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)

Previous studies have shown an association between serum C-reactive protein (CRP) and cardiovascular disease (CVD) risk. The roles of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFalpha) are less well established. The aim of the present study was to analyze the associations of CRP, IL-6 and TNFalpha with incident coronary heart disease (CHD) events, CVD events, and total mortality. A random population sample, including men and women aged 25-64 years was examined in Finland in 1992. The sample size was 7,927 and 6,051 (76%) participated. The cohort was followed up until the end of 2001. During the follow-up, 151 incident CHD events, 205 CVD events and 183 deaths from any cause were observed. A stratified random subsample (n=313) was used as the comparison group. After adjustment for conventional CVD risk factors, CRP showed a significant association with CHD risk in men (HR=2.39, 1.08-5.28, comparing fourth quartile to the first quartile). This association remained significant after further adjustment for TNFalpha. TNFalpha also was a significant predictor of CHD among men, but the association was nonlinear (HR=2.21, 1.18-4.14 comparing the three upper quartiles to the first quartile). Further adjustment for CRP did not change this association substantially. Both CRP and TNFalpha predicted also all CVD events and total mortality among men. Among women the findings were nonsignificant. In conclusion, CRP and TNFalpha were significant, independent predictors of CHD and CVD events and total mortality among men. These findings provide further support to the important role of inflammation in the pathogenesis of CVD.
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PMID:C-reactive protein, interleukin-6 and tumor necrosis factor alpha as predictors of incident coronary and cardiovascular events and total mortality. A population-based, prospective study. 1652 64

Numerous prospective studies support the concept of postprandial glycaemia (PPG) as a risk factor for cardiovascular diseases (CVDs) in individuals with impaired glucose tolerance (IGT). A meta-analysis has demonstrated an exponential relationship between 2-hour postchallenge glucose levels and the incidence of CVD. This relationship is stronger than those observed with fasting glycaemia or glycosylated haemoglobin (HbA(1c)), and persists after adjustment for other vascular risk factors. Although there are fewer data available for the diabetic population, those that are available also support PPG as a risk factor for CVD. Treating PPG with acarbose is associated with a reduction in cardiovascular events in both patients with IGT and diabetes mellitus. Acarbose also reduces the progression of intima-media thickness (IMT), which is a surrogate endpoint for atherosclerosis. It has been suggested that the beneficial effect could be related to an improvement in postprandial hyperglycaemia and associated atherogenic factors - oxidative stress, endothelial dysfunction and pro-coagulation factors - and to an improvement in other cardiovascular risk factors such as systolic blood pressure (by decreasing water and salt absorption), postprandial hypertriglyceridaemia and insulin resistance. Treating PPG with glinides improves IMT as well as interleukin-6 and C-reactive protein levels, while treating PPG with rapid-acting insulin analogues is also associated with improvements in endothelial dysfunction. The Kumamoto study suggests that reduced PPG is strongly associated with reductions in retinopathy and nephropathy. Finally, decreasing PPG in patients with IGT reduces the progression of diabetes. In conclusion, physicians should increase efforts to control PPG in order to further improve HbA(1c), and should also ensure close control of postprandial hyperglycaemic peaks so as to optimise patients' chances of avoiding cardiovascular complications. As for the prevention of CVD, further prospective intervention trials, powered to answer this question, are still required.
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PMID:Should postprandial hyperglycaemia in prediabetic and type 2 diabetic patients be treated? 1652 17

The mortality rate among patients with chronic kidney disease is much higher than among those without. As glomerular filtration rate declines and patients approach end-stage renal disease, the mortality rate increases and patients at this stage are more likely to die than receive renal replacement therapy. The higher mortality and its underlying causes among chronic kidney disease patients is a serious issue. Lack of physician awareness of chronic kidney disease and its association with excess mortality remains a problem. In this review of current literature, we aim to increase this awareness among health care professionals and the general public and to call for action to improve survival in chronic kidney disease patients. The data strongly suggest that advancing kidney dysfunction leads to increased mortality risk. Contributing to the mortality associated with chronic kidney disease are the comorbidities that accompany this disease state. For instance, patients with chronic kidney disease and comorbidities are at 1.3 to 3.6 times more risk than patients without chronic kidney disease. Further, cardiovascular disease is the leading cause of death among chronic kidney disease patients. It appears that both traditional (such as diabetes mellitus, hypertension, and smoking) and nontraditional risk factors (C-reactive protein and interleukin-6 levels) present in the chronic kidney disease population promote the frequent development of cardiovascular disease. Therefore, therapies targeting both progression of chronic kidney disease and comorbidities such as cardiovascular disease are required to reduce mortality among these patients.
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PMID:Increased mortality in chronic kidney disease: a call to action. 1653 76

The lack of social integration has predicted coronary heart disease morbidity and mortality in prospective observational studies; however, the biologic mechanisms by which this may occur are not well understood. The objective of this study was to determine whether social integration is associated with inflammatory risk factors for coronary heart disease, specifically C-reactive protein (CRP) and interleukin-6. The study participants (aged 70 to 79 years; 380 men and 425 women) were from the MacArthur Successful Aging Study, a longitudinal study of 3 community-based cohorts in the United States of older adults with relatively high physical and cognitive functioning at baseline (1988 to 1989). The plasma concentrations of interleukin-6 and CRP were assessed using a high-sensitivity enzyme-linked immunosorbent assay. Cross-sectional logistic regression analyses were performed. Multivariate adjusted analyses indicated that social integration was significantly inversely associated with CRP concentration in men after adjusting for age, race/ethnicity, smoking, alcohol consumption, physical activity, body mass index, cardiovascular disease, other major or chronic conditions, physical functioning, socioeconomic status, and depression (odds ratio 2.23, 95% confidence interval 1.05 to 4.76, for elevated CRP [>3.19 mg/L] in the least socially integrated quartile vs the most socially integrated quartile). No significant associations were found between social integration and interleukin-6 in men or either inflammatory marker in women. In conclusion, social integration was negatively associated with the plasma CRP concentration in men. These findings suggest a potential biologic mechanism for the observed associations between social integration and coronary heart disease in prospective studies. Differences may exist between women and men in the biologic pathways associated with social integration.
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PMID:Relation of social integration to inflammatory marker concentrations in men and women 70 to 79 years. 1656 7

Adrenomedullin (AM) is a vasodilator peptide that originally isolated from pheochromocytoma tissue. However, the mRNA is expressed in the normal adrenal gland, heart, kidney and blood vessels. The human AM gene is located in the short arm of chromosome 11 and is composed of 4 exons. There are 2 single nucleotide polymorphisms in introns 1 and 3, and the 3'-end of the AM gene is flanked by a microsatellite marker of cytosine-adenine repeats that is associated with an increased risk of developing hypertension and diabetic nephropathy. AM gene expression is promoted by various stimuli, including inflammation, hypoxia, oxidative stress, mechanical stress and activation of the renin-angiotensin and sympathetic nervous systems. The AM gene promoter region possessed binding site for several transcription factors, including nuclear factor for interleukin-6 expression (NF-IL6) and activator protein 2 (AP-2). Further, plasma AM levels are increased in patients with various cardiovascular diseases, including hypertension, heart failure and renal failure. These findings suggest that AM plays a role in the development of or response to cardiovascular disease. Indeed, experimental and clinical studies have demonstrated that systemic infusion of AM may have a therapeutic effect on myocardial infarction, heart failure and renal failure. Further, vasopeptidase inhibitors which augment the bioactivity of endogenous AM may benefit patients with hypertension and arteriosclerosis. Finally, the angiogenic and cytoprotective properties of AM may have utility in revascularization and infarcted myocardium and ischemic limbs. Because of the potential clinical benefits of AM, indications for use and optimal dosing strategies should be established.
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PMID:Pathophysiologic and therapeutic implications of adrenomedullin in cardiovascular disorders. 1661 59

An inflammatory cause of atrial fibrillation (AF) has been proposed on the basis of the presence of lymphocytic infiltrates in the biopsy results of patients with lone AF, alterations of C-reactive protein (CRP) and interleukin-6 levels in subjects with AF, and the time course of postoperative AF. Many previous studies exploring inflammatory factors in AF have been confounded by concomitant medical illnesses. Subjects with lone AF provide a unique opportunity to eliminate the effects of associated conditions. We therefore sought to determine CRP levels in homogenous cohorts of patients with lone AF or AF and hypertension. One hundred twenty-one subjects with lone AF, 52 subjects with AF and hypertension, and 75 control subjects were enrolled and studied. Plasma CRP levels were determined using a commercially available immunoassay. There was no significant difference in CRP levels between subjects with lone AF and controls (1.34 vs 1.21 mg/L, p = 0.18). CRP levels in subjects with AF and hypertension were elevated compared with those of controls and those of subjects with lone AF, although this difference was attributable to increased body mass indexes. CRP levels were not elevated in subjects with lone AF compared with controls. In conclusion, these findings clarify previous observations of elevations in CRP levels in subjects with AF and suggest that this marker of systemic inflammation is associated not with the arrhythmia per se, but rather with underlying cardiovascular disease.
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PMID:C-Reactive protein in lone atrial fibrillation. 1699 92

The importance of inflammation in atherosclerosis is well established in cardiovascular disease. However, limited data exist on the relationship between vascular inflammation and the severity of peripheral arterial occlusive disease (PAD). We investigated the relationship between biochemical markers of vascular inflammation and the diagnostic measures of PAD: ankle-brachial pressure index (ABI), maximum treadmill walking distance and angiographic score. In 127 patients (mean age 66 years; 64% males) with angiographically verified PAD, fasting blood samples were drawn for determination of selected soluble cell adhesion molecules, cytokines and chemokines. Tumor necrosis factor-alpha (TNFalpha), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1) and CD40 ligand (CD40L) were all significantly correlated with the angiographic score (p < 0.05 for all). After adjustment for relevant co-variates, MCP-1 and CD40L remained statistically significant (p < 0.01 for both). IL-6 was, independent of other risk factors, inversely correlated with the maximum treadmill walking distance (p < 0.01). Our cross-sectional study in PAD patients showed that the vascular inflammatory markers MCP-1, CD40L and IL-6 were significantly associated with the extent of atherosclerosis, assessed by angiographic score and maximum treadmill walking distance. These findings indicate that vascular inflammation is implicated in PAD, which might be of importance in future diagnosis and treatment of the disease.
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PMID:Markers of vascular inflammation are associated with the extent of atherosclerosis assessed as angiographic score and treadmill walking distances in patients with peripheral arterial occlusive disease. 1666 9

Investigators have suggested that inflammation may play a role in the pathogenesis of valve calcium. Participants in the Framingham Heart Study's offspring cohort had systemic levels of C-reactive protein, intercellular adhesion molecule-1, interleukin-6, and monocyte chemoattractant protein-1 measured at examination cycle 7. Mitral annular calcium, aortic annular calcium, aortic sclerosis, and aortic stenosis were assessed by echocardiography at examination cycle 6. Logistic regression was used to examine the odds of valvular calcium per 1 unit increase in inflammation (ISUM), a summary statistic of all normalized deviates of the individual markers. Two thousand six hundred eighty-three participants (mean age 61 +/- 10 years; 52% women) were analyzed: 8.2% (n = 216) had > or = 1 calcified valve or annulus; 89 had mitral annular calcium, 78 had aortic annular calcium, 135 had aortic sclerosis, and 33 had aortic stenosis. Participants with valvular calcium were older and were more likely to have hypertension and diabetes mellitus. Participants with valve calcium had higher median levels of all markers. For each log unit increase in ISUM, after adjustment for age and gender, there was an associated 1.1-fold increased odds of > or = 1 calcified valve (p = 0.02); the odds ratios were no longer significant after adjustment for cardiovascular disease risk factors (odds ratio 1.0, 95% confidence interval 0.9 to 1.1). Similar results were obtained for the individual markers and the odds of > or = 1 calcified valve. In conclusion, inflammatory markers were elevated in patients with valvular calcium. Our findings suggest that much of the observed association between systemic inflammatory markers and valvular calcium may be due to shared risk factors.
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PMID:Relations of inflammation and novel risk factors to valvular calcification. 1667 93

Soy isoflavones may impede atherogenic processes associated with cardiovascular disease. Research suggests that the postprandial generation of TG-rich remnants contributes to the development of atherosclerosis. The purpose of the current study was to determine if 39 g soy (85 mg aglycone isoflavones, treatment) compared with 40 g milk protein (0 mg aglycone isoflavones, control) in combination with a high-fat meal can modify postprandial, atherogenic-associated events and biomarkers for oxidative stress, inflammation, and thrombosis. Fifteen healthy men (20-47 yr) participated in a double-blind cross-over meal-challenge study occurring on two nonconsecutive days. The study meals consisted of two high-fat apple muffins consumed with either a soy or milk shake (229 mL, 41% fat, 41% carbohydrate, and 18% protein). Blood samples were obtained at baseline (fasted) and hours two, four, and six postprandial. Plasma TG significantly increased in both treatment and control meal challenges compared with baseline. There were no significant differences (P > 0.05) between treatment (soy) and control (milk) for ex vivo copper-induced LDL oxidation, serum C-reactive protein, serum interleukin-6 (IL-6), serum fibrinogen, or plasma lipids (total cholesterol, HDL, LDL, TG). IL-6-concentrations significantly decreased as a function of time during either meal challenge (P = 0.005). These data suggest that consumption of soy or milk protein in conjunction with a high-fat meal does not acutely modify postprandial oxidative stress, inflammation, or plasma lipid concentrations in young, healthy men.
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PMID:Effects of soy or milk protein during a high-fat feeding challenge on oxidative stress, inflammation, and lipids in healthy men. 1671

Epidemiological and experimental studies have indicated a relationship among aging, dietary Mg, inflammatory stress, and cardiovascular disease. Our aim in the present study was to investigate possible links between dietary Mg, oxidant stress parameters, and inflammatory status with aging in rats. We designed a long-term study in which rats were fed for 22 months with moderately deficient (150 mg/kg), standard (800 mg/kg), or supplemented (3200 mg/kg) Mg diets. Comparisons were made with young rats fed with the same diets for 1 month. Compared to the standard and supplemented diets, the Mg-deficient diet significantly increased blood pressure, plasma interleukin-6, fibrinogen, and erythrocyte lysophosphatidylcholine, particularly in aging rats, it decreased plasma albumin. The impairment of redox status was indicated by increases in plasma thiobarbituric acid reactive substances and oxysterols and an increased blood susceptibility to in vitro free-radical-induced hemolysis. We concluded that Mg deficiency induced a chronic impairment of redox status associated with inflammation which could significantly contribute to increased oxidized lipids and promote hypertension and vascular disorders with aging. Extrapolating to the human situation and given that Mg deficiency has been reported to be surprisingly common, particularly in the elderly, Mg supplementation might be useful as an adjuvant therapy in preventing cardiovascular disease.
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PMID:Long-term moderate magnesium-deficient diet shows relationships between blood pressure, inflammation and oxidant stress defense in aging rats. 1681 8


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