diagnosis. The disease evolution of AOSD can be monocyclic, polycyclic or chronic. In chronic disease, joint involvement is often predominant and erosions are noted in one-third of patients. No prognostic factors have been identified to date. Therapeutic strategies are from observational data. Corticosteroids are usually the first-line treatment. With inadequate response to corticosteroids, methotrexate appears the best choice to control disease activity and allow for tapering of steroid use. For refractory disease, biological therapy with agents blocking interleukin-1 (anakinra) and then those blocking interleukin-6 (tocilizumab) seem the most promising.
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PMID:Adult-onset Still disease. 1902 63

A new era in iron chelation therapy began with the successful removal of excess iron load and the maintenance of normal iron stores in thalassemia patients using the International Committee on Chelation (ICOC) protocols. This achievement was based on two phases, firstly the introduction of deferiprone (L1) (80-100 mg/kg/day) and deferoxamine (DFO) (40-60 mg/kg at least 3 days per week) combination therapy, which appears to progressively remove all excess storage iron and thereafter by the introduction of L1 monotherapy that can maintain physiological range levels of serum ferritin, cardiac and liver magnetic resonance imaging (MRI) T2*. This new development is likely to change current practices and set a new gold standard in the treatment of transfusional iron loaded patients leading to an increased survival and the change of thalassemia from a fatal to a chronic disease. A major aspect of the improved therapies is the ability of L1 to mobilize and remove excess cardiac iron and reduce congestive cardiac failure, which is the main cause of death in thalassemia patients. Further, new developments include the use of alternating sequential chelation therapies and selected dose protocols with L1, DFO and deferasirox (DFRA) for overcoming toxicity and efficacy complications observed in some patients treated with monotherapies or combination therapies. The selection and adjustment of dose protocols is crucial for providing optimum chelation therapy for each individual patient.
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PMID:A new era in iron chelation therapy: the design of optimal, individually adjusted iron chelation therapies for the complete removal of iron overload in thalassemia and other chronically transfused patients. 1981 79


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