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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The reliability of a radioimmunometric assay of serum ferritin concentration by a packaged kit was evaluated. In addition, application of the serum ferritin assay to the clinical evaluation of selected anemias was assessed. When appropriate serum dilutions were utilized, this method was sufficiently reproducible and reliable for application to the clinical laboratory. Serum ferritin was found to be a valuable tool in the differential diagnosis of anemia accompanied by hypoferremia, although iron depletion coexisting with either the anemia of chronic disease or active hepatocellular disease may not be clearly appreciated. The primary advantage of the determination was to help characterize the iron status of the patient with a hypochromic microcytic anemia or hypoferremia who would ordinarly require a bone-marrow examination for iron stores.
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PMID:Evaluation of a packaged kit assay of serum ferritin and application to clinical diagnosis of selected anemias. 69 76

Tests to evaluate body iron stores were compared in patients with iron deficiency and the anemia of chronic disease. The serum ferritin assay separated these disorders in 20 of 22 patients. One discrepancy was explained by the concomitant association of both disorders. From this study and review of literature a low serum ferritin level is a good indication for iron therapy. The serum ferritin assay is a clinically useful test in lieu of bone marrow estimation of body iron stores to detect patients with iron deficiency. Total iron binding capacity levels when high-normal or elevated are sometimes helpful as a screening test in separating iron deficiency from the anemia of chronic disorders. Free erythrocyte protoporphyrin values were elevated in both conditions but were higher in iron deficiency than in the anemia of chronic disorders with considerable overlap of values. Urinary iron excretion with deferoxamine was not helpful in separating these disorders but is a useful test to establish iron overload. An elevated serum ferritin level is usually found with disease of iron overload but serum iron levels, deferoxamine iron excretion tests, and liver biopsy for estimation of iron stores are still beneficial diagnostic aids.
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PMID:Serum ferritin, free erythrocyte protoporphyrin, and urinary iron excretion in patients with iron disorders. 86 19

The ferritin content of monocytes, lymphocytes and polymorphs is reduced in patients with iron deficiency anaemia. In patients with the anaemia of chronic disease a reduced serum iron concentration is associated with an increase in the ferritin content of all peripheral blood leucocytes. Iron uptake by all cell types is related to transferrin saturation. In iron deficiency anaemia lymphocyte iron uptake is greatly increased, possibly relfecting intracellular iron depletion. In patients with active rheumatoid arthritis and carcinomatosis there is no alteration in leucocyte iron uptake or ferritin synthesis.
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PMID:Iron uptake and ferritin synthesis by peripheral blood leucocytes from normal subjects and patients with iron deficiency and the anaemia of chronic disease. 97 35

Microcytic anemia is defined as the presence of small, often hypochromic, red blood cells in a peripheral blood smear and is usually characterized by a low MCV (less than 83 micron 3). Iron deficiency is the most common cause of microcytic anemia. The absence of iron stores in the bone marrow remains the most definitive test for differentiating iron deficiency from the other microcytic states, ie, anemia of chronic disease, thalassemia, and sideroblastic anemia. However, measurement of serum ferritin, iron concentration, transferrin saturation and iron-binding capacity, and, more recently, serum transferrin receptors may obviate proceeding to bone marrow evaluation. The human body maintains iron homeostasis by recycling the majority of its stores. Disruptions in this balance are commonly seen during menstruation, pregnancy, and gastrointestinal bleeding. Although the iron-absorptive capacity is able to increase upon feedback regarding total body iron stores or erythropoietic activity, this physiologic response is minimal. Significant iron loss requires replacement with iron supplements. The vast majority of patients respond effectively to inexpensive and usually well-tolerated oral iron preparations. In the rare circumstances of malabsorption, losses exceeding maximal oral replacement, or true intolerance, parenteral iron dextran is effective. In either form of treatment, it is necessary to replete iron stores in addition to correcting the anemia.
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PMID:Microcytic anemia. Differential diagnosis and management of iron deficiency anemia. 157 56

Recent studies have shown that the serum transferrin receptor is a sensitive, quantitative measure of tissue iron deficiency. This study was undertaken to determine the serum transferrin receptor's ability to distinguish iron-deficiency anemia from the anemia of chronic inflammation and to identify iron deficiency in patients with liver disease. The mean transferrin receptor level in 17 normal controls was 5.36 +/- 0.82 mg/L compared with 13.91 +/- 4.63 mg/L in 17 patients with iron-deficiency anemia (p less than 0.001). The mean serum receptor level was normal in all 20 patients with acute infection, including five with acute hepatitis, and was also normal in 8 of 10 anemic patients with chronic liver disease. Receptor levels were in the normal range in all but 4 of 41 patients with anemia of chronic disease. We conclude that unlike serum ferritin levels, which are disproportionately elevated in relation to iron stores in patients with inflammation or liver disease, the serum transferrin receptor level is not affected by these disorders and is therefore a reliable laboratory index of iron deficiency anemia.
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PMID:Serum transferrin receptor distinguishes the anemia of chronic disease from iron deficiency anemia. 158 89

A retrospective study of the 99 surviving heart and lung transplant (HLT) recipients at one center showed that 31% had significant anemia (hemoglobin less than 100g/L) six months after transplantation. Chronic anemia persisted in 18% of HLT recipients two years posttransplantation. A similar study of 100 heart transplant recipients showed no unexplained anemic patients. The prevalence of anemia after HLT was unrelated to the original diagnosis, immunosuppression, or acute rejection. All HLT recipients appeared to be unduly sensitive to the myelosuppressive effects of azathioprine. Detailed studies in 16 representative patients showed a normochromic, anisocytotic anemia with normal reticulocyte counts, B12 and folate levels, and haptoglobin levels and appropriate erythropoietin levels--but increased ESRs, low/normal iron levels and low/normal total iron binding capacity, normal or raised ferritin levels, and autoantibodies in 4 (25%). Bone marrow aspirates in 10 patients showed dyshemopoiesis out of proportion to the degree of anemia and colonies of activated lymphoid cells. The cause for this anemia appears to be a combination of anemia of chronic disease and dyshemopoiesis, both of uncertain etiology.
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PMID:The prevalence, course, and characteristics of chronic anemia after heart and lung transplantation. 160 80

Flow cytometric reticulocyte enumeration measures the fluorescence intensity of the reticulocyte population, the reticulocyte mean channel fluorescence. Reticulocyte mean channel fluorescence, used as an indicator of reticulocyte maturation, is directly proportional to the amount of intracellular RNA. Other factors, such as iron stores, may affect reticulocyte mean channel fluorescence. Iron status in normal controls, patients with anemia of chronic disease, and pregnant women was evaluated by hemoglobin, hematocrit, red blood cell indices, iron, total iron-binding capacity, and ferritin. Reticulocyte mean channel fluorescence was significantly elevated (P less than 0.0001) to 85.6 +/- 4.6 (mean +/- 1 standard deviation) in iron-deficient anemic patients and to 81.1 +/- 8.4 in iron-depleted patients compared to healthy individuals (69.7 +/- 2.6). The reticulocyte mean channel fluorescence in anemia of chronic disease was 71.3 +/- 5.8 and was not significantly different from that of normal controls. Reticulocyte mean channel fluorescence showed significant correlations with total iron-binding capacity (P less than 0.0001, r = 0.62) and ferritin (P less than 0.0001, r = 0.40). A possible explanation for these findings, describing differences in cytoplasmic levels of transferrin receptor mRNA, is discussed.
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PMID:Effect of iron status on reticulocyte mean channel fluorescence. 172 54

We determined serum ferritin, C-reactive protein (CRP), fibrinogen, and the erythrocyte sedimentation rate (ESR) in 73 patients with anemia of chronic disease. Nomograms of CRP, ESR, or fibrinogen vs ferritin concentrations were constructed and used to estimate the iron store in bone marrow. Iron stores estimated from the nomograms were compared with the results of staining cytological bone marrow smears for iron, the reference method for evaluating iron in bone marrow. In contrast to the results of Witte et al. (Clin Chem 1985;31:1011; Am J Clin Pathol 1986;85:202-6 and 1988;90:85-7), we observed that nomograms of CRP, fibrinogen, or ESR (i.e., acute-phase reactants not influenced by changes in iron metabolism) vs ferritin are not suitable to correct for the acute-phase component of changes in ferritin concentrations. For ferritin concentrations less than 70 micrograms/L, we found that iron deficiency, as judged from bone marrow iron stain, apparently was always present.
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PMID:Measurements of serum ferritin used to predict concentrations of iron in bone marrow in anemia of chronic disease. 190 71

In the vast majority of cases, the cause of microcytic hypochromic anemia is clearly suggested by the patient history, physical examination results, red cell indexes, and peripheral blood smear. Thus, further diagnostic testing, if necessary, can be very selective. When the underlying cause of anemia is obscure, the serum ferritin concentration should be measured first. If it is normal or increased, serum iron and free erythrocyte protoporphyrin levels can be determined. The serum iron level is low in anemias caused by iron deficiency and chronic disease but normal or elevated in those resulting from the thalassemias, hemoglobin E disorders, and lead toxicity. The free erythrocyte protoporphyrin level is elevated with iron deficiency, the anemia of chronic disease, and lead toxicity but normal with thalassemias and hemoglobin E disorders. Results of these two test indicate which of the more specific tests is most likely to yield the correct diagnosis.
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PMID:Determining the cause of anemia. General approach, with emphasis on microcytic hypochromic anemias. 202 Jun 45

We investigated the serum erythropoietin (Epo) response in 11 rheumatoid arthritis (RA) patients without anaemia, 7 with RA and iron deficiency (ID) and 12 with RA and anaemia of chronic disease (ACD). In all patients the serum Epo was higher than in healthy subjects. Apparently this increase was insufficient to prevent anaemia in ID and ACD. Serum Epo correlated negatively with serum ferritin. Ten RA patients with ACD were treated with the oral iron chelator 1,2-dimethyl-3-hydroxypyrid-4-one (L1). No obvious toxicity signs occurred after one week of treatment. It effectively released iron from iron stores. The Hb rise (in 70% of the patients) was correlated positively with an Epo increase and negatively with a serum ferritin decrease. We conclude that a serum Epo increase does not overcome ACD. Epo response might correlate inversely with iron stores. L1 treatment effectively chelates iron from iron stores. The effects of L1 on erythropoiesis and serum Epo and its safety need further substantiation after prolonged treatment in more RA patients.
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PMID:Impaired erythropoietin responsiveness to the anaemia in rheumatoid arthritis. A possible inverse relationship with iron stores and effects of the oral iron chelator 1,2-dimethyl-3-hydroxypyrid-4-one. 205 65


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