Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ferritin level in serum was investigated in 9 patients with myocardial infarction, all with a history of chest pain of less than 4 hours before admission. A significant rise in serum ferritin level was found in 8 patients. The rise was generally smaller than that seen in acute infection and not significantly correlated to the size of infarction, as estimated from changes in serum levels of myoglobin, ASAT and LDH. The rise started after a mean of 30 hours, the peak being reached within a week (M 4.3 days). Serum ferritin then fell to 120--300% (M 190) of the initial level, where it remained. An initial rise in serum iron levels was unexpectedly seen within 12 hours in 7 patients.
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PMID:Serum ferritin during inflammation. A study on myocardial infarction. 52 35

A male forestry worker presented with chest pain followed by severe continuing haemoptysis and an extensive bilateral nodular pulmonary infiltrate. A needle biopsy of lung demonstrated micronodular deposits of malignant tissue. The patient died from respiratory failure. Necropsy showed a disseminated haemangiosarcoma arising in the right atrium. Haemoglobin and serum iron levels were normal. Electron microscopy of the lung biopsy showed a close relationship between tumour cells and basement membrane and suggested that haemorrhage occurred directly from the tumour nodules. The ultrastructure of alveoli adjacent to tumour deposits was normal. This case provides further indirect evidence that the clinical and histological features of idiopathic pulmonary haemosiderosis cannot be explained by the mere occurrence of alveolar haemorrhage.
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PMID:Pulmonary haemorrhage in disseminated cardiac haemangiosarcoma. 55 87

Fifty six patients admitted consecutively to the coronary care unit with ischemic chest pain participated in a controlled prospective study of acute changes in iron metabolism. Following myocardial infarction there were significant reductions of plasma iron by 8.1 mumol/L (P = 0.002), total iron binding capacity by 12.9 mumol/L (P = 0.003), and plasma transferrin by 0.70 g/L (P = 0.007). In contrast, there was a significant elevation of serum ferritin by 218 micrograms/L (P = 0.0005). The magnitude and duration of these acute changes in iron metabolism was greater in patients with higher peak serum creating kinase levels, suggesting that these changes are influenced by the extent of tissue necrosis. Comparison with the control group showed that alteration in dietary iron intake was not a significant factor. The possible mechanisms of these acute changes and their similarity to those observed in the anemia of chronic disease are discussed.
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PMID:Acute changes in iron metabolism following myocardial infarction. 406 89

The treatment of anemia in hemodialysis patients is frequently hindered by the presence of suboptimal iron stores. Intravenous iron dextran is in common use to maintain iron stores in this population, but there are little published data regarding the incidence and type of adverse events. The purpose of this study was to evaluate the safety of this medication. Charts from four hemodialysis centers of all 573 patients treated with intravenous iron dextran (INFeD; Schein Pharmaceutical, Inc, Florham Park, NJ) between July 1, 1993, and June 30, 1995, were studied. Twenty-seven patients (4.7%) had adverse reactions that were related to iron dextran. Four patients (0.7%) had reactions classified as serious (one cardiac arrest; three others required hospitalization). Ten patients (1.7%) had reactions classified as anaphylactoid. No patients died or developed permanent disability as a result of reactions. The most common adverse reactions included itching (1.5% of patients) and dyspnea or wheezing (1.5%); others included chest pain (1.0%), nausea (0.5%), hypotension (0.5%), swelling (0.5%), dyspepsia (0.5%), diarrhea (0.5%), skin flushing (0.3%), headache (0.3%), cardiac arrest (0.2%), and myalgias (0.2%). Five of all the reactions occurred during a test dose; four of these were anaphylactoid. Several factors were studied as possible predictors of adverse reactions. A positive history of drug allergy (odds ratio, 2.4; P = 0.03) and history of multiple drug allergy (odds ratio, 5.5; P = 0.0004) were significant predictors of reactions. In summary, we found serious adverse reactions to be uncommon in hemodialysis patients treated with intravenous iron dextran. Future prospective studies will help confirm this finding.
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PMID:The safety of intravenous iron dextran in hemodialysis patients. 1067 41

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.
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PMID:Plasma iron status and lipid peroxidation following thrombolytic therapy for acute myocardial infarction. 956 80

A 72-year-old patient presented himself with typical symptoms of coronary heart disease and was scheduled for invasive diagnostic procedures. Cardiac risk factors were smoking and arterial hypertension. The physical examination was inconspicious. In the laborchemistry a hemoglobin of 79 g/l with a mean corpuscular volume of 63 fl and a mean corpuscular hemoglobin of 20 pg was conspicuous. The serum iron was with 42 micrograms/dl in the lower norm. Transferrin, bili-rubin and lactate dehydrogenase were normal. Then in the gastrointestinal investigations he was diagnosed with a leiomyoma of the intestine that led to chronic anaemia and additionally to chest pain characteristic for angina pectoris. After the removal of the tumor and normalization of hemoglobin this patient was free from symptoms of the disease. The coronary angiography revealed a complex stenosis of the right coronary artery with collaterales and not significant stenosis both of the left coronary arteries. In patients with angina pectoris anaemia as the possible and only cause of angina ought to be verified. It is therefore necessary after normalization of hemoglobin and clarification of the cause for the anaemia to apply a test for coronary ischemia.
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PMID:[Angina pectoris in leiomyoma]. 975 77

A new intravenous (i.v.) iron compound, sodium ferric gluconate complex in sucrose (Ferrlecit, R&D Laboratories, Inc, Marina Del Rey, CA), was administered over 8 consecutive dialysis days in equally divided doses to a total of either 0.5 or 1.0 g in a controlled, open, multicenter, randomized clinical study of anemic, iron-deficient hemodialysis patients receiving recombinant human erythropoietin (rHuEPO). Effectiveness was assessed by increase in hemoglobin and hematocrit and changes of iron parameters. Results were compared with historically matched controls on oral iron. High-dose i.v. treatment with 1.0 g sodium ferric gluconate complex in sucrose resulted in significantly greater improvement in hemoglobin, hematocrit, iron saturation, and serum ferritin at all time points, as compared with low-dose i.v. (0.5 g) or oral iron treatment. Despite an initial improvement in mean serum ferritin and transferrin saturation, 500 mg i.v. therapy did not result in a significant improvement in hemoglobin at any time. Eighty-three of 88 patients completed treatment with sodium ferric gluconate complex in sucrose: 44 in the high-dose and 39 in the low-dose group. Two patients discontinued for personal reasons. The other three discontinued because of a rash, nausea and rash, and chest pain with pruritus, respectively. In comparison with 25 matched control patients, adverse events could not be linked to drug therapy, nor was there a dose effect. In conclusion, sodium ferric gluconate complex in sucrose is safe and effective in the management of iron-deficiency anemia in severely iron-deficient and anemic hemodialysis patients receiving rHuEPO. This study confirms the concepts regarding iron therapy expressed in the National Kidney Foundation Dialysis Outcomes Quality Initiative (NKF-DOQI) that hemodialysis patients with serum ferritin below 100 ng/mL or transferrin saturations below 18% need supplementation with parenteral iron in excess of 1.0 g to achieve optimal response in hemoglobin and hematocrit levels.
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PMID:Sodium ferric gluconate complex in sucrose is safe and effective in hemodialysis patients: North American Clinical Trial. 1067 41

The safety data from the phase II clinical trial of ferumoxtran-10, an ultrasmall superparamagnetic iron oxide contrast agent, are presented. One hundred and four patients with focal liver or spleen pathologies underwent ferumoxtran-10-enhanced magnetic resonance (MR) imaging at doses of 0.8, 1.1, and 1.7 mg Fe/kg. Overall, 15% patients reported a total of 33 adverse events, regardless of causality. The adverse events most frequently seen were dyspnea (3.8%), chest pain (2.9%), and rash (2.9%). No serious adverse events were reported during the 48 hour observation period. There were no clinically significant effects on vital signs, physical examination, and laboratory results. Ferumoxtran-10 is a safe and well tolerated MR contrast agent.
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PMID:Safety profile of ultrasmall superparamagnetic iron oxide ferumoxtran-10: phase II clinical trial data. 1007 27

The National Kidney Foundation recently published guidelines stating that regular use of intravenous iron therapy will prevent iron deficiency and promote better erythropoiesis than oral iron therapy in patients with end stage renal disease (ESRD) who are undergoing hemodialysis. Although intravenous iron dextran has been shown to be clinically effective in maintaining iron stores in such patients, some clinicians are concerned about the incidence of adverse events associated with this mode of iron supplementation. We conducted a retrospective review of adverse events associated with the use of Dexferrum (American Regent Laboratories, Inc., Shirley, NY) in ESRD patients at an outpatient dialysis clinic. During the 6-month study period, only 1 patient out of 62 (1.6%) experienced adverse events (hypotension, chest pain) related to treatment with Dexferrum. No patients developed anaphylactoid reactions.
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PMID:The safety of intravenous iron dextran (Dexferrum) during hemodialysis in patients with end stage renal disease. 1085 89

A 37-year-old male, splenectomized at the age of 1 year, was admitted to the ward with severe chest pain and signs of cardiogenic shock. Clinical investigations revealed the presence of both hemochromatosis and hereditary spherocytosis (HS). HLA typing showed A3,B7 and A24,B57 haplotypes and genetic analysis revealed homozygosity for the C282Y mutation. A family study was performed. The parents and four brothers were heterozygous for the C282Y mutation. Two of the brothers also presented high levels of iron stores and they had been splenectomized because of HS, while two other siblings had neither spherocytosis nor hemochromatosis. The mother had a mild anemia with dehydrated red blood cells (RBC), while the father appeared to have low-density, but normal RBC; none of them presented with spherocytosis. All siblings with spherocytosis and elevated iron stores showed a RBC density distribution similar to the mother. We present the first case with genetically proven hemochromatosis in combination with spherocytosis, focusing on the various possibilities of iron accumulation in individuals with spherocytosis and heterozygosity for the C282Y mutation.
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PMID:Hereditary spherocytosis and hemochromatosis. 1197 22


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