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)

Serum levels of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) have been shown to be predictors of adverse outcomes in patients with coronary artery disease (CAD). We hypothesized that measurement of inflammatory markers could predict atherosclerotic burden and major adverse cardiac events (MACEs). We prospectively measured hs-CRP, IL-6, and TNF-alpha in 249 patients who were admitted with acute chest pain and underwent coronary angiography. We analyzed the relation between serum levels of inflammatory markers and angiographic severity of CAD. A follow-up at 6 months was conducted to assess MACEs, defined as a cumulative of myocardial infarction, all-cause death, or coronary revascularization (percutaneous coronary intervention or coronary artery bypass surgery). After adjusting for conventional CAD risk factors (age, gender, diabetes, hypertension, smoking, and hypercholesterolemia), there was no association between inflammatory markers (hs-CRP, IL-6, and TNF-alpha) and angiographic severity of CAD. There was a significant positive correlation between age, male gender, diabetes mellitus, and hypercholesterolemia with atherosclerotic burden determined by angiography. There was no significant positive association between MACEs and hs-CRP, IL-6, or TNF-alpha level in unadjusted and adjusted models. In conclusion, in patients hospitalized with chest pain, we found no association of serum levels of hs-CRP, IL-6, or TNF-alpha with coronary atherosclerotic burden or MACEs at 6 months after adjustment for traditional CAD risk factors.
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PMID:Inflammatory markers, angiographic severity of coronary artery disease, and patient outcome. 1739 76

The aim of the study was to investigate, whether the degree of metabolic risk factors for atherosclerotic complications in a very rare kind of obesity, the Multiple Symmetrical Lipomatosis, also known as the Launois-Bensaude Syndrome (LBS), are comparable or different from "simple" truncal obesity. 10 patients with LBS (Body mass index 34.4 +/- 1.8 kg/m(2), age: 62 +/- 3 yrs) were compared with 19 BMI - matched patients with "simple" truncal obesity and obstructive sleep apnoea syndrome (OSAS) and 20 BMI- matched patients with "simple" truncal obesity without OSAS. Markers of subclinical inflammation and thrombocyte activation (sCD62p = soluble p-selectin, highly sensitive C-Reactive protein = CRP, Interleukin-6 = IL-6, ICAM-1 = Intracellular Adhesion Molecule-1, Vascular Cell Adhesion Molecule = VCAM -1, leptin), as well as adiponectin and resistin were studied. The prevalence of atherogenic risk factors as hypertension (80%), type 2 diabetes (30%), OSAS (50%), smoking (30%) and alcohol abuse (80%) was high in the (obese) LBS group. The markers of subclinical inflammation and thrombocyte activation showed an indifferent picture with lower levels of circulating IL-6 and sCD62p, comparable CRP and higher ICAM-1 and VCAM-1 than in controls. Leptin and adiponectin were higher than in controls. However, the accumulation of "classic" cardiovascular risk factors in the LBS group was well reflected by the presence of symptomatic cardiovascular disease in 3 of the 10 LBS patients, putting LBS patients - if obese - at an atherosclerotic risk at least comparable to obese persons.
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PMID:Adiponectin, resistin and subclinical inflammation--the metabolic burden in Launois Bensaude Syndrome, a rare form of obesity. 1744 28

It has been suggested that Type 2 diabetes may, in part, be precipitated or accelerated by an acute-phase reaction as part of the innate immune response, in which large amounts of cytokines are released from adipose tissue, creating a low-grade inflammatory milieu. There is also firm evidence that atherosclerosis is an immune-mediated inflammatory disease. Therefore it is reasonable to imply that low-grade inflammation is an important pathogenetic factor in atherosclerosis and cardiovascular events in patients with Type 2 diabetes. Over the last few years, there have been a lot of promising clinical markers proposed to link inflammation and atherosclerosis. Of these markers, hs-CRP (high-sensitivity C-reactive protein) might be a prognostic marker for further cardiovascular events, although this has been refuted recently. In this issue of Clinical Science, Castoldi and co-workers have demonstrated that, in patients with Type 2 diabetes categorized into low (<1.0 mg/l), medium (1.0-3.0 mg/l) and high (>3.0 mg/l) hs-CRP groups, serum levels of hs-CRP correlated with lipopolysaccharide-stimulated release of interleukin-1beta and interleukin-6 in whole blood. This finding may indicate that low-grade inflammatory activity might influence cytokine production in these patients.
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PMID:C-reactive protein: a marker or a player? 1736 4

Inflammatory markers, their relation to maintenance of sinus rhythm after electrical cardioversion for atrial fibrillation (AF), and the effect of candesartan were investigated in a double-blind placebo-controlled study (CAPRAF). One hundred seventy-one patients with persistent AF were randomly assigned to receive candesartan 8 mg/day or placebo for 3 to 6 weeks before and candesartan 16 mg/day or placebo for 6 months after electrical cardioversion. Serum levels of high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-alpha, interleukin-6, P-selectin, E-selectin, CD-40 ligand, and vascular cell adhesion molecule-1 were measured at baseline and end of study. Compared with patients with a relapse of AF, patients still in sinus rhythm at 6 months after cardioversion (n = 40) had lower baseline hs-CRP and E-selectin levels: median 2.36 mg/L (25th, 75th percentiles 1.28, 4.09) versus 3.44 mg/L (25th, 75th percentiles 1.66, 6.05, p = 0.031) and 32 ng/ml (25th, 75th percentiles 23, 42) versus 37 ng/ml (25th, 75th percentiles 28, 51, p = 0.042), respectively. Neither sustained sinus rhythm for 6 months nor treatment with candesartan had an impact on measured concentrations of markers of inflammation. In conclusion, low hs-CRP and E-selectin at baseline were associated with maintenance of sinus rhythm after electrical cardioversion.
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PMID:Effect of candesartan and various inflammatory markers on maintenance of sinus rhythm after electrical cardioversion for atrial fibrillation. 1753 93

We investigated the determinants of endothelial function in 100 asymptomatic, non-diabetic, non-smokers with and without the metabolic syndrome ((MS)--defined by ATP-III criteria). Subjects with MS (n=24) had greater endothelial dysfunction (ED, P<0.001) than subjects without MS. One-way analysis of variance demonstrated a significant negative linear trend between level of ED (F=21.89; P<0.001) and number of ATP-III metabolic diagnostic criteria present in each subject. In a stepwise multivariate logistic regression model presence/absence of MS was the only independent determinant of ED (P=0.01). Age, gender, LDL cholesterol, C-reactive protein, interleukin-6 and tumour necrosis factor-alpha receptor 2 had no independent influence on endothelial function. In the absence of MS as variable there was no independent association between the remaining variables and endothelial function. Receiver operating characteristic (ROC) curves demonstrated that a combination of age, LDL cholesterol and CRP levels and presence/absence of MS can be used to predict ED (area under curve 0.81+/-0.06) and thus potentially may be used as a simple screening test to identify subjects with the greatest level of ED (sensitivity=0.82, specificity=0.72). Our study demonstrated that subjects with MS had greater ED. The extent of ED increased with presence of each additional ATP-III diagnostic criteria. Presence/absence of MS was the only independent predictor of ED and in conjunction with age, LDL cholesterol and CRP levels could be used as a potential simple clinical screening test for ED.
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PMID:Determinants of endothelial function in asymptomatic subjects with and without the metabolic syndrome. 1765 41

A best evidence topic in cardiac surgery was written according to a structured protocol. The question addressed was whether prophylactic administration of steroids is of benefit to children undergoing cardiac surgery? Altogether 302 papers were found using the reported search, of which six represented the best evidence. The author, journal, date and country of publication, patient group studied, study type, relevant outcomes, results, and study weaknesses were tabulated. We conclude that steroids may reduce Troponin I release, CRP and reduce Interleukin-6. In addition, two studies, each in only 30 patients, found some evidence for improvements in clinical parameters such as ICU stay and fluid requirement. These findings need confirmation prior to any firm recommendations as to the clinical benefits of steroids.
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PMID:Is prophylactic administration of steroids of benefit to children undergoing cardiac surgery? 1767 Feb 96

We investigated whether smoking would interact with the interleukin-6 (IL-6) polymorphisms (-174G>C and -572C>G, -597G>A and -1363G>T) in determining circulating levels of inflammatory markers and its consequence to oxidative stress. The G/G genotype (n=26) of the -572C>G in nonsmokers (n=376) was associated with higher IL-6 (P=0.028), fibrinogen (P=0.007) and ox-LDL (P=0.006) than those with C/C (n=209) or C/G (n=141). Results were similar for nonsmokers and smokers (n=268), but in smokers, the -572G/G genotype was associated with a greater difference in levels of IL-6 (P=0.031), fibrinogen (P=0.001), ox-LDL (P=0.037) and PGF(2alpha) (P=0.050). IL-6 had positive relations with CRP, fibrinogen, ox-LDL and PGF(2alpha). There was no evidence of an effect of -572C>G genotype on CRP levels in nonsmokers, however, this polymorphism was associated with a highly significant effect on CRP in smokers (P<0.001) (genotype-smoking interaction P=0.04, adjusted for age, BMI and IL-6). The C allele frequency at the -174 promoter region of IL-6 was very rare (<0.01) and -597G>A and -1363G>T were monomorphic in this study. Our results suggest that IL-6 -572C>G has a greater response over time to the inflammatory effects of smoking and this may result in smokers having higher oxidative stress in subjects with G/G compared to C/C or C/G.
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PMID:Influence of the IL-6 -572C>G polymorphism on inflammatory markers according to cigarette smoking in Korean healthy men. 1768 74

The aim of the study was to analyze the relation between early diabetic retinopathy and the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), vascular endothelial growth factor (VEGF) in children with diabetes mellitus type 1. Two hundred and two children with diabetes mellitus type 1 aged 13.2+/-3.83 years and 85 healthy controls were analyzed. Patients were divided into two subgroups: children with retinopathy (Group 1, n=39) and children without retinopathy (Group 2, n=163). All the children had 24h urine albumin secretion rate, glycosylated hemoglobin HbA1c level, and C-reactive protein level measured, underwent 24h blood pressure monitoring and had ophthalmologic examination performed. Additionally, all the children had serum TNF-alpha, IL-6 and VEGF level measured using an ELISA test (Quantikine High Sensitivity Human). Statistically significant higher blood serum levels of HbA1c, VEGF, TNF-alpha and IL-6 were found in the Group 1 in comparison with the Group 2. Additionally, the children of the Group 1 showed statistically significant correlation between serum VEGF and serum TNF-alpha (R=0.35, p=0.000), CRP level (R=0.23, p=0.006), 24h albumin urine secretion rate (R=0.45, p=0.000) and duration of the disease (R=0.26, p=0.002). The results of the current study suggest that there is a relationship between VEGF, TNF-alpha, IL-6 and the development of the diabetic retinopathy in children with diabetes mellitus type 1.
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PMID:The role of vascular endothelial growth factor, tumor necrosis factor alpha and interleukin-6 in pathogenesis of diabetic retinopathy. 1771 75

LDL apheresis is an extracorporal modality to lower the concentration of atherogenic lipoproteins, e.g., LDL cholesterol. We compared two recently introduced whole-blood LDL apheresis systems inpatients with hypercholesterolemia in a randomized cross-over trial with respect to their effects on lipoproteins as well as on other cardiovascular risk markers. Six patients (4 women, 2 men, median age 62.5 years, median BMI 25.9 kg/m(2)) on regular LDL apheresis were randomly assigned to receive six weekly treatments with either DALI (Fresenius) or Liposorber D (Kaneka). After 6 weeks, the patients were switched to the other device (again six weekly treatments). Blood was drawn before and immediately after LDL apheresis at three time points (last regular apheresis before the study; after six treatments with DALI and after six treatments with Liposorber D). LDL cholesterol concentration before the sixth apheresis (DALI 129 mg/dL, Liposorber D 132 mg/dL) as well as LDL cholesterol reduction during the sixth apheresis (DALI 68.3% and Liposorber D 68.4%) were similar with the two systems. CRP and fibrinogen concentrations were lower but interleukin-6, myeloperoxidase, and resistin concentrations were higher after the last Liposorber treatment compared with DALI (P < 0.05, respectively). No differences were observed concerning adiponectin, ghrelin, and PYY levels. In conclusion, both devices were highly effective in eliminating atherogenic lipoproteins. CRP and fibrinogen were better eliminated with Liposorber D. However, following Liposorber D, interleukin-6 levels were higher than after DALI possibly indicating an increased inflammatory activation.
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PMID:Effects of two whole blood systems (DALI and Liposorber D) for LDL apheresis on lipids and cardiovascular risk markers in severe hypercholesterolemia. 1793 45

The link between cancer and inflammation in an organ or tissue has firmly been established on the basis that cancer tends to occur at sites of chronic inflammation and that local inflammatory processes can accelerate the growth of preexisting tumors in both animals and human beings. In contrast, the relationship between cancer and systemic inflammation has been less studied. In this work, we demonstrated that the growth of the murine fibrosarcoma MC-C, was accompanied by manifestations of systemic inflammation, as demonstrated by an increase in both the number of circulating polymorphonuclear neutrophils (PMN) and the serum concentration of the proinflammatory cytokines interleukin-1beta (IL-1beta), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) and the acute phase proteins C reactive (CRP) and serum A amyloid (SAA). Two temporally separate peaks of systemic inflammation were detected during tumor development. The first was displayed during the first week after tumor inoculation. The second peak began around day 14 and its intensity was proportional to tumor size. In mice bearing a large MC-C tumor, a high number of circulating PMN and myeloid precursors were evident. Most of these cells exhibited activation evidenced by an increased reactive oxygen species generation and high expression of the Gr1+/Mac1+ markers. Inoculation of thioglycolate -which generates a transient systemic inflammation-accelerated the growth of MC-C tumor and reciprocally, inhibition of such systemic inflammation by using indomethacin, prevented that enhancing effect. This suggests that the systemic inflammation that the tumor generates on its own, could be part of its growth strategy.
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PMID:[Systemic inflammation and experimental cancer in a murine model]. 1805 Dec 31


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