Fibrinogen and Cardiovascular Risk

Ernst, E; Resch, K. L.

doi:10.7326/0003-4819-119-12-199312150-00016

Cited by 11 publications

(16 citation statements)

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“…Regarding other covariables, smoking status did not affect plasma fibrinogen (P ϭ 0.37) in our patients, contrary to previous studies in both the general pop- ulation and type 1 diabetic subjects (2,5,14,15). It is possible that this represents a type 2 error due to the limited number of current smokers in the EDIC study.…”

Section: The Study Group Consisted Of 405 Women (A) and 504 Men (B) Wcontrasting

confidence: 99%

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Fibrinogen Is a Marker for Nephropathy and Peripheral Vascular Disease in Type 1 Diabetes

Klein

Hunter²,

Jenkins³

et al. 2003

Diabetes Care

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-We examined whether plasma fibrinogen levels and the ␤-fibrinogen gene G Ϫ455 3 A polymorphism were related to microvascular or macrovascular disease in patients (n ϭ 909) with type 1 diabetes enrolled in the Diabetes Control and Complications Trial/ Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC). Univariate regression showed that fibrinogen levels were correlated with BMI (r ϭ 0.15; P Ͻ 0.0001), HbA 1c (r ϭ 0.11; P ϭ 0.0014), total cholesterol (r ϭ 0.17; P Ͻ 0.0001), and LDL cholesterol (r ϭ 0.16; P Ͻ 0.0001) in all patients. In men, but not women, waist-to-hip ratio (r ϭ 0.20; P Ͻ 0.0001) and triglycerides (r ϭ 0.13; P ϭ 0.0047) also became powerful predictors of fibrinogen level; in women, but not men, fibrinogen was correlated with both diastolic (r ϭ 0.16; P ϭ 0.0011) and systolic (r ϭ 0.11; P ϭ 0.0241) blood pressure. Fibrinogen was correlated with urinary albumin excretion rates in men (r ϭ 0.13; P ϭ 0.0033), but not in women. In both sexes, however, the development of proteinuria (albumin excretion Ͼ300 mg/24 h) was accompanied by 1.5-fold increment in plasma fibrinogen compared with patients with normal excretion or microalbuminuria. In addition, high fibrinogen levels were associated with a lower average ankle-brachial index in women (r ϭ Ϫ0.13; P ϭ 0.0075), but not men. Multiple regression analyses demonstrated that plasma fibrinogen was independently correlated with high albumin excretion rate in men, and with low average ankle-brachial index in women. Fibrinogen was not correlated with the severity of retinopathy. Carotid artery intima-medial thickness was not correlated with fibrinogen, and the G Ϫ455 3 A polymorphism in the 5Ј promoter region of the ␤-fibrinogen gene did not influence circulating fibrinogen levels. However, the presence of the more common G Ϫ455 allele was associated with greater intima-medial thickness in the internal carotid artery (ANCOVA P ϭ 0.045). Last, hyperfibrinogenemia in type 1 diabetes is associated with components of the insulin resistance syndrome trait cluster, and the association is influenced by sex.

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Section: The Study Group Consisted Of 405 Women (A) and 504 Men (B) Wcontrasting

confidence: 99%

“…In addition, hyperfibrinogenemia may be an indicator of inflammatory vascular changes and endothelial dysfunction (12). Alternatively, fibrinogen may be directly involved in atherosclerosis and thrombosis (13)(14)(15). Hyperfibrinogen levels lead to enhanced coagulant activity and are associated with increased blood viscosity.…”

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confidence: 99%

Fibrinogen Is a Marker for Nephropathy and Peripheral Vascular Disease in Type 1 Diabetes

Klein

Hunter²,

Jenkins³

et al. 2003

Diabetes Care

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“…Given the cross-sectional design of this study, it is impossible to sort out whether inflammation plays a pathogenetic role in the development of diabetic nephropathy or increased inflammatory markers represent a response to renal injury. Fibrinogen may be associated with GBM thickening not only via inflammatory mechanisms but also through endothelial damage, coagulant activity, and platelet activation (11)(12)(13)(14)(15). SAA is an acute-phase protein that has been investigated poorly in human physiology and pathology.…”

Section: Discussionmentioning

confidence: 99%

“…In type 2 diabetes, fibrinogen levels have been demonstrated to predict the progression to overt nephropathy (10). Hyperfibrinogenemia, an indicator of inflammation, is also associated with the presence of endothelial dysfunction, insulin resistance, hypercoagulability, and increased blood viscosity and is a marker of unstable atherosclerotic lesions (11)(12)(13)(14)(15). The aim of the present study was to explore the relationships between low-grade inflammation markers, glomerular structure, and renal function in patients with type 2 diabetes.…”

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confidence: 97%

Acute-Phase Markers of Inflammation and Glomerular Structure in Patients with Type 2 Diabetes

Vestra¹,

Mussap

Gallina³

et al. 2005

Journal of the American Society of Nephrology

245

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Type 2 diabetes is frequently associated with an inflammatory status; the relationships between low-grade inflammation and diabetic nephropathy are still unclear. The aim of this study was to evaluate the relationships between acute-phase markers of inflammation, glomerular structure, and albumin excretion rate (AER) in type 2 diabetes. In 74 patients with type 2 diabetes (23 normoalbuminuric, 30 microalbuminuric, and 21 proteinuric) fibrinogen, serum amyloid A protein (SAA), C-reactive protein (CRP), and IL-6 were determined. AER was measured on three 24-h urine collections; GFR was measured by 51 Cr EDTA plasma clearance. A kidney biopsy was performed, and mesangial fractional volume [Vv(mes/glom)] and glomerular basement membrane (GBM) width were estimated by electron microscopic morphometric analysis. CRP, fibrinogen, SAA, and IL-6 differed among groups, with proteinuric patients having the highest levels. SAA and fibrinogen correlated with AER (P < 0.03 and P < 0.001, respectively). GBM width and Vv(mes/glom) increased from normoalbuminuric to proteinuric patients [P < 0.005 normoalbuminuric and microalbuminuric versus proteinuric for GBM, P < 0.01 normoalbuminuric versus proteinuric for Vv(mes/glom)]. In patients with increased GBM width (>396 nm), CRP, SAA, and IL-6 were higher than in patients with normal GBM width (P < 0.003, P < 0.004, and P < 0.0004, respectively). GBM width was directly correlated with fibrinogen (r ‫؍‬ 0.33, P < 0.002) and IL-6 (r ‫؍‬ 0.25 P < 0.05). In conclusion, this study demonstrates that acute-phase markers of inflammation are associated with nephropathy status and GBM thickening, suggesting a role for inflammation in the pathogenesis of diabetic glomerulopathy. T ype 2 diabetes is frequently associated with an acutephase reaction, suggestive of a low-grade inflammatory status (1,2). In fact, markers of acute-phase response, including serum amyloid A (SAA), C-reactive protein (CRP), and IL-6, the main mediators of the response, have been shown to be elevated in patients with type 2 diabetes and with the metabolic syndrome (2). It is well known that in the general population, as well as in diabetes, these acute-phase markers are associated with increased cardiovascular risk, because chronic inflammation is one of the pathogenetic mechanisms of atherosclerosis (3). In contrast, the relationships between lowgrade inflammation and diabetic microangiopathy are still unclear. As far as nephropathy is concerned, several studies have examined the relationships with inflammation, leading to conflicting results (4 -11). Overall, however, most studies have reported an increase in acute-phase markers in patients with nephropathy and also in patients with microalbuminuria (5,7-9). The coexistence of an inflammatory condition with diabetic nephropathy could explain in part the tremendously increased cardiovascular risk among these patients.Also fibrinogen has been reported to be associated with both cardiovascular risk and nephropathy in type 1 and type 2 diabetes (10,11). The Diabetes Cont...

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“…[3][4][5] Because of this, several investigators have suggested that CRP might prove useful in clinical practice, 6,7 whereas others have favored fibrinogen. 8,9 Although there are important details to work out before either of these markers enters the clinical domain, this interest provides a clear and compelling imperative for understanding how inflammation integrates into both normal physiology and atherothrombotic pathophysiology.…”

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confidence: 99%

Is Visceral Adiposity the “Enemy Within”?

Tracy

2001

ATVB

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"Has it ever struck you that there's a thin man inside every fat man, just as they say there's a statue inside every block of stone?" George Orwell, Coming Up For Air (1939) R ecently, data from diverse areas of investigation have come together to implicate chronic low-level inflammation as an important pathogenetic factor in atherosclerotic cardiovascular disease (CVD). As recently summarized by Ross, 1 studies in cell biology, animal models, clinical research, and epidemiology have been remarkably consistent in validating the early work of Virchow 2 and others, suggesting that atherosclerotic lesions are essentially an inflammatory response. In clinical research and epidemiology, 2 inflammation blood markers in particular, fibrinogen and C-reactive protein (CRP), have been used. Many studies have confirmed that these markers predict future cardiovascular events independently of more traditional cardiovascular risk factors, such as plasma lipid levels. [3][4][5] Because of this, several investigators have suggested that CRP might prove useful in clinical practice, 6,7 whereas others have favored fibrinogen. 8,9 Although there are important details to work out before either of these markers enters the clinical domain, this interest provides a clear and compelling imperative for understanding how inflammation integrates into both normal physiology and atherothrombotic pathophysiology. See p 961 and 968Focusing on CRP, population-based research efforts have revealed that in general, women have slightly higher values than men, blacks have higher values than whites, and those with clinical CVD have higher values than those without [10][11][12][13] et al, manuscript in preparation). In those without clinical CVD, metabolic variables consistently correlated with CRP include body mass index (BMI), glucose tolerance status/diabetes status, and level of coagulation activation. In addition, depending on the population being studied, other correlates of CRP may include smoking status, plasma lipids (especially HDL cholesterol), hypertension, evidence of chronic infection, and measures of subclinical atherosclerotic disease, such as ankle-brachial blood pressure index (ABI).

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Fibrinogen and Cardiovascular Risk

Cited by 11 publications

References 0 publications

Fibrinogen Is a Marker for Nephropathy and Peripheral Vascular Disease in Type 1 Diabetes

Fibrinogen Is a Marker for Nephropathy and Peripheral Vascular Disease in Type 1 Diabetes

Acute-Phase Markers of Inflammation and Glomerular Structure in Patients with Type 2 Diabetes

Is Visceral Adiposity the “Enemy Within”?

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