Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the potential role of interleukin-6 as a mediator of the acute-phase reaction (APR) in patients with acute myocardial infarction. Of the six patients studied, five demonstrated increased plasma interleukin-6 levels. Interleukin-6 levels began to increase at 14 hours (mean; range = 8 to 20 hours) after the initial complaints and reached maximal levels of 28 to 250 U/mL (normal values less than 10 U/mL) after 36 hours (mean; range = 24 to 52 hours). No correlation was seen between the size of the interfaction as indicated by creatine kinase MB assays and the extent of the interleukin-6 increases (r = 0.44; p = 0.38). As an indicator of the APR, plasma C-reactive protein (CRP) levels were measured. CRP levels began to increase after 16 hours (mean; range = 8 to 24 hours) and reached maximum levels of 56 to 322 mg/L (normal values less than 3 mg/L) after 65 hours (mean; range = 48 to 92 hours). The increase of the interleukin-6 level preceded the increase of the CRP level in three patients and was simultaneous in two patients. Maximal interleukin-6 levels correlated significantly with maximal CRP levels (r = 0.96; p = 0.002). Thus these findings indicate that interleukin-6 is an important endogenous mediator for the APR in patients with acute myocardial infarction.
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PMID:Interleukin-6 release and the acute-phase reaction in patients with acute myocardial infarction: a pilot study. 158 14

Interleukin-6 (IL-6) plays a key role in the synthesis of human acute-phase protein and several acute-phase responses occur in patients with acute myocardial infarction (AMI). We examined the plasma levels of IL-6 in 23 consecutive patients with AMI over the course of 4 weeks and in 30 control subjects. In patients with AMI, the plasma IL-6 levels (in picograms per milliliter) were increased at all sampling points from admission to discharge (ranging from 28.5 +/- 6.6 to 46.5 +/- 7.8) compared with levels in control subjects (11.4 +/- 2.9; p < 0.01). Cardiac catheterization did not influence plasma IL-6 levels. The plasma IL-6 level reached its peak approximately 3 days (46.5 +/- 7.8) and approximately 1 week after admission in patients with AMI. There was a significant positive linear correlation between the peak level of plasma IL-6 minus the level on admission and the peak level of plasma C-reactive protein in patients with AMI. The peak IL-6 level did not correlate with the peak levels of creatine kinase, pulmonary capillary wedge pressure, or left ventricular ejection fraction at 4 weeks. We conclude that the plasma IL-6 level is increased over a time course of 4 weeks in patients with AMI.
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PMID:Elevated plasma interleukin-6 levels in patients with acute myocardial infarction. 824 85

We have observed that acute myocardial infarction is associated with the immunological response characterized a transient rise of serum immunoglobulin E (IgE). We wondered whether this reaction was specific for myocardial infarction or whether it reflected a more generalized phenomenon, perhaps triggered by tissue injury. We, therefore, made a large prospective study on patients undergoing various surgical procedures. These were the patients undergoing coronary artery bypass graft, who did (n = 39) or did not (n = 42) develop perioperative myocardial infarction, patients subjected to thoracic operations (n = 33) patients having cholecystectomy (n = 17) or repair of the inguinal hernia (n = 18) and 30 healthy volunteers forming the control group. Blood samples were drawn before the operation and then after the operation at 8, 16, 24, 48, 72, 120, 168 and 216 hours. In all samples, concentrations of serum immunoglobulins E were determined on blinded specimens by an automated microparticle enzyme immunoassay while immunoglobulins G, A and M were determined using nephelometry. In all groups studied, except the control group, serum IgE began to rise shortly after the operations reached a peak by the fifth day, and then gradually declined. This behaviour of IgE serum levels was in striking contrast to that of the remaining serum immunoglobulins G, A and M which showed a rapid fall after surgical interventions, followed by a gradual return to the initial values. The stimulation of hypothalamus-adrenal axis and release of glucocorticosteroids, interacting with de novo synthesized interleukin-6, could explain this newly observed phenomenon of the immunoglobulin E response to the tissue injury. Behaviour of serum IgE, as described by us, bears much resemblance to that of acute phase proteins. In conclusion, we hypothesize that immunoglobulin E may act in human organism as an acute phase protein.
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PMID:[Humoral immune response to tissue injury, characterized by a rise in serum immunoglobulin E]. 861 12

Three cases of patients with cardiac myxoma who had attacks of acute myocardial infarction are presented. Cineangiographic study showed normal coronary arteries. Immunohistochemical and serologic examination revealed that both interleukin-6 and interleukin-8 were secreted in cardiac myxoma. The authors discuss the relation between these cytokines and myocardial infarction with normal coronary arteries.
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PMID:Myocardial infarction in myxoma patients with normal coronary arteries. Case reports. 871 87

Interleukin-6 (IL-6) is one of the cytokine mediators of the acute phase response. The value of IL-6 determination in the investigation of patients suspected of acute myocardial infarction and unstable angina is not fully established. In 26 patients being investigated for AMI and UA, IL-6, Creatine Kinase (CK) and Troponin T (TnT) were elevated with peak values at 12 hours (for IL-6 and CK) and at 0 and 24 hours (for TnT) following admission. CK values in AMI were significantly different from UA patients at 0, 6, 12, and 25 hours following admission, whereas, IL-6 values showed significant difference only at 24 hours. TnT showed a significant difference between the groups at 0 and 24 hours following admission. There was poor negative correlation between IL-6 and CK levels and percentage left ventricular ejection fraction. This study showed that, although IL-6 was elevated in AMI and UA patients, the spread of the data indicated that its measurement is of limited value in the diagnosis of AMI.
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PMID:The value of serum interleukin-6 measurement in the investigation of patients suspected of myocardial infarction. 896 84

While an overproduction of interleukin-6 (IL-6) has been observed in patients with acute myocardial infarction (AMI), its clinical significance and localization in the ischemic myocardium have not been elucidated. We examined immunohistochemically the expression of IL-6 in 12 autopsied patients with AMI who had died within seven days of the infarction. Twenty sections of ischemic myocardium and nine of the coronary arteries involved were stained with anti-IL-6 and anti-atrial natriuretic peptide (ANP). The diameter of the myocardium was analyzed. The greatest expression of IL-6 in the infarcted myocardium occurred in patients who had died three to four days after the onset (2.7 +/- 0.4), as judged by a scheme for grading IL-6 expression. Patients who died within one to two days (1.0 +/- 0.3) or five to eight days (0.6 +/- 0.4) less frequently showed an overproduction of IL-6. The IL-6-positive myocardium co-expressed ANP and was significantly (p < 0.05) hypertrophied, when compared with the IL-6-negative myocardium. The diameter of IL-6-positive myocardial myocytes was significantly (p < 0.02) increased in patients who died within one to two days (1.6 +/- 0.2), three to four days (1.8 +/- 0.3), or five to eight days (2.0 +/- 0.2) after the AMI. The involved coronary arteries expressed IL-6 in the intimal and smooth muscle cells, as did atherosclerotic coronary arteries not involved in AMI. An overproduction of IL-6 was confirmed in the injured myocardium with hypertrophy in patients who died of AMI within seven days after onset. The hypertrophied injured myocardium co-expressed IL-6 and ANP. The expression of IL-6 in the myocardium in AMI appears to be associated with the mechanism of cardiac hypertrophy.
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PMID:Expression of interleukin-6 in the ventricles and coronary arteries of patients with myocardial infarction. 950 63

Magnesium (Mg) inhibits the influx of calcium in vascular smooth muscle cells. The purposes of this study were to test the hypothesis that an intravenous administration of magnesium might effect the complement response and to determine the effects of a magnesium pretreatment of patients with acute myocardial infarction (AMI) on the incidence of reperfusion injuries. Thirty-eight AMI patients were treated with coronary reperfusion therapy within 6 hours of onset. They were randomly divided into two groups: group pretreated with intravenous magnesium sulfate (0.27 mmol/kg) (magnesium group, n = 19), and nonpretreated controls (placebo group). The reperfusion injuries observed within 1 hour after the coronary reperfusion included arrhythmias, aggravated chest pain, and ST segment elevation in 12-lead electrocardiograms. Coronary recanalization was performed in 36 patients. The incidence of reperfusion arrhythmia was significantly lower in the magnesium group than in the placebo group (17% vs 78%, p<0.001). At the postreperfusion stage, there was a tendency for the degree of ST segment reelevation in the magnesium group lower than in the placebo group (2.5 +/- 2.3 mm vs 4.7 +/- 3.8 mm, p = 0.07). No marked difference was observed in the incidence of chest pain aggravation between the two groups (67% vs 73%, ns). The peak serum levels of interleukin-6 (IL-6) were significantly lower in the magnesium group than those in the placebo group (38.9 +/- 25.0 vs 92.3 +/- 76.5 pg/mL, p = 0.016). The peak serum levels of matrix metalloproteinase-1 (MMP-1) were lower than those in the placebo group (16.2 +/- 4.8 vs 19.7 +/- 9.0 ng/mL, p = 0.09), but the difference was not significant. A positive correlation was observed between the peak MMP-1 values and the peak IL-6 values (r = 0.57, p = 0.001) in all patients. Increased serum ionized Mg2+ may inhibit arrhythmic recurrence and the production of IL-6 and MMP-1 after reperfusion and prevent the increase of myocardial lesions caused by calcium overload on myocytes. The increased IL-6 production may induce MMP-1, leading to tissue organ injury. Pretreatment with magnesium sulfate may protect the myocardium of AMI patients from reperfusion injuries.
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PMID:Effect of magnesium sulfate pretreatment and significance of matrix metalloproteinase-1 and interleukin-6 levels in coronary reperfusion therapy for patients with acute myocardial infarction. 1043 97

The euthyroid sick syndrome is reported to exist in acute myocardial infarction(AMI). Previous reports showed serum levels of triiodothyronine(T3) are low and thyroid stimulating hormone(TSH) is normal or subnormal levels in patients with AMI. However, the mechanism of altered thyroid hormone metabolism is unknown. Interleukin-6(IL-6) is reported to be a key role in the pathogenesis of AMI and euthyroid sick syndrome. We measured circulating TSH, free T3(FT3), free thyroxine (FT4), IL-6, soluble IL-6 receptor, soluble transducing 130-kD glycoprotein, atrial natriuretic peptide(ANP) and brain natriuretic peptide in 25 patients and 32 healthy subjects. Circulating FT3 levels in patients with AMI became lower than in control group(p < 0.05). IL-6 levels were significantly(p < 0.05) higher than those of healthy subjects. The peak levels of IL-6 was 30.5 +/- 46.9 pg/ml at 25-27 hours(the first peak) and 64.4 +/- 24.6 pg/ml at 70-72 hours(the second peak). FT3 was negatively related to IL-6(p < 0.05) and hANP(p < 0.05) in patients with AMI. These results indicate that the lower levels of FT3 show the greater severity of AMI. We conclude that euthyroid sick syndrome occurs in patients with AMI and euthyroid sick syndrome may regulated by IL-6 through suppressed of thyroid function.
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PMID:[Studies on circulating interleukin-6 and thyroid functions in acute myocardial infarction]. 1080 37

The plasma levels of endothelin(ET), serum levels of tumor necrosis factor(TNF) and interleukin-6(IL-6) in 35 patients with coronary heart disease(CHD) and 20 healthy people were studied by radioimmunoassay and enzymebinded immunosorbent assay(ELISA). The results showed that the plasma ET level and the serum TNF level in the CHD group, especially the acute myocardial infarction(AMI) group, were much higher than those of the control group (P < 0.01). There was no obvious statistical difference on IL-6 levels between the narrowed coronary artery group and the control group (P > 0.05). But the serum level of IL-6 in the AMI group was significantly higher than that of the other groups (P < 0.01). These findings indicate that ET and cytokine levels may play an important role on the pathogenesis of coronary heart disease.
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PMID:[Effect on endothelin and cytokines on the pathogenesis of coronary heart disease]. 1080 72

Although acute myocardial infarction (AMI) may involve both plaque rupture and ischemia-reperfusion injury, the pathogenesis of these phenomena is unclear. To elucidate the pathogenesis of AMI, serial measurements of platelet activating factor (PAF), interleukin-6 and cell adhesion molecules were made in patients with AMI. The PAF levels were measured upon hospital admission and at 24 and 72h in 8 patients with AMI. Serum levels of interleukin-6, soluble E-selectin (sE-selectin), soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule- 1 (sVCAM- 1) were measured upon admission and at 24 h and 4 weeks in 30 patients with AMI and 15 patients with stable effort angina. PAF levels were higher in patients with AMI than in normal volunteers; the increased levels lasting at least 72h. In contrast, interleukin-6 increased at 24h. sE-selectin was elevated at admission and sVCAM-1 increased later. sE-selectin levels upon admission in patients with additional ST-segment elevation after reperfusion were significantly higher than those in patients without ST-elevation. In patients with AMI, the time-course of changes in blood levels of cytokines varied according to the individual substances. Although it is unclear what is the precise role of each of the cytokines in the pathophysiology of AMI, sE-selectin may be possibly related to the reperfusion injury in the infarcted myocardium.
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PMID:Role of cytokines and adhesion molecules in ischemia and reperfusion in patients with acute myocardial infarction. 1094 15


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