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)

Desferrioxamine was used to treat six patients who had rheumatoid arthritis refractory to conventional treatment, on the basis that levels of intra-articular iron would be reduced and inflammation lessened. After a period of initial intensive treatment which was limited by side effects, five patients continued on once-weekly maintenance doses. Two patients had temporary improvement in their symptoms, but relapsed in spite of continuing treatment. The remaining three patients completed six months of treatment with no improvement in their rheumatoid disease. There were no significant changes in rheumatological parameters, immunological markers of disease activity nor radiological evidence of improvement. Treatment did lead to significant falls in haemoglobin concentration (p less than 0.01), mean corpuscular volume (p less than 0.05) and serum ferritin levels (p less than 0.02). Therefore, in spite of a reduction in iron available for haem synthesis and a fall in tissue storage iron the rheumatoid inflammatory process persisted.
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PMID:Treatment of rheumatoid arthritis with desferrioxamine. 365 52

Twenty-four patients affected by beta-thalassemia major were studied by means of combined EEG, VEP and BAEP recordings. All the subjects were treated with regular blood transfusions and chelating therapy (DFO). An elevated incidence of EEG abnormalities (70.8%) consisting of diffused slow waves and/or diffused small sharp spikes was seen. VEP P100 latency was abnormally prolonged in eight patients (33.3%). Furthermore, a voltage increase of N75-P100 (29%) and P100-N145 (33.3%) VEP components was observed. Mean latency and voltage values were significantly increased when compared with those of a control group. No BAEP alterations were observed. No correlations were found between electrophysiological data, serum ferritin levels and transfusional treatment duration. The possible mechanisms involved in provoking such electrophysiological abnormalities are discussed.
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PMID:Electrophysiological (EEG, BAEP, VEP) study in patients with beta-thalassemia major. 367 92

Administration of 3,5,5-trimethylhexanoyl ferrocene in the diet of male Wistar rats results in a substantial increase in hepatic ferritin protein (greater than 2-fold) and of ferritin iron (4-8-fold). The iron-loading in liver, under the conditions used, appears to be essentially in parenchymal cells rather than in reticulo-endothelial cells. It is suggested that the model represents a useful system for the study of the potential efficacy of new iron chelators for the mobilization of hepatic storage iron. The ability of desferal (DFO) and of a new siderophore, desferrithiocin (DFT), to mobilize hepatic ferritin iron is observed in this model of iron overload. Desferrithiocin stimulates ferritin iron mobilization, when administered either by gavage or by intraperitoneal injection, whereas desferal is active intraperitoneally but inactive orally. Our studies lead to the conclusion that DFT merits further examinations, for its activity as an orally active iron chelator.
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PMID:An animal model of iron overload and its application to study hepatic ferritin iron mobilization by chelators. 377 98

It is not known which message and mechanism triggers the cell to mobilize iron from ferritin. In this paper we present the results of incubation experiments with 59Fe-labelled hepatocytes. Anemic serum gives a significant higher rate of iron mobilization than normal serum. The involvement of apo-transferrin is ruled out because it did not increase iron mobilization. Citrate increased iron mobilization which is not the result of an increase in NADH/NAD+-ratio because addition of ethanol did not stimulate iron mobilization. Desferrioxamine is used clinically in iron overloaded patients and it is known that iron removal is a very slow process. Although desferrioxamine can mobilize iron from ferritin in hepatocytes, a considerable amount remains inside the cell as a low molecular weight fraction. This fraction represents chelator bound iron and is slowly released into the circulation.
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PMID:Iron mobilization from isolated hepatocytes. 380 97

Previous work suggested that during the catabolism of haemoglobin a physico-chemical form of iron was released which was more readily chelatable by desferrioxamine than normal storage forms, as ferritin-haemosiderin. Desferrioxamine chelation was therefore investigated in five patients with major fractures in which haemoglobin catabolism is greatly enhanced by the red cell destruction which proceeds in the associated haematoma. Considerable increases in the amounts of iron mobilized by desferrioxamine were observed from the second day after injury. In severe interstitial haemorrhage, these values tended to increase until 10 to 20 days, and sometimes were as high as chelation values seen in haemochromatosis. These results are considered to support the hypothesis that a highly chelatable form of iron is found at some stage during haemoglobin catabolism.
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PMID:Iron chelation in haematomas at fracture sites. 595 23

Delivery of iron to K562 cells by diferric transferrin involves a cycle of binding to surface receptors, internalization into an acidic compartment, transfer of iron to ferritin, and release of apotransferrin from the cell. To evaluate potential feedback effects of iron on this system, we exposed cells to iron chelators and monitored the activity of the transferrin receptor. In the present study, we found that chelation of extracellular iron by the hydrophilic chelators desferrioxamine B, diethylenetriaminepentaacetic acid, or apolactoferrin enhanced the release from the cells of previously internalized 125I-transferrin. Presaturation of these compounds with iron blocked this effect. These chelators did not affect the uptake of iron from transferrin. In contrast, the hydrophobic chelator 2,2-bipyridine, which partitions into cell membranes, completely blocked iron uptake by chelating the iron during its transfer across the membrane. The 2,2-bipyridine did not, however, enhance the release of 125I-transferrin from the cells, indicating that extracellular iron chelation is the key to this effect. Desferrioxamine, unlike the other hydrophilic chelators, can enter the cell and chelate an intracellular pool of iron. This produced a parallel increase in surface and intracellular transferrin receptors, reaching 2-fold at 24 h and 3-fold at 48 h. This increase in receptor number required ongoing protein synthesis and could be blocked by cycloheximide. Diethylenetriaminepentaacetic acid or desferrioxamine presaturated with iron did not induce new transferrin receptors. The new receptors were functionally active and produced an increase in 59Fe uptake from 59Fe-transferrin. We conclude that the transferrin receptor in the K562 cell is regulated in part by chelatable iron: chelation of extracellular iron enhances the release of apotransferrin from the cell, while chelation of an intracellular iron pool results in the biosynthesis of new receptors.
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PMID:Effect of iron chelators on the transferrin receptor in K562 cells. 609 56

The effects of slow subcutaneous (s.c.) infusions of desferrioxamine (Desferal: DF) on iron metabolism and excretion were studied in 6 thalassaemia major patients in the course of a ferrokinetic study with 59Fe as a label; s.c. DF infusions were performed every 4th day starting 4 days after that of the 59Fe injection. Serum iron and total iron binding capacity (TIBC) increased after s.c. infusion, whereas serum ferritin levels remained unchanged. 59Fe urinary specific activity decreased in all subjects from the first to subsequent infusions, whereas faecal specific activity remained almost constant throughout the experiment. These data support the hypothesis that iron reaching RE cells concentrates initially in a readily chelatable pool from which then it moves to a larger and not readily chelatable pool, whereas iron reaching parenchymal hepatic cells remains permanently available to chelant.
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PMID:A study of the mechanisms and sites of action of desferrioxamine in thalassaemia major. 642 Oct 46

Several reports have suggested that iron deficiency might explain "sports anemia" especially in long distance runners. The present study was made to further study the iron metabolism in runners as the proposed cause of "sports anemia" is abstruse considering the good iron nutrition in these athletes. Based on a screening of 43 elite male runners, using bone marrow hemosiderin, serum ferritin and transferrin saturation, two groups of subjects were selected for a very extensive study on iron metabolism. In group 1 (n = 5) iron depletion was suggested in at least one of the screening studies. In group 2 (n = 7) at least one test strongly indicated good iron repletion. This experimental design was chosen to obtain two groups with similar body composition and exercise load but different iron metabolism. The studies comprised determinations of red cell and plasma volumes, plasma iron turnover and red cell incorporation of radioiron, red cell indices, plasma iron and transferrin, red cell protoporphyrin, serum ferritin, serum haptoglobin, urinary iron losses, iron absorption, bone marrow hemosiderin, dietary intake of energy and nutrients and a Desferal test. Pooling the results together it was obvious that none of the subjects were truly iron-deficient. A few occasional findings suggesting low iron stores cannot be satisfactorily explained and indicate that further studies are needed.
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PMID:Iron metabolism and "sports anemia". I. A study of several iron parameters in elite runners with differences in iron status. 649 74

In RDT hemosiderosis appears to be an inevitable complication only in the small number of patients in need of frequent transfusions. To prevent clinical consequences (e.g. cardiomyopathy) known from polytransfused patients without renal disease, transplantation should be considered in RDT patients in need of frequent transfusions. Iron substitution - preferably oral - to replace dialysis-related iron loss does not cause clinically significant hemosiderosis provided iron stores are monitored adequately. A sufficient method of controlling iron stores in RDT patients under iron substitution or regular transfusion therapy is a twice annual determination of serum ferritin concentration. The treatment of choice for hemosiderosis in nontransfused RDT patients is discontinuation of iron substitution. When polytransfused RDT patients with severe hemosiderosis cannot be transplanted and submitted consecutively to phlebotomy, DFO treatment is indicated. Quantitative data regarding optimal dosage and application of DFO in RDT patients are not yet available. Constant infusion of DFO during hemodialysis may be superior to bolus application.
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PMID:Therapy and monitoring of hypersiderosis in chronic renal insufficiency. 671 93

In seven patients with hemochromatosis, arthropathy was an early symptom, or first clinical symptom, of the hemochromatosis. In all seven patients, serum iron, transferrin saturation, and parameters of storage iron (serum ferritin, Desferal-test) were clearly elevated. In 5 patients hemochromatosis was associated with the HLA loci A3 and B7. Bone scan proved a sensitive detection method for hemochromatosis arthropathy. In one case joint involvement was detected by bone scan prior to clinical symptoms. Parameters of iron metabolism correlated well with other organ manifestations of hemochromatosis. In contrast, joint involvement did not correlate with parameters of iron metabolism or severity of hemosiderosis of other organs, and was not relieved by phlebotomy. These 7 cases confirm that joint symptoms can be an early or leading symptom of hemochromatosis, can lead to early therapy and thereby prevent major organ damage. It remains undecided, however, whether the arthropathy is a consequence of iron storage or an independent disease which is genetically associated with hemochromatosis.
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PMID:[Arthropathy as an early symptom of hemochromatosis. Overview of the literature and 7 case reports]. 672 20


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