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Query: UMLS:C0004153 (atherosclerosis)
77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In three groups of patients, we investigated the hypothesis that body weight is not the factor underlying the relation between hyperuricemia and cardiovascular disease. Among 111 subjects with asymptomatic hyperuricemia followed for 108 months, atherosclerotic heart disease (ASHD) developed in six; their mean was 77.4 kg (172 pounds) compared with 79.7 kg (177 pounds) in the remainder; in 25 of the 111 patients hypertension developed; their mean weight was not significantly higher than that of the remainder. Among 156 patients with established gout followed for 133 months, clinical atherosclerosis developed in 25 after a mean of 95 months; their mean weight was 78.3 kg (174 pounds) contrasted with 79.7 kg (177 pounds) in those 81 of the remaining patients who had a weight recorded with 75 +/- 12 months after their initial attack of gout. Among 1,356 men aaged 60 to 69 years who had their serum uric acid recorded in 1967, subsequent deaths from cardiovascular disease showed a stepwise increase when deaths were arranged according to the serum uric acid levels but not when they were arranged according to body weight. Hyperuricemia thus predicts future cardiovascular disease independently of body weight.
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PMID:High uric acid as an indicator of cardiovascular disease. Independence from obesity. 736 8

Intact arterial vessel wall is not thrombogenic. Disorders of the endothelium in connection with pathological coditions such such as atherosclerosis, hyperlipidaemia, hypertension and hyperuricemia induce interaction of surfaces of high thromboplastic activity with the blood stream. In such situations local formation of thrombin will take place immediately. Evidence is presented for the essential and unique activation of the extrinsic pathway of the plasmatic coagulation system. The local formation of thrombin at pathologically altered arterial wall seems to be an important trigger for arterial thrombosis and haemostasis. It could be that in vivo the initial step of thrombogenesis depends upon the formation of the activator complex between tissue-thromboplastin and factor VII.
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PMID:Thromboplastic activity of human arterial walls and its interaction with the plasmatic coagulation system. 744 Nov 81

When compared to values obtained in 40 normalweight normolipemic healthy control subjects, serum uric acid levels were found to be significantly increased in 68 subjects with type II-b and especially in 68 subjects with type IV hyperlipoproteinemia. A much lesser increase of uricemia occurred in 22 patients with type II-a. A significant positive correlation between uricemia and serum triglyceride level could be demonstrated but no such correlation was found with serum cholesterol. Overweight and hypertensive hyperlipemic subjects were presenting higher levels of serum uric acid than normalweight normotensive ones. On the other hand, clinical atherosclerosis and diabetes mellitus had no additive effects upon uricemia in hyperlipoproteinemic patients. It is suggested that hyperinsulinism and accelerated turnover of lipoproteins, often encountered in obese and hypertriglyceridemic subjects, might lead to an enhanced synthesis of purines and subsequently increased production of uric acid.
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PMID:Behaviour of uricemia in hyperlipoproteinemic subjects. 745 83

The individual components of the metabolic syndrome such as central obesity, dyslipidemia with increased triglycerides and decreased HDL-cholesterol, hyperuricemia, hypertension and progressive glucose intolerance are markers for an increased risk of atheroma and type 2 (non-insulin-dependent) diabetes. All components, with the exception of hyperuricemia, are associated with skeletal muscle insulin resistance, leading to compensatory chronic hyperinsulinemia. Insulin resistance/hyperinsulinemia, in turn, is associated with a series of hypertensiogenic and atherogenic side effects, aggravating the individual components of the metabolic syndrome. From a more pathophysiologically orientated point of view, early identification of individuals obviously at risk for atheroma and type 2 diabetes, as well as early intervention aimed at the improvement of reduced insulin action may play a central role in an integrated life-style approach of primary prevention of atherosclerosis and type 2 diabetes.
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PMID:[The metabolic syndrome. Pathophysiologic causes, diagnosis, therapy]. 784 93

From 1970 to 1990, 57 patients 50 years old or younger were treated for hypertension caused by atherosclerotic renal artery disease. Predisposing factors for atherosclerosis included smoking in 43 cases, hyperlipidemia in 15, diabetes in 8 and hyperuricemia in 8. Of the patients 47 had a family history of atherosclerotic vascular disease or a significant related disorder. Evidence of generalized atherosclerosis was present in 55 patients. Atherosclerotic renal artery disease was present unilaterally in 16 cases, bilaterally in 39 and in a solitary kidney in 2. Of the patients 34 were treated surgically, 20 medically and 2 by percutaneous angioplasty. Surgically treated patients experienced significant postoperative improvement in blood pressure (p = 0.001) and renal function (p = 0.05). Medically treated patients experienced significant improvement in blood pressure (p = 0.03) but renal function deteriorated. Younger patients with atherosclerotic renal artery disease suffer from a more severe and accelerated form of atherosclerosis than older patients. Although blood pressure control can be achieved with medical treatment, surgical revascularization offers the best opportunity for stabilization or improvement of renal function.
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PMID:Management of atherosclerotic renal artery disease in younger patients. 825 82

Recently atherosclerotic diseases, such as coronary heart disease and cerebrovascular disease have been considered as an important complication of hyperuricemia and gout. However, it is still controversial whether or not hyperuricemia is an independent risk factor of atherosclerotic diseases. On the other hand, several risk factors for coronary heart disease, for example hyperlipidemia and hypertension, are frequently observed in the patients with gout. Atherosclerosis in relation to hyperuricemia was discussed in view of definite and probable risk factors.
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PMID:[Gout and atherosclerosis]. 897 9

A group of metabolic disorders including insulin resistance and hyperinsulinemia, impaired glucose tolerance, visceral obesity, hypertension, dyslipidemia, hyperuricemia, hypercoagulability and microalbuminuria determine the risk for the development of atherosclerosis, coronary artery disease and cerebral vascular disorders. Although available studies on the pathogenesis of the metabolic syndrome are equivocal, it is most frequently hypothesized that hereditary of insulin resistance leads to the remaining metabolic disorders including diabetes mellitus, atherosclerosis and coronary artery disease. Despite pathogenetic controversies, there are convincing arguments for the diagnosis of the metabolic syndrome and search for therapy improving insulin sensitivity and reducing hyperinsulinemia thus preventing the development of diabetes mellitus and coronary artery disease.
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PMID:[Insulin resistance and hyperinsulinemia--clinical aspects]. 899 30

Usual risk factors for coronary artery disease account for only 25-50% of increased atherosclerotic risk in diabetes mellitus. Other obvious risk factors are hyperglycemia and dyslipidemia. However, hyperglycemia is a very late stage in the sequence of events from insulin resistance to frank diabetes, whereas lipoprotein abnormalities are manifested during the largely asymptomatic diabetic prodrome and contribute substantially to the increased risk of macrovascular disease. The insulin-resistant diabetes course affects virtually all lipids and lipoproteins. Chylomicron and very-low-density lipoprotein (VLDL) remnants accumulate, and triglycerides enrich high-density lipoprotein (HDL) and low-density lipoprotein (LDL), leading to high levels of potentially atherogenic particles and low levels of HDL cholesterol. Hyperglycemia eventually impairs removal of triglyceride-rich lipoproteins, the accumulation of which accentuates hypertriglyceridemia. As triglycerides increase-still within the so-called normal range-abnormalities in HDL and LDL became more apparent. Thus, when triglycerides are >200 mg/dL, LDL particles are small and dense (when they are <90 mg/dL, the particles are of the large, buoyant variety). The atherogenicity of small, dense LDL particles is attributed to their increased susceptibility to oxidation, but in many patients they may be a marker for insulin resistance or the presence of atherogenic VLDL. Hypertriglyceridemia is associated with atherosclerosis because (1) it is a marker for insulin resistance and atherogenic metabolic abnormalities; and (2) the small size of triglyceride-enriched lipoproteins enables them to infiltrate the blood vessel wall where they are oxidized, bind to receptors on macrophages, and ingested, leading to the development of the atherosclerotic lesion. Various studies (primary prevention with gemfibrozil: Helsinki Heart Study; secondary prevention with simvastatin and pravastatin: Scandinavian Simvastatin Survival Study [4S] and Cholesterol and Recurrent Events [CARE], respectively) have demonstrated that lipid-lowering therapy in type 2 diabetes is effective in decreasing the number of cardiac events. Risk reduction was 22% to 50% (statins) and approximately 65% (fibrate) relative to placebo. It was also noted (in 4S and CARE) that the risk of major coronary events in untreated diabetic patients was 1.5-1.7-fold greater than in untreated nondiabetic patients. Although gemfibrozil (fibric acid derivative) is more effective in decreasing triglycerides and increasing HDL cholesterol in diabetic patients than the statins, it does not change and may even increase LDL-cholesterol levels (fenofibrate may be an exception, decreasing LDL cholesterol by 20-25% in some studies). However, gemfibrozil does increase LDL particle size. Nevertheless, the statins are the current lipid-lowering drugs of choice because the change in LDL-cholesterol-to-HDL-cholesterol ratio is better than with gemfibrozil. Moreover, the diabetic patient may be more likely to benefit from statin therapy than the nondiabetic patient. It should be noted that, in theory, nicotinic acid can correct or improve all lipid or lipoprotein abnormalities in patients with type 2 diabetes. Unfortunately, it is relatively contraindicated because it causes insulin resistance and may precipitate or aggravate hyperglycemia (in addition to its other well-known side effects such as flushing, gastric irritation, development of hepatotoxicity, and hyperuricemia). It is unknown at present whether newer formulations such as once-daily Niaspan may be better tolerated in diabetes. In any case, most patients with type 2 diabetes have risk factors for coronary artery disease and qualify for aggressive LDL cholesterol-lowering therapy. At the same time, it is presently unknown whether improved glycemic control decreases coronary artery disease risk in such patients.
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PMID:Diabetic dyslipidemia. 991 65

The objective of this study was to determine the prevalence of carotid atherosclerosis in black Cameroonian adults presenting cardiovascular risk factors (CVRF). It was based on 77 subjects over the age of 40 years (50 men and 27 women) with at least one major CVRF, such as hypertension (HT), smoking, dyslipidaemia or diabetes mellitus. Obesity [body mass index (BMI), waist/hips ratio (W/H)] and hyperuricaemia were also taken into account. Duplex ultrasound examination of the carotid arteries was performed with a Siemens apparatus equipped with a 7.5 MHz transducer array. An atheromatous plaque was defined as medio-intimal thickening > or = 1.5 mm, with either protrusion or hyperechogenicity. Risk factors were distributed as follows in our serie: HT: 82%, Obesity: 49% (W/H) and 32% (BMI); Diabete: 32%; Smoking: 23%; Hyperuricaemia: 21%; Hypercholesterolaemia: 13%. 19 subjects (25%) (12 men and 7 women with a mean age of 63 years) presented one or more atheromatous plaques in the carotid arteries. Hyperuricaemia and hypercholesterolaemia were significantly correlated with the presence of plaques, with a marked tendency in subjects over the age of 70. In this study, hyperuricaemia and advanced age appeared to be independent arterial risk factors on multivariate analysis. In conclusion, our data show that carotid atherosclerosis does exist in our populations, especially in elderly subjects with cardiovascular risk factors. The particular role of hyperuricaemia as a predictive factor of atheromatous plaques in black Cameroonian subjects needs to be defined.
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PMID:[Ultrasonic demonstration of carotid atherosclerosis in black Cameroonian adults with cardiovascular risk]. 992 49

Aim of this paper is to describe and discuss, on the basis of the available current literature, the case of a female patient affected by a tophaceous gout associated with plurimetabolic syndrome. Hyperuricemia and gout may be seen today in all the populations of developed countries, with increasing frequency on the last fifty years. Increased production or reduced urinary excretion of uric acid (and hypoxanthine and xanthine) are the most important pathogenetic mechanisms of primary or secondary hyperuricemia. Gout is an acute rheumatic disorder (characterized by a limited range of manifestations) which occurs in humans in connection with deposition of crystals of monosodium urate (the final product of purine metabolism) in the articular and soft periarticular tissues. Hyperuricemia and/or gout are often associated with hyperinsulinemia, obesity, diabetes mellitus, hyperlipemia, hypertension and atherosclerosis to form the syndrome called "Plurimetabolic syndrome" or "Syndrome X". Here we report the clinical case of a 64-year-old female patient who had android obesity, type 2 diabetes mellitus, hypertension, dyslipidemia and hyperuricemia and had been suffering (over many years) from intermittent episodes of severe pain and inflammatory joint swelling (first metacarpo- and metatarso-phalangeal joints) with development of pronounced multiple tophi in bone articular and soft periarticular tissues. Hyperuricemia and acute episodes had never been treated with anti-hyperuricemic drugs because gouty arthritis had never been diagnosed. This severe tophaceous gout associated to multiple metabolic disorders prompted us to present knowledge on gout and to focus on the interrelationships between hyperuricemia and/or gout and plurimetabolic syndrome, important risk factors for coronary heart disease.
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PMID:[Tophaceous gout in plurimetabolic syndrome]. 1021 66


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