The association of leukocyte count, fibrinogen and c-reactive protein with vascular risk factors and ischemic vascular diseases

Grau, Armin J.; Buggle, Florian; Becher, Heiko; Werle, E; Hacke, Werner

doi:10.1016/0049-3848(96)00071-0

Cited by 109 publications

(67 citation statements)

References 34 publications

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“…Nevertheless, we have shown a close relation between OS and the metabolic control of The second important outcome of this study is the PMN contribution to chronic inflammation in diabetes. The existence of chronic inflammation in diabetes is mainly based on the increased plasma concentrations of C-reactive protein, fibrinogen, interleukin-6, interleukin-1, and tumor necrosis factor (44,45). Our in vivo data of increased diabetic PMN counts, combined with the decreased in vitro PMN survival rate, is evidence that primed PMNs contribute to chronic inflammation in diabetes.…”

Section: Shurtz-swirski and Associatesmentioning

confidence: 58%

Involvement of Peripheral Polymorphonuclear Leukocytes in Oxidative Stress and Inflammation in Type 2 Diabetic Patients

et al. 2001

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OBJECTIVE -To determine the extent to which peripheral polymorphonuclear leukocytes (PMNs) contributed to oxidative stress (OS) and inflammation in type 2 diabetic patients.RESEARCH DESIGN AND METHODS -PMNs and plasma were separated from blood withdrawn from 18 type 2 diabetic patients and 16 age-and sex-matched normal control subjects. The rate of superoxide release from phorbol 12-myristate 13-acetate (PMA)-stimulated PMNs and the plasma glutathione (GSH) levels served as measures of OS. Inflammation was assessed by PMN recruitment, expressed by peripheral blood PMN counts, and the in vitro survival of PMNs, which reflects cell necrosis.RESULTS -PMA-stimulated PMNs from diabetes released superoxide significantly faster, and plasma-reduced GSH was lower in diabetic patients than in normal control subjects. The rate of superoxide release from diabetic PMNs showed no correlation with the plasma glucose concentrations, whereas a positive linear correlation with HbA 1c was found. The in vitro survival of diabetic PMNs was lower than normal control PMNs when each was incubated in its own serum. The in vitro survival of normal control PMNs was reduced when incubated with diabetic serum, whereas normal control sera promoted the survival of diabetic PMNs. Peripheral PMN counts were higher in diabetic patients than in normal control patients.CONCLUSIONS -Type 2 diabetes is accompanied by a priming of PMNs, resulting in OS and increased self-necrosis. Necrosis starts a chain of inflammatory reactions that result in cell recruitment and in the long run, with OS, may result in endothelial dysfunction. Understanding the contribution of PMNs to OS and inflammation in diabetes may illuminate new mechanisms through which endothelial dysfunction evolves and causes angiopathy and atherosclerosis.

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Section: Shurtz-swirski and Associatesmentioning

confidence: 58%

Involvement of Peripheral Polymorphonuclear Leukocytes in Oxidative Stress and Inflammation in Type 2 Diabetic Patients

et al. 2001

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“…Indeed, CRP appeared to predict risk independently of LDL and HDL cholesterol (13,15) and to provide predictive power beyond that derived from using Framingham risk scores (14). CRP levels are also increased in conditions that are associated with increased cardiovascular risk, including obesity (16)(17)(18)(19)(20), insulin resistance (17,18), hypertension (21,22) , the metabolic syndrome (16,(23)(24)(25), type 2 diabetes (16,17,26), hypertriglyceridemia (24,27,28), a low level of HDL cholesterol (17,24,28), and smoking (28,29). CRP levels are also increased in other chronic inflammatory conditions, such as periodontal disease (30,31) and rheumatoid arthritis (32), which are more weakly associated with increased risk for cardiovascular disease.…”

Section: Crpmentioning

confidence: 99%

Thematic review series: The Immune System and Atherogenesis. Lipoprotein-associated inflammatory proteins: markers or mediators of cardiovascular disease?

Chait

Oram

Heinecke

2005

Journal of Lipid Research

209

159

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In humans, a chronically increased circulating level of C-reactive protein (CRP), a positive acute-phase reactant, is an independent risk factor for cardiovascular disease. This observation has led to considerable interest in the role of inflammatory proteins in atherosclerosis. In this review, after discussing CRP, we focus on the potential role in the pathogenesis of human vascular disease of inflammation-induced proteins that are carried by lipoproteins. Serum amyloid A (SAA) is transported predominantly on HDL, and levels of this protein increase markedly during acute and chronic inflammation in both animals and humans. Increased SAA levels predict the risk of cardiovascular disease in humans. Recent animal studies support the proposal that SAA plays a role in atherogenesis. Evidence is accruing that secretory phospholipase A 2 , an HDL-associated protein, and platelet-activating factor acetylhydrolase, a protein associated predominantly with LDL in humans and HDL in mice, might also play roles both as markers and mediators of human atherosclerosis. In contrast to positive acute-phase proteins, which increase in abundance during inflammation, negative acutephase proteins have received less attention. Apolipoprotein A-I (apoA-I), the major apolipoprotein of HDL, decreases during inflammation. Recent studies also indicate that HDL is oxidized by myeloperoxidase in patients with established atherosclerosis. These alterations may limit the ability of apoA-I to participate in reverse cholesterol transport. Paraoxonase-1 (PON1), another HDL-associated protein, also decreases during inflammation. PON1 is atheroprotective in animal models of hypercholesterolemia. Controversy over its utility as a marker of human atherosclerosis may reflect the fact that enzyme activity rather than blood level (or genotype) is the major determinant of cardiovascular risk. Thus, multiple lipoprotein-associated proteins that change in concentration during acute and chronic inflammation may serve as markers of cardiovascular disease. In future studies, it will be important to determine whether these proteins play a causal role in atherogenesis.

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“…18 -21 This association has been interpreted as confirmation of the role of inflammation in the pathogenesis of coronary heart disease, but any contribution of C-reactive protein to the pathogenesis of stroke has received little attention. 6,9,20 We used data from the Third National Health and Nutrition Examination Survey (NHANES III) 22 to examine the possible association between C-reactive protein and cerebrovascular disease.…”

mentioning

confidence: 99%

Serum C-Reactive Protein and Self-Reported Stroke

Ford

Giles

2000

ATVB

142

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Abstract-C-reactive protein may predict the risk of coronary heart disease, but its association with stroke has not been well studied. We used data from the Third National Health and Nutrition Examination Survey, conducted from 1988 to 1994, to examine the association between serum C-reactive protein concentrations and self-reported past history of stroke among 8850 US men and women aged Ն40 years. The unadjusted geometric mean of C-reactive protein concentration was higher among participants with stroke than those without stroke (0.

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The association of leukocyte count, fibrinogen and c-reactive protein with vascular risk factors and ischemic vascular diseases

Cited by 109 publications

References 34 publications

Involvement of Peripheral Polymorphonuclear Leukocytes in Oxidative Stress and Inflammation in Type 2 Diabetic Patients

Involvement of Peripheral Polymorphonuclear Leukocytes in Oxidative Stress and Inflammation in Type 2 Diabetic Patients

Thematic review series: The Immune System and Atherogenesis. Lipoprotein-associated inflammatory proteins: markers or mediators of cardiovascular disease?

Serum C-Reactive Protein and Self-Reported Stroke

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