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 objective of the study was to evaluate the diagnostic efficiency of laboratory tests, including serum transferrin receptor (TfR) measurements, in the diagnosis of iron depletion. The patient population consisted of 129 consecutive anemic patients at the University Hospital of Turku who were given a bone marrow examination. Of these patients, 48 had iron deficiency anemia (IDA), 64 anemia of chronic disease (ACD), and 17 patients had depleted iron stores and an infectious or an inflammatory condition (COMBI). Depletion of iron stores was defined as a complete absence of stainable iron in the bone marrow examination. Serum TfR concentrations were elevated in the vast majority of the IDA and COMBI patients, while in the ACD patients, the levels were within the reference limits reported earlier for healthy subjects. TfR measurement thus provided a reliable diagnosis of iron deficiency anemia (AUC(ROC) 0.98). Serum ferritin measurement also distinguished between IDA patients and ACD patients. However, the optimal decision limit for evaluation of ferritin measurements was considerably above the conventional lower reference limits, complicating the interpretation of this parameter. Calculation of the ratio TfR/log ferritin (TfR-F Index) is a way of combining TfR and ferritin results. This ratio provided an outstanding parameter for the identification of patients with depleted iron stores (AUC(ROC) 1.00). In anemic patients, TfR measurement is a valuable noninvasive tool for the diagnosis of iron depletion, and offers an attractive alternative to more conventional laboratory tests in the detection of depleted iron stores.
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PMID:Serum transferrin receptor and its ratio to serum ferritin in the diagnosis of iron deficiency. 902 38

Iron is essential to all microorganisms. To obtain iron from the very low concentrations present in their environment, microorganisms have developed sophisticated mechanisms such as the siderophore system. As a primitive defense mechanism, humans have developed mechanisms to withhold iron from microorganisms. Iron-binding proteins such as transferrin, ferritin, and lactoferrin have a central role in human ferrokinetics. These iron-binding proteins also participate in the process of decreasing iron availability for the microorganisms. They do so by decreasing iron reutilization. Anemia of inflammation (previously called anemia of chronic disease) is seen in the setting of infectious, inflammatory, and neoplastic diseases. It results, in part, from changes in the intracellular metabolism of iron. Alterations of iron physiology seen in many clinical circumstances make excess iron available to microorganisms, thus enhancing their pathogenicity. Understanding the molecular basis of iron withholding by the human host, both in the absence of and during infection, and that of iron acquisition by microorganisms may provide us with new and innovative antimicrobial agents and vaccines.
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PMID:Iron, infections, and anemia of inflammation. 935 4

Numerous large-scale studies have conclusively established that North American blacks have a lower population mean of serum hemoglobin concentrations than North American whites. An increasing number of researchers interpret the reduced hemoglobin levels as a genetic racial trait and recommend lowering the normal range for blacks. However, other hematological parameters among blacks indicate an alternative view. The same medical surveys also document higher ESR (erythrocyte sedimentation rate) and higher serum ferritin means in the black population. These, in association with low hemoglobin levels, are the definition of the anemia of chronic disease. A range of disorders, from infectious and inflammatory diseases to neoplasia, lead to the anemia of chronic disease. The prevalence of this hematological profile in North American blacks may indicate that the population has a higher morbidity than whites. A literature review suggests that these particular hematological means differ from whites, regardless of socioeconomic class, because of increased frequency and virulence of disease among blacks. The increase appears to be the consequence of social, rather than racial, causes.
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PMID:Interpretations of differences in population hemoglobin means: a critical review of the literature. 938 48

ESR is a time-honored, simple, inexpensive test, but unfortunately it lacks sensitivity and specificity. Clinicians need to be aware of appropriate uses, because any test is expensive when ordered often, and evaluation of false-positive results may incur substantial costs and place the patient at risk from additional procedures. ESR should not be used to screen asymptomatic persons for disease. If an increased ESR is encountered and no explanation is immediately apparent, clinicians should repeat the test in several months rather than pursue an exhaustive search for occult disease. ESR may be useful in establishing a "sickness index" in elderly persons who have nonspecific changes in health status and a moderate probability of underlying disease; in screening for infection in specific settings (e.g., orthopedic surgery, pediatrics, gynecology); in diagnosing and monitoring temporal arteritis, polymyalgia rheumatica, and possibly other rheumatic diseases; in monitoring patients with treated Hodgkin's disease; and in assessing iron deficiency in anemia of chronic disease (when correlated with serum ferritin level). An ESR value exceeding 100 mm/hr has a 90% predictive value for serious underlying disease, most often infection, collagen vascular disease, or metastatic tumor. In asymptomatic persons with a markedly elevated ESR value, a minimal number of tests usually reveal the cause.
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PMID:The erythrocyte sedimentation rate. Still a helpful test when used judiciously. 959 Sep 99

The reticuloendothelial (RE) system plays an important role in the changes in iron metabolism associated with the anemia of chronic disease (ACD). We previously reported that the acute-phase protein alpha1-antitrypsin (alpha1-AT) reduced growth and proliferation in cells of the erythroid cell system by interfering with transferrin (Tf)-mediated iron uptake. The regulation of iron metabolism in cells of the RE system is distinctly different from that in other cell systems; moreover, monocytes and macrophages play an essential part in the regulation of the production and clearance of alpha1-AT. In the present study we examined the effect of alpha1-AT on cells of the monocyte-macrophage lineage. Alpha1-AT completely inhibited the binding of Tf to its receptor (TfR) on THP-1 human myelomonocytic cells and cultured human monocytes. Results of equilibrium saturation and kinetic studies indicated that this inhibition was competitive. No other acute-phase protein demonstrated the same inhibitory potency. Furthermore, alpha1-AT almost completely prevented internalization of the Tf-TfR complex in a dose-dependent manner. Interestingly, and in sharp contrast to the results of our studies with erythroid cells, this inhibition did not reduce the growth and proliferation of THP-1 cells. Furthermore, alpha1-AT significantly increased the concentration of intracellular ferritin in THP-1 cells and monocytes, whereas the number of TfR remained unchanged. Because alpha1-AT showed no enhancing effect on ferritin transcription and translation, we believe that an as-yet unidentified posttranslational mechanism may be responsible for this phenomenon. In addition, our results indicate that the increase in ferritin concentration caused by alpha1-AT is mediated independently of iron supply, as has previously been shown for several proinflammatory cytokines. These data provide further evidence that alpha1-AT is a mediator of the alterations in iron metabolism characteristic of ACD.
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PMID:Modulation of iron metabolism in monocytic THP-1 cells and cultured human monocytes by the acute-phase protein alpha1-antitrypsin. 976 45

Iron plays an essential role in a spectrum of metabolic processes. Cellular iron uptake is facilitated by transferrin receptor (TfR)-mediated endocytosis. In recent years more insight has been obtained in TfR physiology and the regulation of cellular iron homeostasis. The synthesis of TfR and the iron storage protein ferritin is regulated reciprocally at the post-transcriptional level according to the cellular iron status. As a result of externalization of TfR during the endocytic cycle, a soluble form of TfR can be detected in serum. The serum TfR (sTfR) level is closely related to erythroid TfR turnover and the prime determinants of the sTfR concentration are cellular iron demands and erythroid proliferation rate. In the absence of a hyperplastic erythropoiesis the sTfR level is a sensitive parameter of early tissue iron deficiency. The entire spectrum of body iron status can be assessed by measurement of serum ferritin and sTfR levels, with ferritin as marker of tissue iron stores and sTfR as index of tissue iron needs. The sTfR may be a promising tool to detect iron deficiency in inflammatory states and in the anaemia of chronic disease as its concentration is, in contrast to ferritin levels, not influenced by the acute phase response. Determination of sTfR levels may also improve assessment of body iron stores during pregnancy and in neonates. Finally, the sTfR may be a useful parameter to monitor erythropoiesis in various clinical settings, for instance in the prediction of the haematological response to erythropoietin treatment. However, standardization of the sTfR assay, with definition of reference and pathological ranges, is necessary for the definitive introduction of the sTfR as major parameter of iron metabolism.
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PMID:Structure, function and clinical significance of transferrin receptors. 1009 72

The most common cause of anaemia in the elderly is anaemia of chronic disease (ACD). However, iron deficiency anaemia (IDA) may coexist, and can be difficult to diagnose. The serum transferrin receptor (sTfR) blood test may be a better indicator of iron status as it is not affected by inflammation nor by advancing age. We evaluated it in four groups (10 males, 10 females each): 'young' controls, 'elderly' controls, IDA and ACD. All patients in the IDA group had elevated sTfR levels (mean +/- SD 65.2 +/- 17.7 nmol/l). All 'young' controls had normal sTfR (22.3 +/- 7.3 nmol/l) and ferritin levels (92.7 +/- 61.1 micrograms/l). Although all subjects in the 'elderly' controls and ACD group had normal, and raised or normal serum ferritin, respectively (88 +/- 62.3 micrograms/l; 631.2 +/- 509.5 micrograms/l), three (15%) 'elderly' controls and four (20%) ACD patients had raised sTfR levels, suggesting depleted iron stores. Bone-marrow aspirates were available in 3/4 ACD patients with raised sTfR. Haemosiderin was absent in two. The sTfR blood test is comparable to serum ferritin in diagnosing IDA in the elderly but also seems capable of differentiating ACD from IDA. Its potential as a non-invasive test of iron status, especially in elderly anaemic patients, deserves further evaluation.
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PMID:Serum transferrin receptor assay in iron deficiency anaemia and anaemia of chronic disease in the elderly. 1075 Dec 43

In nutritional studies to assess the prevalence of iron deficiency, it has been common practice to define 3 stages of increasing severity: iron storage depletion as defined by low serum ferritin, mild iron deficiency without anemia based on laboratory evidence of iron deficient erythropoiesis (IDE), and overt iron deficiency anemia (IDA). While this approach provides a broad perspective of impaired iron status, the main liabilities of iron lack are associated only with the more advanced stage of IDA. Consequently, the hemoglobin determination can be used to screen for nutritionally significant iron deficiency. Having identified anemia, more specific laboratory studies are needed to establish iron lack as the cause. The traditional measurements of iron deficient erythropoiesis (IDE) such as a low transferrin saturation, elevated erythrocyte protoporphyrin, or decreased mean corpuscular volume are commonly used. The major drawback in using these parameters is that they are affected similarly in individuals with the anemia of chronic disease (ACD), a common form of anemia in low socioeconomic populations. Because iron stores are invariably absent in individuals with uncomplicated IDA, a low serum ferritin concentration below 20 micrograms/L confirms the diagnosis of IDA when anemia is present. The main limitation of the serum ferritin is that it is falsely elevated to within the normal range when IDA develops in individuals with concurrent infection or chronic inflammation. When this occurs in a clinical setting, a bone marrow examination is commonly performed to identify IDA. Recent investigations indicate that this cumbersome procedure can be avoided by measuring an important new iron-related measurement, the serum transferrin receptor (TfR). Because the synthesis of TfR is upregulated with tissue iron deficiency, IDA can be identified readily by an elevated serum TfR. Importantly, the serum TfR is normal in individuals with the ACD but becomes elevated if these individuals develop IDA. The optimal combination of laboratory measurements for detecting IDA is the hemoglobin, serum ferritin and serum TfR.
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PMID:The nutritional assessment of iron status. 1097 31

We encountered two patients who presented with hypochromic-microcytic anemia and were refractory to iron therapy. The symptoms were suggestive of anemia of chronic disease (ACD); however, there was no evidence of any such disease, either inflammatory or malignant. These patients were reminiscent of patients originally described as having primary defective iron reutilization. The hematologic picture consisted of hypochromic-microcytic anemia, low serum iron, low to normal iron binding capacity, high serum ferritin, and increased bone marrow iron in the absence of ringed sideroblasts. These patients had symptomatic anemia and received danazol (200 mg orally) three times per day to which they responded very well with an increase of approximately 3 g in the hemoglobin concentration over 1 year and amelioration of their symptoms. Danazol was well tolerated and did not cause any virilizing side effects. Doses were lowered in maintenance after 1 year to 200 mg once per week, and responses were sustained up to 36 months of follow-up duration. In the differential diagnosis of hypochromic-microcytic anemia, especially in postmenopausal women, one has to consider this type of treatable anemia when more common types such as iron deficiency, chronic inflammation, malignancy, sideroblastic anemia, or thalassemia have been ruled out.
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PMID:Treatment of primary defective iron-reutilization syndrome: revisited. 1098 70

Anemia should not be accepted as an inevitable consequence of aging. A cause is found in approximately 80 percent of elderly patients. The most common causes of anemia in the elderly are chronic disease and iron deficiency. Vitamin B12 deficiency, folate deficiency, gastrointestinal bleeding and myelodysplastic syndrome are among other causes of anemia in the elderly. Serum ferritin is the most useful test to differentiate iron deficiency anemia from anemia of chronic disease. Not all cases of vitamin B12 deficiency can be identified by low serum levels. The serum methylmalonic acid level may be useful for diagnosis of vitamin B12 deficiency. Vitamin B12 deficiency is effectively treated with oral vitamin B12 supplementation. Folate deficiency is treated with 1 mg of folic acid daily.
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PMID:Anemia in the elderly. 1103 74


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