Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

New diagnostic tests are mainly evaluated by determining the sensitivity and specificity of the test. These test characteristics were originally meant to be used in making diagnoses. For evaluative purposes their usefulness is weakened by their susceptibility to selection and their dependence on the cut-off points that are used for test positivity. The plotting of a receiver operating characteristic (ROC) curve might be a solution to these problems. Furthermore, the ROC curve yields a measure for the diagnostic power of the test expressed in one number instead of two, namely the area under the curve (AUC). Finally, the ROC curve and its AUC permit easy comparison of different tests and the performance of different interpreters of one test. The construction and use of ROC curves are described and illustrated with data of a case-referent investigation into the relationship between iron status parameters and the presence of acute myocardial infarction. The AUCs of ferritin and serum iron, 0.61 and 0.68 respectively, are too low to suggest meaningful usefulness in clinical practice.
 ...
PMID:ROC curves for the initial assessment of new diagnostic tests. 149 May 47

Recent studies have noted an association between both increased serum ferritin and dietary iron intake and acute myocardial infarction (AMI). The possible role of increased serum ferritin and dietary iron intake in the promotion of infection, and in the etiology of AMI, is discussed. In addition, the possible role of infection in the etiology of coronary heart disease and AMI is also discussed.
 ...
PMID:Short note: iron, infection and acute myocardial infarction. 802 32

The authors investigated the association of the amount and intensity of conditioning leisure time physical activity with serum ferritin and blood hemoglobin concentrations in 1,743 eastern Finnish men who were aged 42-60 years during the period 1984-1989. The duration and frequency of physical activity were associated inversely with serum ferritin (p = 0.003 for duration and p < 0.001 for frequency) and blood hemoglobin (p = 0.002 for duration and p = 0.019 for frequency) in multivariate regression models, after adjustment for major confounders. Men in the highest quartile of duration (> 2.6 hours/week) had a 16.8% lower mean serum ferritin concentration and men in the highest category of frequency (> 3 sessions/week) had a 19.9% lower mean serum ferritin concentration than men with a low duration (< 0.4 hour/week) and frequency (< 1 session/week), respectively. For blood hemoglobin, the respective differences were 1.3% and 1.0%. The intensity of physical activity was significantly associated only with blood hemoglobin (p = 0.011). Together with the authors' previous finding concerning the association between high serum ferritin and an excess risk of acute myocardial infarction, these data suggest that a reduction in stored iron levels could be one mechanism through which conditioning leisure time physical activity decreases the risk of coronary heart disease.
 ...
PMID:Higher levels of conditioning leisure time physical activity are associated with reduced levels of stored iron in Finnish men. 802 3

In a recent Finnish study, an association of high serum ferritin levels with excess risk of myocardial infarction in men was reported. This was the first such report in the literature so we decided to review the clinical records of 298 male patient seen over a 10-year period in Southern West Virginia, in whom serum ferritin levels were obtained. Of the 32 patients who experienced an acute myocardial infarction, there were no significant statistical differences between their mean ferritin levels and the ferritin levels of the 266 patients with no myocardial infarct. Only two of the 32 patients with myocardial infarct showed an elevated serum ferritin level, so our findings do not support the hypothesis that high serum ferritin levels are associated with myocardial infarct.
 ...
PMID:Serum ferritin and myocardial infarct. 812 58

Elevated serum ferritin concentrations between 200 and 500 microg/l have been found to be a strong risk factor for acute myocardial infarction in Finnish men, but the reason for this association is still uncertain. In the Finnish population ferritin concentrations correlated with factors of insulin resistance syndrome. As these factors have been found to be associated with an LDL subfraction phenotype of increased concentrations of small, dense LDL particles, we hypothesized an association between ferritin and an atherogenic LDL subfraction profile, a finding which could be an explanation for the observed relationship between ferritin and atherosclerosis. Therefore we determined serum ferritin levels, metabolic cardiovascular risk factors, and the LDL subfraction phenotype in 93 healthy men without signs for infection or coronary heart disease. We found that men with moderately elevated ferritin levels (200-500 microg/l; n = 31) had a significantly worse coronary risk profile than men with lower levels ( < 200 microg/l; n = 62). Elevated ferritin concentrations were associated with significantly higher values for serum triglycerides, VLDL cholesterol, VLDL apolipoprotein B (P < 0.01), IDL cholesterol, fasting glucose (P < 0.05) and uric acid (P < 0.01), and lower levels for HDL2b and HDL2a cholesterol and apolipoprotein A-I (P < 0.05), and lipoprotein(a) (P < 0.01). Elevated ferritin levels were, however, not associated with an unfavourable LDL subfraction profile of increased concentrations of small, dense LDL particles.
 ...
PMID:Relationship of serum ferritin concentrations with metabolic cardiovascular risk factors in men without evidence for coronary artery disease. 905 Jul 80

Serum ferritin level was determined in 20 patients with acute myocardial infarction (AMI) during the first 10 days post infarction. Starting on the second day, a gradual increase in serum ferritin level was detected, reaching a maximum of four times the initial level on the sixth day after the infarction. In addition, a significant increase in ferritin content was found in the peripheral blood monocytes on the fifth day after the event. The control group comprised six patients suffering from chest pains not due to AMI. In all of them the serum ferritin level was found to be within normal limits. Peripheral blood monocytes derived from healthy individuals incubated with hydrocortisone, showed a significant enhancement of their ferritin content, a finding suggesting that these cells activated by steroids during stress could be a source of the increased serum ferritin level following AMI. It is concluded that measurement of serum ferritin may be used as a complementary tool for confirming the diagnosis of AMI.
 ...
PMID:Elevated serum ferritin level in acute myocardial infarction. 918 Oct 48

Free radical species have been implicated as important agents involved in myocardial ischemic and reperfusion injuries. Superoxide is capable of mobilizing iron from ferritin and the released iron can cause hydroxyl formation from H2O2. The aim of this study was to evaluate the time-dependent increase in lipid peroxidation assessed by plasma thiobarbituric acid reactive substances (TBARS) and the relationship between lipid-peroxidation and the iron status. Peripheral venous blood samples were obtained from 17 men with acute myocardial infarction (AMI) before thrombolytic treatment (T0) and 1, 2, 3, 4, 8, 12, 16, 20, 24 and 48 hours after commencing fibrinolytic treatment. The concentration of TBARS, the parameters of iron metabolism, serum myoglobin, creatine kinase, and creatine kinase-MB were measured. Early reperfusion was judged by regression of sinus tachycardia (ST) elevation and reduction of chest pain. Recanalization of coronary artery was evaluated by a late coronary angiography 24-96 hours after thrombolysis. After thrombolytic therapy, the TBARS level was raised from 2.98 +/- 0.80 (T0) to 4.57 +/- 1.24 (peak), and decreased to 2.96 +/- 0.40 nmol/mL plasma at T48 (T0 vs peak: P < 0.001, peak vs T48: P < 0.001, T0 vs T48: NS). The mean time of the peak was observed at 9.7 +/- 7.5 hours. The iron increased significantly from 0.67 +/- 0.34 (T0) to 1.15 +/- 0.52 mg/L (peak), and returned to the pre-reperfusion to levels: 0.53 +/- 0.28 UI/L at T48 (TO vs peak: P < 0.001, peak vs T48: P < 0.001, T0 vs T48: NS). The mean time of the peak was observed at 9.4 +/- 7.3 hours. In return, no correlation was found between the increase of plasma creatine-kinase activity, myoglobin and iron or between the biochemical markers and time of fibrinolytic therapy. The results confirmed the importance of the temporal relationship between lipid peroxidation and iron status after thrombolytic therapy. Our results are in agreement with the concept that antioxidant agents used in association with thrombolytic therapy might be useful.
 ...
PMID:Plasma iron status and lipid peroxidation following thrombolytic therapy for acute myocardial infarction. 956 80

We investigated whether there is an association between serum ferritin or soluble transferrin receptor (sTfR) concentrations and coronary artery disease (CAD) or its clinical presentations. This is a case-control study that included 892 patients (664 cases with angiographically proven CAD and 228 controls without CAD). Blood was collected before angiography for determination of sTfR, ferritin and C-reactive protein (CRP). The values (median, 25th-75th percentiles) of sTfR (2.6 [2.1; 3.2]mg/l versus 2.4 [2.1; 3.0]mg/l, P = 0.13) or ferritin (140.1 [74.8; 248.3]ng/ml versus 120.1 [74.9; 218.0]ng/ml, P = 0.11) did not differ significantly between cases or controls. The values of sTfR in the case subjects with 1-vessel, 2-vessel, and 3-vessel CAD were: 2.4 [2.0; 3.0], 2.6 [2.0; 3.2], and 2.8 [2.2; 3.3]mg/l, respectively (P = 0.003). In multivariate analysis, neither sTfR (chi2 = 0.14, P = 0.70) nor ferritin (chi2 = 2.8, P = 0.09) correlated independently with the presence of CAD. In case subjects with stable angina, unstable angina, and acute myocardial infarction (MI), ferritin concentrations were: 127.5 [69.5; 214.0], 138.9 [86.1; 278.0], and 175.0 [93.5; 314.5]ng/ml, respectively (P < 0.001). Our results showed that serum concentrations of sTfR or ferritin do not predict the risk for coronary artery disease. In subjects with pre-existing CAD, those with more severe disease had increased levels of sTfR. Patients with CAD presenting with acute coronary syndromes showed increased levels of serum ferritin.
 ...
PMID:Value of serum ferritin and soluble transferrin receptor for prediction of coronary artery disease and its clinical presentations. 1513 58

More than 20 years ago it was proposed that differences in body iron stores may account for differential heart disease prevalence in men and women. In 1992 Finnish investigators presented intriguing supportive evidence for this proposal by showing that middle-aged men with normal but elevated serum ferritin, a biomarker of body iron stores, were at increased risk for acute myocardial infarction. During the past dozen years many studies have followed leading to intense debate on the role of iron in the development of heart disease. A meta-analysis of prospective studies found, however, no support for the iron-heart disease hypothesis. As new disease associations with iron status continue to be explored, consideration needs to be given to the lessons learned from these studies. Moreover, additional efforts need to be made to find a simple, high throughput and more satisfactory measure of the forms of iron in the body that are liable to do damage.
 ...
PMID:The iron-heart disease connection: is it dead or just hiding? 1523 Dec 42

Organic nitrates are a group of very effective anti-ischemic drugs. They are used for the treatment of patients with stable angina, acute myocardial infarction and chronic congestive heart failure. A major therapeutic limitation inherent to organic nitrates is the development of tolerance, which occurs during chronic treatment with these agents. The mechanisms underlying nitrate tolerance remain incompletely defined and are likely multifactorial. One mechanism seems to be a diminished bioconversion of nitroglycerin, another seems to be the induction of vascular oxidative stress, and a third may include neurohumoral adaptations. Recent studies have revealed that mitochondrial reactive oxygen species (ROS) formation and a subsequent oxidative inactivation of nitrate reductase, the mitochondrial aldehyde dehydrogenase (ALDH-2), play an important role in the development of nitrate and cross-tolerance. The present review focus first on the role of oxidative stress and second on the role of ALDH-2 in organic nitrate bioactivation leading to the development of tolerance and cross-tolerance (endothelial dysfunction) in response to nitroglycerin treatment. Recently, the role of mitochondrial oxidative stress in the development of nitrate tolerance was demonstrated in a mouse model with a heterozygous deletion of manganese superoxide dismutase (MnSOD(+/-)), which is the mitochondrial isoform of this enzyme. Studies from our own laboratory have provided evidence for cross-talk between mitochondrial and cytosolic (Nox-dependent) sources of ROS. We close this review by focusing on the protective properties of the organic nitrate pentaerithrityl tetranitrate, which upregulates enzymes that have strong antioxidative activity, such as heme oxygenase-1 and ferritin, thereby preventing the development of tolerance and endothelial dysfunction.
 ...
PMID:Nitrate tolerance as a model of vascular dysfunction: roles for mitochondrial aldehyde dehydrogenase and mitochondrial oxidative stress. 1930 91


1 2 Next >>