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)

Polymorphisms at the beta-fibrinogen locus have been shown to be associated with plasma concentration of fibrinogen and coronary heart disease. The effect of the genetic heterogeneity of fibrinogen on carotid atherosclerosis has not been determined so far. We examined the influence of the C148 --> T polymorphism on carotid disease in a large cohort of middle-aged to elderly subjects without evidence of neuropsychiatric disease. This polymorphism is located close to the consensus sequence of the interleukin-6 element and may represent a functional sequence variant. The genotype of 399 randomly selected, neurologically asymptomatic individuals, aged 45 to 75 years, was determined by denaturing gradient gel electrophoresis. Carotid atherosclerosis was assessed by color-coded duplex scanning and was graded on a five-point scale ranging from 0 (=normal) to 5 (=complete luminal obstruction). The C/C, C/T, and T/T genotypes were noted in 226 (56.6%), 148 (37.1 %), and 25 (6.3%) individuals, respectively. The T/T genotype group demonstrated higher grades of carotid atherosclerosis than did the C/C and C/T genotypes (P=.003). Logistic regression analysis created a model of independent predictors of carotid atherosclerosis that included apolipoprotein B (odds ratio [OR], 1.17/10 mg/dL), age (OR, 2.46/10 years), lifetime tobacco consumption (OR, 1.03/1000 g), presence of the beta-fibrinogen promoter T/T genotype (OR, 6.17), plasma fibrinogen concentration (OR, 1.05/10 mg/dL), and cardiac disease (OR, 1.80). These data suggest that the beta-fibrinogen promoter T/T148 genotype represents a genetic risk factor for carotid atherosclerosis in the middle-aged to elderly.
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PMID:Beta-fibrinogen gene polymorphism (C148-->T) is associated with carotid atherosclerosis: results of the Austrian Stroke Prevention Study. 951 19

Stroke is the second cause of mortality in industrialized countries. Atherosclerotic plaque rupture with atheromatous debris distal embolization is the pathogenetic mechanism responsible for cerebrovascular events due to atherosclerotic carotid disease. Plaque composition rather than lesion burden seems to be the determinant factor producing rupture and subsequent thrombosis. Histologic features of vulnerability are : a large lipid core, a thin fibrous cap, and an inflammatory infiltrate rich of monocytes and macrophages. In the clinical practice, it is difficult to predict the risk of experiencing a major cerebrovascular events especially in asymptomatic patients. New invasive techniques such as intravascular ultrasound with termography, optical coherence tomography, fotons spectroscopy and elastography have been developed to detect atherosclerotic lesion tissue composition. However, such techniques are difficult to apply on a large scale basis in primary prevention. On the contrary, new serologic biomarkers such as Pregnancy Associated Plasma Protein-A, Lp-PLA2, Interleukin-6, Interleukin-12, metalloproteinases, lipoprotein-(a), and plaque oxidative products have been recently proposed for screening general and high risk population. The present paper will briefly review the current histologic characteristics of vulnerable plaque and the new imaging tools proposed for its detection, focusing on the most recent serologic biomarkers evaluated in the clinical practice to increase our accuracy in predicting not only the plaque but moreover the patient at risk for an acute cerebrovascular event.
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PMID:From carotid plaque biology to serologic markers of vulnerability to predict the risk of cerebrovascular events. 1751 60