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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lactoferrin turnover was studied in the rabbit with 125I- and 131I-labelled human lactoferrin. Plasma lactoferrin activity showed a rapid decrease during the first 24 h, followed by a 'final slope' with a T1/2 of about 25 h. Turnover studies after transfer of plasma from one rabbit (A) 3 h after injection to another rabbit (B), showed a recovery of 100% compared to 30% in A rabbits but otherwise a similar disappearance curve. The rapid turnover was confirmed in whole body studies. Concomitantly with the initial dissapearance from the plasma, there was a marked accumulation of proteinbound activity only in the liver in both A and B rabbits. From these results, the rate of synthesis in normal man can be estimated at around 25 mg per d. The disappearance pattern and hepatic uptake are discussed in relation to knowledge about lactoferrin receptors in macrophages, asialo elimination, and fucose group recognition. Concerning the significance of lactoferrin turnover for iron metabolism it is concluded that the plasma turnover results are insufficient to explain the disturbance in iron kinetics seen in the anaemia of chronic disorders; however, it is likely that lactoferrin plays a role in iron metabolism within the extravascular space.
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PMID:Turnover of human lactoferrin in the rabbit. 12 4

Chronic granulocytic leukemia is a rare myeloproliferative disorder in dogs. The present study investigated various functions of leukemic granulocytes in a dog that presented with thrombocytopenic purpura, anaemia and a classical leukemic hemogram. All analyses were performed in parallel with a control dog. Purification of the leukemic granulocytes by density gradient centrifugation revealed three neutrophil and neutrophil precursor populations with different densities. Comparison of cell morphology and density showed that cell density increased with increasing maturity. The control dog possessed only one neutrophil population, with a density greater than 1.077. Analysis of cellular contents of the granular enzymes, elastase, myeloperoxidase and lysozyme showed that leukemic neutrophils were quantitatively markedly different from normal neutrophils with respect to enzyme activities. There were no major differences between leukemic and normal cells as regards aggregatory and migratory responses to different stimuli. The phagocytic capacity of the leukemic cells, however, was dramatically increased compared with the control, and exceeded all previously encountered responses in the assay employed. In a similar fashion, superoxide generation and secretion of elastase and lysozyme in response to zymosan and phorbol myristate acetate were substantially higher than in the control dog. Priming of cell function to a level exceeding that normally attainable in neutrophils appears to have taken place in peripheral blood of the leukemic dog. The only endogenous mediator known to prime neutrophil functions to the extent seen in the present case is the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), which is intimately involved in regulation of myelopoiesis in mammals. On the basis of the enzymological and functional findings in the leukemic dog, we hypothesize that a lactoferrin deficiency in leukemic neutrophils leads to enhanced GM-CSF synthesis, which is ultimately the cause of the observed cellular hyperresponsiveness and contributes to the monocytosis seen in the patient.
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PMID:Enhanced granulocyte function in a case of chronic granulocytic leukemia in a dog. 165 Oct 30

Immunoreactive serum erythropoietin concentrations were measured in 35 patients with anaemia associated with active rheumatoid arthritis. Based on an evaluation of stainable iron in the bone marrow (marrow iron grade 0-4) and serum ferritin concentrations (concentrations less than or equal to 60 micrograms/l compatible with iron deficiency) the anaemia was found to be complicated by iron deficiency in 19/35 (54%) of the patients. The mean serum erythropoietin level (57.6 (SD) 27.3) U/l) was sufficiently raised for the degree of anaemia irrespective of the size of the marrow iron stores. Thus the data do not support the contention that suppressed secretion of erythropoietin is involved in the pathogenesis of anaemia of chronic disorders. There was a significant inverse correlation between the haemoglobin concentration and log serum erythropoietin in the patients with rheumatoid arthritis. In the patients with adequate iron stores, but not in the iron depleted patients, there was a tendency for serum erythropoietin concentrations to correlate positively both with C reactive protein and erythrocyte sedimentation rate. Red cell distribution width (mean (SD) 16.3 (1.8)%) was above normal (11.5-14.5%) both in the iron replete and the iron depleted patients, and the mean red cell distribution width values did not differ significantly among the two subpopulations. The plasma lactoferrin concentration (mean (SD) 137.6 (109.9) micrograms/l) was normal and did not differ significantly between the iron deficient patients and those with adequate iron.
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PMID:Anaemia of rheumatoid arthritis: serum erythropoietin concentrations and red cell distribution width in relation to iron status. 238 57

This study was designed to examine whether lactoferrin, a glycoprotein contained in neutrophils which binds free iron, mediates the anemia associated with renal cell carcinoma. Preoperative hematocrit, urinalysis, serum iron, total iron binding capacity, and ferritin levels were obtained in 24 patients with hypernephroma. At the time of radical nephrectomy, a tumor specimen was obtained from all 24 patients and corresponding normal renal tissue was obtained from eight patients. Fifteen patients had low serum iron, whereas nine patients had normal serum iron. All tissue samples were snap frozen at the time of surgery and were subsequently sectioned into 3-microns slices using the cryostat. Then all the sectioned specimens were stained with FITC (fluorescein isothiocyanate) and peroxidase conjugated rabbit derived anti-human lactoferrin. Ten of the 15 patients with low serum iron had positive anti-lactoferrin staining in both the FITC and peroxidase systems. None of the tumors from patients with normal serum iron and none of the normal renal parenchyma exhibited positive anti-lactoferrin uptake. Stains for iron in the bone marrow of two patients with low serum iron showed increased iron stores. These studies suggest that lactoferrin mediates the anemia often seen in association with renal cell carcinoma.
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PMID:The relationship of lactoferrin to the anemia of renal cell carcinoma. 353 15

The anemia of chronic disease (ACD) is defined as a mild anemia associated with a chronic inflammatory, infectious or neoplastic illness and with a characteristic disturbance of iron metabolism. Many of the findings in ACD can be accounted for by release of a monokine called leukocyte endogenous mediator (LEM), endogenous pyrogen, or interleukin-1. This substance is released from "activated" monocytes. Bacterial endotoxins, certain lymphokines and phagocytic challenges are among the factors stimulating its biosynthesis. LEM induces fever, leukocytosis, biosynthesis. LEM induces fever, leukocytosis, and a variety of biochemical changes, including hypoferremia and alterations in plasma protein synthesis, collectively known as the "acute phase response." It is proposed that ACD results from the long-term elaboration of LEM and that release of this material is the common pathogenetic factor found in the illnesses that are associated with ACD. Some suggestions are made for testing the hypothesis. The hypoferremia associated with ACD is probably caused by defective release of iron from cells--particularly from macrophages, but also from hepatocytes and intestinal epithelium. Two possible mechanisms for this abnormality have been proposed: liberation of lactoferrin from neutrophilic leukocytes and induction of apoferritin synthesis. Neither mechanism has been established. Erythrokinetic studies in ACD have detected a modest reduction of erythrocyte survival without an adequate compensatory increase in the rate of red cell production. The reduced erythrocyte survival is probably related to an increase in phagocytic activity by activated macrophages. Impaired bone marrow response is partly related to the restricted iron supply, but there is substantial evidence for an additional defect in erythropoietin secretion. In some malignant diseases, there is evidence of an additional abnormality: impaired marrow response to a normal amount of erythropoietin. The nature of the erythropoietic defects and the relation of LEM to them remain to be established.
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PMID:The anemia of chronic disease. 634 57

Iron is essential for the organism. In ionized forms (Fe++, Fe ), it constitutes an integrated part of a lot of different functional proteins (Figure 1). The most important functions are participation in oxygen transport in blood, oxygen storage in muscle tissues and oxidation of nutrients in the mitochondria. Iron is an essential part of cytochrome C and alpha-glycerolphosphate dehydrogenase, and early stages of iron deficiency may, therefore, cause disturbances in tissue metabolism before development of anaemia. Thus, haemoglobin determinations is not very suitable for diagnosing early iron deficiency. The content of iron in roughages, apart from root crops (Table II), is usually sufficient to cover the requirement of domestic animals (Table III), which is met by about 50 mg per kg feed dry matter. Iron deficiency is very often caused by a reduced absorption in the intestinal tract because of components in the feed forming complexes with iron of very low solubility or inhibitors reducing the absorption processes. The immune status of the organism and its resistance against infections depends on the iron supply. Iron deficiency inhibits the myeloperoxidase activity and thus decreases the bacteriocide effect of the leucocytes. In spite of this, when exposed to infections the physiological mechanisms reduce the blood concentration of available iron. By this mode of action, invading pathogens, needing iron like the host animals, will be restrained. The low content of iron in milk (Table II) combined with a high content of iron binding lactoferrin, is ideal to protect newborn and milk fed young animals against intestinal infections.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Iron deficiency in domestic animals]. 643 95

Lactoferrin is an iron-binding protein present in high concentrations in human milk. The efficacy of supplementing iron bound to lactoferrin to iron-deficient and iron-sufficient young mice was evaluated in comparison with supplementation of iron as iron chloride. Mice fed a nonsupplemented milk diet (approximately 1 mg Fe/L) for 4 weeks had a microcytic, hypochromic anemia and low tissue iron concentrations. Iron supplementation of the diet with lactoferrin-iron, or iron chloride at a level of 5 mg Fe/L prevented the anemia and resulted in tissue iron levels similar to levels found for mice fed a stock commercial diet. There was no significant difference in any of the parameters analyzed between the groups of mice receiving the two iron supplements following a diet deficient in iron. Apolactoferrin when supplemented to the diet had no negative effect on the iron status of the mice. These results show that lactoferrin may be a useful vehicle for supplementation of iron.
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PMID:Supplementation of milk with iron bound to lactoferrin using weanling mice: L. Effects on hematology and tissue iron. 664 50

In order to evaluate the diagnostic and pathogenetic importance of s-ferritin and p-lactoferrin in the anemia of rheumatoid arthritis (RA), 38 patients were examined. Twenty-one out of 38 randomly selected anemic patients with classical or definite RA had iron deficiency, as estimated from the iron content in stained bone marrow aspiration. S-ferritin concentrations below 60 micrograms per litre had sensitivity and a specificity for iron deficiency of 86% and 88%, respectively, which was much better than such commonly used variables as s-iron, p-transferrin, MCV, and MCHC. Although this cut-off level is higher than in patients without inflammatory disease, s-ferritin was not correlated to disease activity. In 7 out of 8 patients, the s-ferritin level rose during iron therapy. P-lactoferrin values were within the normal range and did not vary with the anemia or with disease activity. Thus p-lactoferrin appears to be of no pathogenetic importance in the anemia of RA.
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PMID:Serum ferritin and the assessment of iron deficiency in rheumatoid arthritis. 665 99

Cyclic neutropenia is the most frequent of the cyclic haematopoietic disorders characterized by its regular 21 d cyclic fluctuations in the number of blood neutrophils, and in many cases simultaneous fluctuations in the other blood cell lines. In this paper we describe a 77-year-old woman with a cyclic pancytopenia including all the myeloid cell lines and to some extent the lymphocytes with a constant and predictable oscillation period of about 100 d. Serial bone marrow biopsies and plasma lactoferrin measurements indicated a similar fluctuating pattern in the bone marrow production of neutrophils. Serial measurements of plasma GM-CSF concentration pointed at a simple feed-back inhibitory system. The condition was present for at least 4 years, after which it gradually improved, although the thrombocyte count still showed a fluctuating tendency after a further 4 years of observation. The clinical consequences were mild symptoms of anaemia and a few episodes of respiratory infections occurring during pancytopenic periods. We think this is the first case described in the literature with this variant of a cyclic haematopoietic disorder. The precise pathophysiological mechanism behind this condition is obscure, but probably it is due to a regulatory disturbance at a very early step in the haematopoietic stem cell hierarchy.
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PMID:Reversible adult-onset cyclic haematopoiesis with a cycle length of 100 days. 845 64

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


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