Gene/Protein Disease Symptom Drug Enzyme Compound
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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mounting data support a causal connection between high-normal fibrinogen levels and atherosclerotic cardiovascular disease. There is clearly a thrombogenic component to atherosclerosis and the onset of clinical manifestations. This offers the possibility to better identify high-risk candidates and also to protect them by reducing blood fibrinogen concentration or blocking its action. The relationship of antecedent fibrinogen to the subsequent development of cardiovascular disease is examined, based on 18 years of surveillance of a cohort of 1274 men and women aged 47 to 79 years who participated in the Framingham Study. The association with the development of peripheral arterial disease and cardiac failure is now examined in addition to previously studied relationships to coronary heart disease and stroke. In men and women, there is a significant age-adjusted relationship of fibrinogen level to coronary heart disease and to cardiovascular disease in general. In women, a significant relationship to cardiac failure and peripheral arterial disease, but not to stroke, was also found. These data on women are unique as they are not available elsewhere. Age-adjusted cardiovascular, all-cause, and coronary heart disease mortality were all related to fibrinogen in both sexes. In men, fibrinogen impact was the greatest for stroke and the least for peripheral arterial disease. For women, the impact on coronary heart disease was greatest. The absolute risk for an elevated fibrinogen level was greatest for coronary heart disease in both sexes. Average fibrinogen values are higher in women and in persons with other risk factors, including hypertension, cigarette smoking, diabetes, obesity, and elevated hematocrit. However, there is an independent contribution of fibrinogen to cardiovascular disease in general and coronary disease in particular, on adjustment for coexistent risk factors. Fibrinogen enhances the risk of cardiovascular disease in hypertensives, diabetics, and cigarette smokers. About half the cardiovascular risk of cigarette smoking appears due to the higher fibrinogen values. Now, five prospective studies document the excess incidence of cardiovascular events in persons with elevated fibrinogen levels within the "normal range." Each standard deviation increase in fibrinogen is associated with a 30% increment of coronary heart disease in men and a 40% increase in women. Fibrinogen should be added to the list of major cardiovascular risk factors. Trials of intervention to lower fibrinogen in high-risk coronary candidates are needed.
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PMID:Update on fibrinogen as a cardiovascular risk factor. 134 96

Fibrinogen has turned out to be an independent risk factor for coronary heart disease (CHD). It is not known whether or not this parameter could be a prognostic factor for restenosis following percutaneous transluminal coronary angioplasty (PTCA), which represents the main problem limiting the long-term efficacy of this procedure. Therefore, we studied fibrinogen concentrations in a series of 50 males (mean age: 55, range: 38-70 years) with CHD and successful PTCA. Follow-up coronary angiography was performed 12 months following PTCA. Twenty-two patients had restenosis, and 28 patients were without restenosis. Both groups did not differ significantly in medical history (smoking habits, hypertension, positive family history for cardiovascular diseases), in routine lipid profile (total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides, apolipoproteins A1 and B). Fibrinogen values were 405 +/- 128 mg/dl (range: 202-725) in patients with restenosis and 352 +/- 94 mg/dl (range: 187-568) in patients without restenosis (not significant). Elevated fibrinogen levels of more than 400 mg/dl were found in 8 patients in each group. Although fibrinogen is a proven marker for CHD in men, fibrinogen is not a risk factor for restenosis following PTCA.
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PMID:Fibrinogen values in patients with and without restenosis following percutaneous transluminal coronary angiography. 145 Nov 21

Dipeptidylpeptidase IV (DPP IV) activity has been found in glomeruli of the rat and other previously investigated animal species, but has not been detected in the glomeruli of the normal human kidney. Under pathological conditions, enzyme activity may be registered. Following investigations on 155 human renal biopsies using polyclonal antisera against IgG, IgA, IgM, C3C, Fibrinogen, and DPP IV, we found glomerular enzyme activity in 43 cases of various histological diagnoses, but never in normal renal tissue. Identical results could be found by the Gly-Prol-beta-MNA substrate reaction. The localization of glomerular enzyme activity in capillary walls could not be definitely determined, possibly enzyme activity occurs in podocytes. Correlation of glomerular DPP IV activity to the deposition of immunoglobulins was not found. Nevertheless, the appearance of DPP IV in human glomeruli seems to be in correlation with some clinical findings, e.g. hypertension. The importance of DPP IV activity in pathohistologically changed glomeruli of human kidney is definitely large, but needs further investigation.
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PMID:Demonstration of glomerular DPP IV activity in kidney diseases. 168 53

Hyperglycaemia, a raised fibrinogen, an increased serum triglyceride and a reduced HDL-cholesterol are common metabolic features of non-insulin dependent diabetes mellitus (NIDDM). Hypertension is frequently associated with NIDDM, however the influence of antihypertensive therapy on these combined factors in the diabetic is at present unclear. In a double-blind placebo-controlled crossover study in 20 stable NIDDM subjects with hypertension, the metabolic effects of 6 weeks' treatment with the alpha-blocker, doxazosin, was compared with treatment with the beta-blocker, atenolol. Similar and significant reductions in BP were produced by both drugs. Significant increases in weight, HbA1, apoprotein B, serum triglyceride and cholesterol/HDL ratio were observed with atenolol therapy. Doxazosin therapy was associated with opposite patterns of changes in fasting glucose, lipids and lipoproteins but only for serum triglyceride was difference between treatments significant. Fibrinogen was not altered by either treatment. Conclusions from this study indicate; 1) adrenergic mechanisms may be an important influence on glucose homeostasis and lipid metabolism in NIDDM and 2) the beta-blocker, atenolol, has a small adverse effect on weight, glycaemic control and the atherogenic lipid profile, whereas the alpha-blocker, doxazosin, has no such effect and may, in part, correct the disturbances of lipoprotein metabolism characteristic of NIDDM.
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PMID:Alpha-blocker therapy; a possible advance in the treatment of diabetic hypertension--results of a cross-over study of doxazosin and atenolol monotherapy in hypertensive non-insulin dependent diabetic subjects. 198 Sep 30

Fibrinogen level is an independent predisposing factor for coronary heart disease and has a prognostic significance comparable with that of cigarette smoking, serum cholesterol level and hypertension. In our study fibrinogen levels were measured in 45 patients with cardiovascular disease of which 25 (55%) had a high fibrinogen level and in 45 persons healty, of which only 3 (6.6%) increased fibrinogen. The impact of fibrinogen level on the risk of cardiovascular disease was more consistent in men of all ages considered. The authors note that the independent contribution of fibrinogen to the cardiovascular risk may reflect hypercoagulability, hyperviscosity and increased platelet aggregation. Therefore they consider, the dosing of fibrinogen level important in the research of cardiovascular risk factors.
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PMID:[Fibrinogen, a cardiovascular risk factor]. 262 36

The relationship between plasma fibrinogen levels and the severity of coronary atherosclerosis was examined in 229 patients, aged 25-82 years (162 men and 67 women), undergoing coronary angiography. Severity of coronary atherosclerosis was assessed in terms of the number of vessels with a 75% or greater stenosis and Gensini's severity score. Fibrinogen levels increased progressively with the severity of coronary atherosclerosis, determined by both the number of involved vessels and Gensini's severity score in men, and the relationships were statistically significant. Similar patterns were noted among women, but the trends were not statistically significant. The association was evident even after adjustment for age, hypertension, total cholesterol, cigarette smoking, alcohol intake, high density lipoprotein cholesterol and body mass index. These results provide evidence that in the Japanese also plasma fibrinogen levels can serve as an independent indicator of the progression of coronary atherosclerosis.
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PMID:Plasma fibrinogen levels as an independent indicator of severity of coronary atherosclerosis. 275 52

Plasma and whole blood viscosity and its determinants were measured in 86 diabetic patients (29 hypertensive and 57 normotensive) and compared with 52 non-diabetic control subjects to assess whether hypertension has an additive and adverse effect on blood viscosity. Whole blood viscosity (corrected for haematocrit), at high and low shear rates (95 and 0.95 s-1), was significantly higher in both Type 1 (5.1 +/- 0.5 (+/- SD), 19.8 +/- 2.9) and Type 2 (5.2 +/- 0.3, 21.1 +/- 2.0) diabetic patients compared with control subjects (4.9 +/- 0.6, 17.4 +/- 2.6 mPa s, p less than 0.01). Corrected whole blood viscosity at high shear rate was significantly higher in hypertensive than in normotensive Type 2 diabetic patients (5.5 +/- 0.4 vs 5.2 +/- 0.3 mPa s, p less than 0.01). Plasma viscosity was significantly higher in diabetic patients compared with control subjects (1.4 +/- 0.1 vs 1.3 +/- 0.1 mPa s, p less than 0.01), but there was no difference between hypertensive and normotensive diabetic patients (1.4 +/- 0.1 vs 1.4 +/- 0.2 mPa s). Fibrinogen levels were similar in all the groups.
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PMID:Association of hypertension with blood viscosity in diabetes. 297 42

The objectives of the present study were to determine whether an intracisternal injection of fibrinogen-sodium citrate, a model of neurogenic pulmonary edema (NPE), produces protein-rich or protein-poor pulmonary edema, and to determine whether the edema is associated with pulmonary vascular hypertension and pulmonary congestion. Fibrinogen (6-10 mg/ml) dissolved in 0.055 M sodium citrate was injected into the cisterna magna of six New Zealand White rabbits. Six additional rabbits were injected with saline to control for the effects of intracranial hypertension and pulmonary vascular hypertension. The fibrinogen-sodium citrate solution or sodium citrate alone, as opposed to saline, produced systemic and pulmonary vascular hypertension, pulmonary edema, hypoxemia, hypercapnia, and acidosis. The lungs from fibrinogen-injected rabbits were edematous, congested, and liverlike in appearance. Tracheal froth that was blood tinged and protein rich was present in five of the six rabbits. Microscopic examination of lung biopsies revealed erythrocytes and plasma in the alveoli and focal injury to the pulmonary microvascular endothelium. Fibrinogen-sodium citrate increased (P less than 0.05) the extravascular lung water (EVLW) (10.3 +/- 2.0 vs. 5.5 +/- 0.6 g, means +/- SE), lung blood weight (9.7 +/- 1.3 vs. 3.8 +/- 0.6 g), total dry lung weight (3.2 +/- 0.4 vs. 2.0 +/- 0.1 g), and the EVLW-to-blood-free dry lung weight ratio (7.0 +/- 0.8 vs. 4.0 +/- 0.3 g) from saline-control values. There was no difference in the blood-fre dry lung weight (1.4 +/- 0.1 vs. 1.3 +/- 0.1 g) between the two groups. These findings demonstrate that pulmonary congestion, pulmonary vascular hypertension, and focal endothelial injury contribute to the development of NPE.
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PMID:Endothelial injury and pulmonary congestion characterize neurogenic pulmonary edema in rabbits. 311 22

Fibrinogen and blood viscosity were measured in 72 stable non-insulin dependent diabetic subjects, 31 without hypertension, and 41 who had treated hypertension. The hypertensive group had higher plasma fibrinogen levels and blood viscosity. As both these rheological variables have been associated with micro- and macro-vascular disease, these findings may provide a possible explanation for the mechanism of the increased vascular disease seen in hypertensive compared with normotensive diabetic subjects.
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PMID:Diabetic hypertension--the importance of fibrinogen and blood viscosity. 324 46

In over 30 years of surveillance of 2873 women, 574 developed initial clinical manifestations of CHD. A number of antecedent metabolic risk factors proved atherogenic, including blood lipids, glucose tolerance, uric acid, and menopause. Serum total cholesterol predicts as strongly in women as in men. The predictive power of cholesterol is strengthened when the total cholesterol is partitioned into its atherogenic LDL and protective HDL fractions. Contrary to the case in men, triglyceride may be a contributor to risk in older women. A total-to-HDL cholesterol ratio exceeding 7.5 equalizes the risk in men and women. Impaired glucose tolerance also eliminates the female CHD risk advantage over men, conferring a three-fold increased risk. Serum uric acid, although lower in women than in men, is equally predictive in the sexes. Central obesity confers an increased CHD risk in women and predisposes to diabetes, hyperuricemia, hypertension, and an unfavorable LDL/HDL cholesterol ratio. A combination of obesity, low HDL cholesterol, and impaired glucose tolerance predisposes especially. Age-adjusted risk of CHD is increased two- to threefold compared to pre menopausal women, even when induced surgically without removing the ovaries. It is not clear whether post menopausal estrogen replacement eliminates this excess risk. Fibrinogen is higher in women than in men, and is increased with hypertension, diabetes, hypercholesterolemia, high hematocrit, and cigarette smoking. At any level of multivariate risk, fibrinogen added to the CHD risk in women.
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PMID:Metabolic risk factors for coronary heart disease in women: perspective from the Framingham Study. 360


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