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)

Iron overload is relatively common and is now detected more frequently because of inclusion of serum iron measurement in automated clinical chemistry panels. Secondary hemosiderosis and hemochromatosis result from increased iron absorption associated with increased erythropoiesis compensating for hemolysis, increased dietary iron, inappropriate prolonged oral iron therapy or chronic multiple transfusions. Primary hemochromatosis is a genetic metabolic disorder associated with the HLA locus on chromosome 6 resulting in increased iron absorption, though erythropoiesis and dietary iron are normal, and abnormal diversion of iron from reticuloendothelial (RE) to parenchymal cells. A genetic increase of intracellular iron carrier is a proposed basic mechanism. Only in the cirrhotic stage of primary hemochromatosis do RE iron and serum ferritin increase. Since both serum iron and serum ferritin may remain normal in the precirrhotic stage and may be falsely positive in the absence of iron overload, direct measurement of body iron stores is often useful. Measurement of tissue iron in liver biopsy specimens is widely used. However, quantitation of total mobilizable body iron by measurement of a 6-hour urine collection after intravenous injection of 59Fe-DTPA is noninvasive, sensitive, relatively accurate, and together with other laboratory and clinical data provides a practical means of establishing the correct diagnosis and therapy early enough to minimize organ damage.
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PMID:Iron overload syndromes. 395 74

Secondary haemosiderosis may be accompanied by a decrease in the phagocytic function of neutrophils (PMNs). This dysfunction has been attributed to an exaggerated generation of oxidants induced by intracellular iron. However, an accumulation of iron has so far not been reliably demonstrated in neutrophils harvested from iron-overloaded patients. Six polytransfused haemodialysed patients, with a serum ferritin level higher than 1000 micrograms/l, and 10 healthy controls were investigated. The iron status of PMNs was evaluated by iron determination using atomic absorption spectrometry and by ferritin measurement using radioimmunoassay. The phagocytic performance was measured by cytofluorometry. The results confirm that PMNs from the haemosiderosis patients have a decreased phagocytosis. Moreover, they demonstrate for the first time that these PMNs have an increased cellular iron and ferritin content. Both latter concentrations were 4 to 5 times more elevated in secondary haemosiderosis than in healthy controls. This iron accumulation may be toxic for the PMNs and may, at least partially, explain the three-fold higher risk of bacteraemia which has been reported in those patients.
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PMID:Neutrophils from patients with secondary haemosiderosis contain excessive amounts of autotoxic iron. 840 31