Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The multiple cholesterol emboli syndrome (MCES) is a rare, multi-organ disease than can occur spontaneously or after arterial or cardiac catheterization, arteriography, angioplasty, cardiovascular surgery, oral or intravenous anticoagulation, systemic fibrinolysis and cardiorespiratory resuscitation, predominantly in male subjects with disseminated atherosclerosis over the age of 60 years. Clinical signs of MCES vary considerably depending on the organs involved, but the signs most frequently encountered are renal failure, skin lesions (livedo reticularis, purple toc, ulcers, etc) and transient eosinophilia. Optimal treatment of this syndrome is controversial and is often symptomatic. However, the most effective measure remains prevention based on identification of high-risk patients, treatment with platelet antiaggregants and careful handling of catheters. This syndrome has a serious prognosis in the majority of cases. In this article, the authors describe a case of MCES. After thoracic aortography, this 73-years-old patient presented typical clinical sign of MCES (angina, cerebrovascular accident, bilateral blindness, transient renal failure and splenic infarction). The clinical course was favourable in response to heparin therapy and splenectomy and caudal pancreatectomy. Histology confirmed the presence of cholesterol emboli in the lumen of splenic arterioles. Except in the case of severe bleeding diathesis, the authors recommend early heparin therapy for MCES caused by catheterization, angioplasty or cardiovascular surgery. However, complementary studies must be performed to more clearly define the effects of heparin on MCES.
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PMID:[Multiple cholesterol emboli syndrome: beneficial effects of early heparin therapy. A case report]. 1255 63

Age-related maculopathy (ARM) is a degenerative disease of the retina and the leading cause of incurable blindness and visual impairment in industrialized countries. By definition, ARM is confined to the age-category above 50 years. The aetiology of ARM is still unknown, despite intensive research on many fronts. In this paper, we provide a review of the epidemiology of ARM. The most prominent findings were an exponential increase in frequency with age, a significant familial and genetic component, and a strong association with smoking. Other risk factors that were found less consistently were atherosclerosis, low intake of antioxidant nutrients, and cataract extraction. Future studies, both observational and experimental, will hopefully identify more risk factors that are amenable to prevention.
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PMID:Epidemiology of age-related maculopathy: a review. 1456 Oct 43

Diabetes mellitus has been referred to as a vascular disease because of its effect on the vascular endothelial wall. In recent years, research has identified specific effects of hyperglycemia and insulin resistance on the vasculature of the diabetic patient. Atherosclerosis is known to develop earlier in the diabetic patient and is more aggressive due to the metabolic effects of hyperglycemia and insulin resistance. The results of many large, randomized, prospective trials have provided practice changes in the management of the patient with diabetes. Trials such as the Framingham Study identified risk factors associated with atherosclerosis. Additional studies, such as the Diabetes Control and Complications Trial and the United Kingdom Prospective Diabetes Study, provided information about risk factors for diabetes and contributed to treatment recommendations for the person with type 1 or type 2 diabetes. Results of these and many other trials continue to change the recommendations for the person with diabetes to reduce mortality and prevent coronary heart disease, blindness, renal failure, and amputation. This paper will identify the effects of diabetes on the vascular system and outline best practice recommendations on the basis of clinical trials.
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PMID:Effects of diabetes on the vascular system: current research evidence and best practice recommendations. 1498 97

Blind randomized placebo-control research included 39 women. The following criteria were: menopause period for more then 1 year long; diabetes mellitus; arterial hypertension; hypercholesterolemia. The patients were divided into two groups. Women from the first group (N = 24) were given 30 mg lycopene (composed with "Tomatol") per day during 24 weeks. The second group (N = 15) were given placebo. It was showed that during 12-week "Tomatol" intake we state that lycopene concentration in serum increased twice (337.0 +/- 133.0 nM), total cholesterol (CH) and CH LDL decreased by 12% and 16% respectively. The lipoproteins spectrum normalization correlated to serum antioxidative activity (r = 0.30, p < 0.05), and malonic dialdehyde concentration decrease by 44.8% correlated to lycopene increase (r = -0.51, p < 0.05). Our results give us a possibility to use "Tomatol" as an additional medicine for the prevention of atherosclerosis.
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PMID:[Effect of lycopene on blood lipoproteids in women with type 2 diabetes mellitus in postmenopause]. 1504 52

Diabetic vascular complication is a leading cause of acquired blindness, end-stage renal failure, a variety of neuropathies and accelerated atherosclerosis, which could account for disabilities and high mortality rates in patients with diabetes. Chronic hyperglycemia is essentially involved in the pathogenesis of diabetic micro- and macrovascular complications via various metabolic derangements. In this review, we discuss the molecular mechanisms of diabetic retinopathy and nephropathy, especially focusing on advanced glycation end products (AGEs) and their receptor (RAGE) system. Several types of AGE inhibitors and their therapeutic implications in diseases, including diabetic microangiopathy, will be discussed in the next review article.
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PMID:Role of advanced glycation end products (AGEs) and their receptor (RAGE) in the pathogenesis of diabetic microangiopathy. 1522 2

A 31-year-old woman presented with recurrent transient monocular blindness. As transient ischaemic attacks were suspected further investigations were targeted at evaluation of premature atherosclerotic lesions in the internal carotid artery. Initially laboratory tests were not performed. After referral to a cardiovascular-disease prevention outpatient clinic, laboratory evaluation disclosed a marked isolated polycythaemia that turned out to be secondary to right-left shunting through multiple pulmonary arteriovenous malformations. The ultimate diagnosis was hereditary haemorrhagic telangiectasia. Later on, physical signs such as telangiectasia and central cyanosis were noticed. In the clinical decision-making process, laboratory tests associated with causes of transient monocular visual loss were not carried out and therefore clues important for the ultimate diagnosis were not obtained. In only a minority of young patients with transient monocular visual loss can this be ascribed to premature atherosclerosis. For these reasons, a proper physical examination and laboratory tests directed towards other causes must be part of the initial diagnostic work-up in young patients with visual disturbances and suspected transient ischaemic attacks.
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PMID:[Clinical reasoning and decision-making in practice. A 31-year-old woman with transient monocular blindness and polycythaemia]. 1579 48

Diabetic vascular complication is a leading cause of end-stage renal failure, acquired blindness, a variety of neuropathies and accelerated atherosclerosis, which could account for disabilities and high mortality rates in patients with diabetes. Recent large prospective clinical studies have shown that intensive glucose control reduces effectively microvascular complications among patients with diabetes, and insulin resistance and postprandial hyperglycemia seem to be involved in diabetic macrovascular complications. Chronic hyperglycemia is a major initiator of diabetic vascular complications. Indeed, high glucose, via various mechanisms such as increased production of advanced glycation end products, activation of protein kinase C, stimulation of the polyol pathway and enhanced reactive oxygen species generation, regulates vascular inflammation, altered gene expression of growth factors and cytokines, and platelet and macrophage activation, thus playing a central role in the development and progression of diabetic vascular complications. This article summarizes the molecular mechanisms of diabetic vascular complications and the potential therapeutic interventions that may prevent these disorders even in the presence of hyperglycemia, control of which is often difficult with current therapeutic options.
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PMID:Diabetic vascular complications: pathophysiology, biochemical basis and potential therapeutic strategy. 1602 67

DNA damage is related to a variety of degenerative diseases such as cancer, atherosclerosis and neurodegenerative diseases, depending on the tissue affected. Increasing evidence indicates that reactive oxygen species (ROS) play a key role in the pathogenesis of primary open angle glaucoma (POAG), the main cause of irreversible blindness worldwide. Oxidative DNA damage is significantly increased in the ocular epithelium regulating aqueous humor outflow, i.e., the trabecular meshwork (TM), of glaucomatous patients compared to controls. The pathogenic role of ROS in glaucoma is supported by various experimental findings, including (a) resistance to aqueous humor outflow is increased by hydrogen peroxide by inducing TM degeneration; (b) TM possesses remarkable antioxidant activities, mainly related to superoxide dismutase-catalase and glutathione pathways that are altered in glaucoma patients; and (c) intraocular-pressure increase and severity of visual-field defects in glaucoma patients parallel the amount of oxidative DNA damage affecting TM. Vascular alterations, which are often associated with glaucoma, could contribute to the generation of oxidative damage. Oxidative stress, occurring not only in TM but also in retinal cells, appears to be involved in the neuronal cell death affecting the optic nerve in POAG. The highlighting of the pathogenic role of ROS in POAG has implications for the prevention of this disease as indicated by the growing number of studies using genetic analyses to identify susceptible individuals and of clinical trials testing the efficacy of antioxidant drugs for POAG management.
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PMID:The role of oxidative stress in glaucoma. 1641 23

Accelerated atherosclerosis and microvascular complications are perhaps the leading cause of coronary heart disease, blindness and renal failure, which could account for disabilities and high mortality rates in patients with diabetes. Several thrombogenic abnormalities have been shown to play a central role in the pathogenesis of these devastating complications. However, the molecular mechanism for thrombogenic diathesis in diabetes is not fully elucidated. A recent clinical study, the Diabetes Control and Complications Trial-Epidemiology of Diabetes Interventions and Complications (DCCT-EDIC) Research, has revealed that the reduction in the risk of progressive retinopathy and nephropathy resulting from intensive therapy in patients with type 1 diabetes persist for at least several years, despite increasing hyperglycemia. Further, intensive therapy during the DCCT resulted in decreased progression of carotid intima-media thickness six years after the end of the trial as well. These clinical studies strongly suggest that so-called 'hyperglycemic memory' causes chronic abnormalities in diabetic vessels that are not easily reversed, even by subsequent, relatively good control of blood glucose. Among various biochemical pathways activated under diabetes, the process of formation and accumulation of advanced glycation end products (AGEs) and their mode of action are most compatible with the theory 'hyperglycemic memory'. In this review, we discuss the role of AGEs in thrombogenic abnormalities in diabetes.
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PMID:Role of advanced glycation end products (AGEs) in thrombogenic abnormalities in diabetes. 1647 28

The metabolic syndrome consists of a combination of cardiovascular risk factors that include hyperglycemia with or without type 2 diabetes mellitus, visceral obesity, elevated blood pressure, and atherogenic dyslipidemia. These interrelated disorders and their associated lipotoxicity, oxidative stress, and inflammatory state predispose to a constellation of cardiovascular conditions leading to high risk of heart attack, stroke, renal failure, blindness, and lower extremity amputation. Visceral obesity, a prime risk factor for type 2 diabetes and a major component of the metabolic syndrome, potentiates atherogenesis, atherosclerosis, organ lipotoxicity, and oxidative tissue damage.Peroxisome proliferator-activated receptors (PPARs) are relatively recently discovered nuclear transcription factors that are modulated by dietary fatty acids, including the essential polyunsaturated fatty acids, arachidonic acid and its metabolites, and are essential to the control of energy metabolism. Of the three PPAR isoforms (alpha, gamma, and delta), synthetic pharmaceutical ligands that activate PPARalpha (the antidyslipidemic fibric acid derivatives ['fibrates']) and PPARgamma (the antidiabetic thiazolidinediones) have been studied extensively. Recently developed dual PPARalpha/gamma agonists may combine the therapeutic effects of these drugs, creating the expectation of greater efficacy, and perhaps other advantages in the treatment of type 2 diabetes and the metabolic syndrome. However, thiazolidinediones are hampered by adverse effects related to increased weight gain and fluid overload. It remains to be seen whether the dual PPARalpha/gamma agonists currently under development have similar limitations. Nevertheless, existing clinical data imply that the combined effects of thiazolidinediones and fibrates are likely to be emulated by dual PPARalpha/gamma agonists, providing superior efficacy to these classes for the treatment of type 2 diabetes, the metabolic syndrome, and their cardiovascular and other end-organ complications.
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PMID:Dual Peroxisome Proliferator-Activated Receptor-alpha/gamma Agonists : In the Treatment of Type 2 Diabetes Mellitus and the Metabolic Syndrome. 1654 49


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