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 clinical features and therapy of chronic iron overload are reviewed. Chronic iron overload is classified as primary or secondary hemochromatosis. In primary hemochromatosis a genetic defect in iron metabolism results in increased absorption of iron from the gastrointestinal tract. The excess iron in secondary hemochromatosis may be derived from increased gastrointestinal absorption due to ineffective erythropoiesis or from medicinal, dietary, or transfusional sources. Phlebotomy is the treatment of choice in patients with primary hemochromatosis. Iron chelation therapy is indicated in patients who are not candidates for phlebotomy. Deferoxamine mesylate, the only commercially available iron chelator, is usually administered subcutaneously or intravenously over 10-12 hours/day. Serum ferritin concentrations are measured every three to six months to monitor the effectiveness of therapy. The adverse effects of deferoxamine include local skin reactions, ototoxicity, cataracts, growth impairment, and increased susceptibility to infectious organisms. Patient compliance may be compromised by the routes of administration and cost of deferoxamine. Early detection and prompt treatment are necessary to prevent organ damage. Phlebotomy and iron chelation therapy are effective in the treatment of chronic iron overload.
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PMID:Treatment of chronic iron overload. 174 62

Chronic iron overload (CIO) enhances nitric oxide (*NO) production in the liver, which may represent a hepatoprotective mechanism against CIO toxicity. In order to test this hypothesis, the influence of CIO (diet enriched with 3% (wt/wt) carbonyl-iron for 8 weeks) in the absence or presence of the (*)NO synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) on NOS activity, extracellular signal-regulated kinase (ERK1/2) and NF-kappaB activation was studied, in relation to ferritin expression and liver morphology. CIO increased liver NOS activity, ERK1/2 phosphorylation, NF-kappaB DNA binding, and ferritin expression, with normal liver histology. These changes were suppressed by combined CIO and L-NAME treatment, with the resulting inflammatory response of the liver. It is concluded that (*)NO response induced by CIO represents a molecular mechanism affording protection against iron toxicity, which is related to both the activation of the ERK/NF-kappaB pathway involving inducible NOS expression and ferritin upregulation, changes that may be interrelated.
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PMID:Hepatoprotective role of nitric oxide in an experimental model of chronic iron overload. 1687 48