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)

Type I dyserythropoietic anaemia was diagnosed in an infant, who presented with respiratory distress and hepatosplenomegaly soon after birth. Anaemia became manifest during the neonatal period. The case clearly proves the congenital nature of the disease. Abnormalities of the myelopoietic series indicate that it might be a stem cell disease and the presence of skeletal anomalies of the hands suggests a genetic relationship to some cases of Fanconi and Diamond anaemia. No serum lipid or vitamin E deficiency was present as in type II congenital dyserythropoietic anaemia. Serial serum ferritin determinations indicated that iron stores are increased early in type I congenital dyserythropoietic anaemia despite no transfusion load.
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PMID:Type I congenital dyserythropoietic anaemia with myelopoietic abnormalities and hand malformations. 69 20

A newborn male with a large diaphragmatic hernia presented in severe respiratory distress. Additional features included a paucity of subcutaneous tissue, mild facial dysmorphism, webbing of the neck, genital hypoplasia, and flexion contractures of the fingers. His karyotype showed a previously unreported de novo interstitial deletion of the long arm of chromosome 1 [46,XY,del(1)(pter----q32.3::q42.3----qter)]. Regional mapping of five human genes that have been provisionally assigned to chromosome 1 was performed by restriction analysis of genomic DNA from this patient. Glucocerebrosidase, H4 histone, renin, and alpha-spectrin genes mapped outside the deleted region, whereas an H subunit of the ferritin gene mapped to 1q32----q42. These results indicate the utility of chromosomal deletions in gene mapping, and the importance of karyotype analysis in newborns with diaphragmatic hernias.
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PMID:Association of a new chromosomal deletion [del(1)(q32q42)] with diaphragmatic hernia: assignment of a human ferritin gene. 316 27

We investigated serum ferritin levels as a predictor of the acute respiratory distress syndrome (ARDS) because: (1) proinflammatory cytokines, which are implicated in ARDS, increase ferritin synthesis; and (2) oxidative stress in patients at risk for ARDS might liberate iron from ferritin, accelerating toxic hydroxyl radical (.OH) formation. Serum ferritin levels measured by radioimmunoassay (RIA) were greater in 75 patients at risk for ARDS (women, p < 0.0001; men, p < 0.0001) and 8 patients with ARDS (women, p = 0.001; men, p = 0.0009) than in healthy control subjects. Serum ferritin levels were also greater in female (p = 0.003) and male (p = 0.003) at-risk patients who developed ARDS than in patients who did not develop ARDS. In women, a value exceeding 270 ng/ml predicted ARDS with an 83% sensitivity, 71% specificity, 67% positive, and 86% negative predictive value. In men, a value exceeding 680 ng/ml predicted ARDS with a 60% sensitivity, 90% specificity, 75% positive, and 82% negative predictive value. Serum ferritin levels did not correlate with C-reactive protein levels, were not different in medical or surgical at-risk patients, and were not accounted for by liver disease. Evaluating serum ferritin levels in at-risk patients may help predict the development of ARDS and thereby improve study and treatment of ARDS. Elevated serum ferritin levels may also regulate the participation of iron in the oxidative responses that contribute to ARDS.
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PMID:Serum ferritin as a predictor of the acute respiratory distress syndrome. 900 Dec 83

Iron, through its participation in reactions that generate reactive oxygen species, may contribute to the oxidative lung injury observed in patients with acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS). A number of investigators have shown that the endogenous iron storage protein ferritin increases in the blood of patients with and at-risk for ALI and ARDS, but the significance of these increases are not known. In the present investigation, we measured lung tissue levels of thiobarbituric acid reactive substances (TBARS) and lung leak in isolated rat lungs perfused with xanthine oxidase (XO) and purine, an enzymatic system which generates reactive oxygen species. We found that adding ferritin (100 ng/mL) or desferrioxamine (DFO, 10 mM), an iron chelator, to the vascular perfusate solution decreased oxidant-induced leak in isolated rat lungs perfused with XO and purine. Addition of ferritin or DFO also decreased TBARS in isolated rat lungs perfused with XO and purine; neither ferritin nor DFO, however, decreased XO activity in vitro. Our results suggest that oxidative lung leak may be altered by the availability of reactive iron and that ferritin may contribute to protection against oxidative lung injury.
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PMID:Ferritin and desferrioxamine attenuate xanthine oxidase-dependent leak in isolated perfused rat lungs. 1218 28

We report a case of a young woman with pyrexia and progressive lung disease who developed acute respiratory distress syndrome (ARDS) and required prolonged mechanical ventilator support. The patient had a markedly elevated serum ferritin concentration of 7880 micrograms/L, a specific finding for the adult onset Still's disease (AOSD). Treatment of the patient with supportive and immunosuppressive therapy, resulted in patient survival and cure. The early consideration of the diagnosis of AOSD in patients with fever of unknown origin and a compatible clinical course may modify its severe complications.
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PMID:Adult onset Still's disease as a cause of ARDS and acute respiratory failure. 1219 35

Acute respiratory distress syndrome (ARDS) is associated with altered plasma and lung iron chemistry. Iron can promote microbial virulence and catalyse pro-oxidant reactions, thereby contributing to the oxidative stress that characterises the syndrome. Therefore, the expression of ferritin and transferrin receptors (TfR) were sought in the lungs and hearts of rodents treated with lipopolysaccharide (LPS), and measurements of TfR and ferritin protein expression were taken from lung biopsy specimens from patients with ARDS and appropriate controls. TfR messenger ribonucleic acid (mRNA) was significantly upregulated in the lungs and significantly downregulated in the hearts of rats 4 h after LPS. Ferritin mRNA levels (light and heavy chains) remained unaltered. Protein TfR levels were significantly upregulated in lungs and downregulated in hearts 4 h post-LPS. Ferritin protein levels were significantly downregulated in lungs compared to baseline values but were unaltered in hearts. Nonhaem iron levels were increased in lungs and decreased in hearts, and iron-regulatory-protein activity increased in hearts but not lungs. TfR protein levels were significantly increased in lung biopsies from patients with ARDS compared to controls. Transferrin receptors are upregulated in rodent lungs during inflammation but are downregulated in the heart. Transferrin receptor protein levels were significantly increased in the lungs in clinical acute respiratory distress syndrome. These findings have implications for the pathogenesis of acute respiratory distress syndrome, especially in relation to the role of iron as a mediator of oxidative stress.
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PMID:Variable tissue expression of transferrin receptors: relevance to acute respiratory distress syndrome. 1295 70

A TRIAD OF FEATURES: Adult onset Still's disease (ASD) is an uncommon disorder usually associating high spiking fever, evanescent skin rash constituted of small salmon pink macules, and arthritis. NUMEROUS SYSTEMIC MANIFESTATIONS: A sore throat is common and often misleading. More than 60% of the patients develop mobile and indolent lymph nodes, usually in the cervical area. Liver involvement is common and usually limited to a mild or moderate cytolysis. However, several observations of severe hepatitis have been reported justifying strict monitoring of the liver biology in these patients. Amongst the other numerous systemic manifestations that have been reported, pericarditis is common and sometimes responsible for tamponade, the pulmonary involvement may lead to an acute respiratory distress, and the rare neurological manifestations include aseptic meningitis or cranial nerve palsy. FROM A BIOLOGICAL POINT OF VIEW: The sedimentation rate is consistently elevated and there is usually a marked elevation in the polymorphonuclears. The bacteriological survey is negative as are the immunological tests. An increase in the serum level of IL-18 might be both diagnostic and prognostic. It is the increase of the serum level of ferritin and the marked decrease in its glycosylated fraction below 20% that seem to be of more potent diagnostic value.
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PMID:[Clinical and biological manifestations of adult-onset Still's disease]. 1552 51

Adenovirus pneumonia is uncommon but its severe infection has a mortality as high as 10%, and survivors may have residual airway damages, manifested by bronchiectasis, bronchiolitis obliterans, or pulmonary fibrosis. We report a case of adenovirus pneumonia demonstrating fatal respiratory distress. Adenovirus was isolated from pharyngeal specimens using cell culture and typed as serotype 3 by a combination of polymerase chain reaction (PCR) and restriction fragment length polymorphism analysis. The patient characteristically showed hypercytokinemia, characterized by increased levels of lactate dehydrogenase, ferritin, and several cytokines including interferon-gamma and interleukin-6. We treated the patient with pulse methylprednisolne therapy (25 mg/kg/day, for 3 days), resulting in the rapid amelioration of respiratory distress. This is the first report describing the treatment of pulse methylprednisolone therapy in fatal adenovirus pneumonia. During the clinical course, serum Krebs von den Lungen-6 (KL-6), which is a marker for the activity of diffuse interstitial lung disease, was elevated, suggesting that serum KL-6 could be available as a marker of pulmonary prognosis in viral pneumonia.
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PMID:Pulse methylprednisolone therapy in type 3 adenovirus pneumonia with hypercytokinemia. 1663 25

As a result of a direct exchange with the external environment, the lungs are exposed to both iron and agents with a capacity to disrupt the homeostasis of this metal (e.g. particles). An increased availability of catalytically reactive iron can result from these exposures and, by generating an oxidative stress, this metal can contribute to tissue injury. By importing this Fe(3+) into cells for storage in a chemically less reactive form, the lower respiratory tract demonstrates an ability to mitigate both the oxidative stress presented by iron and its potential for tissue injury. This means that detoxification is accomplished by chemical reduction to Fe(2+) (e.g. by duodenal cytochrome b and other ferrireductases), iron import (e.g. by divalent metal transporter 1 and other transporters), and storage in ferritin. The metal can subsequently be exported from the cell (e.g. by ferroportin 1) in a less reactive state relative to that initially imported. Iron is then transported out of the lung via the mucociliary pathway or blood and lymphatic pathways to the reticuloendothelial system for long term storage. This coordinated handling of iron in the lung appears to be disrupted in several acute diseases on the lung including infections, acute respiratory distress syndrome, transfusion-related acute lung injury, and ischemia-reperfusion. Exposures to bleomycin, dusts and fibers, and paraquat similarly alter iron homeostasis in the lung to affect an oxidative stress. Finally, iron homeostasis is disrupted in numerous chronic lung diseases including pulmonary alveolar proteinosis, transplantation, cigarette smoking, and cystic fibrosis.
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PMID:Disruption of iron homeostasis and lung disease. 1910 Mar 11

Intestinal ischemia/reperfusion (I/R) is one of common causes of acute lung injury (ALI). Early and accurate diagnosis of patients who are like to develop serious acute respiratory distress syndrome (ARDS) would give a therapeutic advantage. Ferritin and heme oxygenase-1 (HO-1) are increased by oxidative stress and are potential candidates as a predictive biomarker of ARDS. However, the mechanisms responsible for the increases of ferritin and HO-1, and their relationship to ALI, are unclear. In order to elucidate the interactions between ferritin and HO-1, we studied the changes in ferritin and HO-1 levels in serum and bronchoalveolar lavage (BAL) fluid after intestinal I/R injury in rats. Leukocyte number and protein contents in BAL fluid were elevated following I/R, and the increases were attenuated by mepacrine pretreatment. Both serum ferritin and HO-1 concentrations were progressively elevated throughout the 3 h observation period. Mepacrine pretreatment attenuated the increase of serum and BAL fluid ferritin concentrations, but did not suppress the increase of serum HO-1. Moreover, BAL fluid HO-1 levels did not change after I/R or after mepacrine pretreated I/R compared with sham rats. Unlike ferritin, HO-1 levels are not exactly matched with the ALI. Therefore, there might be a different mechanism between the changes of ferritin and HO-1 in intestinal I/R-induced ALI model.
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PMID:Ischemia/reperfusion Lung Injury Increases Serum Ferritin and Heme Oxygenase-1 in Rats. 1988 35


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