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 concentration of ferritin was measured in the pleural fluid of 108 patients with pleural effusions. In all groups of patients the ferritin concentration was higher in pleural fluid than in serum. The greatest differences, with up to 100 times more ferritin in the pleural fluid, were found for patients with rheumatoid pleurisy, malignant effusions, and empyema. In patients with non-malignant inflammatory pleural effusions the concentration of ferritin in pleural fluid correlated significantly with other pleural fluid indices of inflammation: there was a positive correlation with lactate dehydrogenase activity and a negative correlation with concentrations of glucose and complement components C3 and C4. Ferritin was detected immunocytochemically only in the macrophages found among the pleural fluid cells. Our study shows that large amounts of ferritin accumulate locally in the pleural cavity in certain types of pleural inflammation. The accumulation is probably partly the result of increased local reticuloendothelial system activity. Determination of the concentration of ferritin in pleural fluid may provide corroborative information for differential diagnosis and may further our understanding of the pathogenetic events that lead to the perpetuation of inflammatory activity in pleural effusions.
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PMID:Pleural fluid ferritin concentrations in human disease. 401 3

Pleural effusion is a common diagnostic problem. The analysis of serum and body fluids for tumor markers has been intensively applied to clinical diagnosis. The aim of the present study was to determine the usefulness of simultaneous quantification of carbohydrate antigen 19.9, carbohydrate antigen 125, neuron specific enolase, mucinous-carcinoma-associated antigen, and ferritin in samples of pleural fluids in the malign pleural effusion and its differentiation from benign effusions. A total of 61 pleural effusions were collected from the patients, who were subjected either to simple needle aspiration or to tube drainage for the diagnosis of pleural effusion. Tumor markers were determined in benign patient groups with nonspecific pleurisy, tuberculous pleurisy, empyema, congestive heart failure and in malignancy groups consisting of adenocarcinoma, small cell lung carcinoma, mesothelioma, epidermoid lung cancer. The tumor markers CA-19.9, CA-125, NSE, and ferritin levels were quantified by the sandwich assay using the streptavidin technology of ELISA in an ES-300 Boehringer-Mannheim analyser. MCA was measured by employing a two-side solid phase EIA method. MCA measurements were done by the Cobas-Core. For all patients, the effusions correctly or incorrectly identified by the different procedures as being malignant or nonmalignant are defined as true positive, false positive, true negative, and false negative, the term 'positive' referring to histologically proven malignant pleural effusion while nonmalignant effusions are referred to as 'negative'. Therefore, sensitivity, specificity, positive predictive value, and negative predictive value were defined as diagnostic parameters. The cut-off values calculated were 352 U/ml for CA-125, 54 U/ml for CA-19.9, 555 for ferritin, 11.1 for MCA and 8.7 for NSE. In our study, the highest sensitivity is found to be MCA with 100%; specificity, CA-19.9 with 97%; PPV, CA-19.9 and MCA with 95% and NPV, MCA with 100%. Our data imply that the co-measurement of MCA+CA-19.9+CA-125 levels may further improve their diagnostic value in malignant pleural effusion compared with that of each tumour marker alone and may be useful in distinguishing malignant from benign pleural effusions.
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PMID:Diagnostic usefulness of tumour marker levels in pleural effusions of malignant and benign origin. 1095 62

Bilirubin is the end product of heme catabolism by heme oxygenases. The inducible form of these enzymes is heme oxygenase-1 (HO-1), which is the rate-limiting enzyme that can degrade heme into equimolar quantities of carbon monoxide (CO), biliverdin, and free iron. Biliverdin is very rapidly converted to bilirubin by the enzyme biliverdin reductase, and free iron upregulates the expression of ferritin. HO-1 is a ubiquitous stress protein and is induced in many cell types by various stimuli. Induced HO-1 exerts antiinflammatory effects and modulates apoptosis. Expression of HO-1 in vivo suppresses the inflammatory responses in endotoxic shock, hyperoxia, acute pleurisy, and organ transplantation, as well as ischemia-reperfusion injury, and thereby provides salutary effects in these conditions. Accumulating evidence indicates that biliverdin/bilirubin can mediate the protective effects of HO-1 in many disease models, such as IRI and organ transplantation, via its antiinflammatory, antiapoptotic, antiproliferative, and antioxidant properties, as well as its effects on the immune response. This review attempts to summarize these protective roles as well as the molecular mechanisms by which biliverdin/bilirubin benefit IRI and solid-organ transplantation, including chronic rejection, and islet transplantation.
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PMID:Therapeutic applications of bilirubin and biliverdin in transplantation. 1791 67