Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular disease is a leading cause of mortality in rheumatoid arthritis (RA). Endothelial dysfunction often precedes manifest atherosclerosis. Both traditional, Framingham risk factors and inflammation-associated factors are involved in RA-associated atherosclerosis. Among imaging techniques, the early determination of common carotid intima-media thickness (ccIMT), flow-mediated vasodilation (FMD), and nitroglycerine-mediated vasodilation (NMD) may be useful to determine atherosclerosis and endothelial dysfunction. We and others found increased ccIMT and impaired FMD in RA patients. Among immunological and metabolic laboratory markers, anticyclic citrullinated peptide (anti-CCP) antibodies, IgM rheumatoid factor, circulating immune complexes, pro-inflammatory cytokines including tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), Th0/Th1 T cells, homocysteine, dyslipidemia, decreased folate and vitamin B12 production, and impaired paraoxonase activity may all be involved in the development of vascular disease in RA. The early diagnosis of endothelial dysfunction and atherosclerosis, active immunosuppressive treatment, the use of drugs that control atherosclerosis, changes in sedentary lifestyle, and the close follow-up of RA patients may help to minimize cardiovascular risk in these individuals.
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PMID:Accelerated atherosclerosis in rheumatoid arthritis. 1789 98

Neuropathy is a common complication of diabetes mellitus, which reduces the quality of life and may be life-threatening. The etiology is complex and multifactorial: hyperglycemia and dyslipidemia give rise to oxidative stress and formation of advanced glycation and lipoxidation end products. These stimulate inflammatory processes, nuclear factor kappa B (NFkappaB) activation being of central importance. Many of the drugs that have been developed for treatment of diabetic complication at least in part work through suppressing either NFkappaB activation itself, or the production of cytokines that stimulate NFkappaB, such as tumor necrosis factor (TNF) alpha. To date there have been few tests of drugs that are specific inhibitors of the NFkappaB / TNFalpha axis. However preliminary results in animal models are encouraging and go some way in establishing the NFkappaB cascade as an important therapeutic target for diabetic vascular complications in general, and neuropathy in particular.
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PMID:Pro-inflammatory mechanisms in diabetic neuropathy: focus on the nuclear factor kappa B pathway. 1822 Jul 13

Psoriasis is a chronic and debilitating inflammatory disease associated with serious comorbidities. Psoriasis can have a significant impact on a patient's quality of life and is associated with loss of productivity, depression, and an increased prevalence of malignancy. Emerging comorbidities of psoriasis include cardiovascular disease and metabolic syndrome. Psoriasis patients have an increased prevalence of the core components of metabolic syndrome, including obesity, dyslipidemia, and insulin resistance. The relationship between psoriasis and comorbidities such as metabolic syndrome and cardiovascular disease is likely linked to the underlying chronic inflammatory nature of psoriasis. The molecular mechanisms involved in psoriasis-associated dysregulation of metabolic function are believed to be due, in large part, to the action of increased levels of proinflammatory factors, such as tumor necrosis factor-alpha, that are central to the pathogenesis of psoriasis. Recent studies investigating the effects of tumor necrosis factor antagonists on the treatment of cardiovascular disease and metabolic syndrome support this concept.
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PMID:Psoriasis comorbidities. 1827 20

Obesity is associated with the changes of plasminogen activator inhibitor-1 (PAI-1), tumor necrosis factor-alpha (TNFalpha) and transforming growth factor beta (TGFbeta) levels. However, the precise effect of the 4G allele on obesity is still contradictory. Here, we aimed to elucidate the role of the 4G/5G polymorphism of the PAI-1 gene on the PAI-1 level and determine the associations between cytokines, glucose and lipid metabolism parameters in obese children. Thirty-nine obese children (mean age 11.4 +/- 3.3 years) and 38 age-matched healthy control group (mean age 10.3 +/- 3.5 years) were included in the study. In all cases, serum levels of glucose, lipid and insulin were measured, homeostasis model assessment of insulin resistance (HOMA-IR) was calculated, and 4G/5G polymorphism of PAI-1 gene, plasma PAI-1 level and serum TNFalpha and TGFbeta levels were studied. The mean relative body mass index (BMI) and HOMA-IR score, VLDL, TG, insulin, PAI-1, TNFalpha levels were higher, and HDL and TGFbeta levels were lower in the obese group. The frequency of the 4G/4G genotype was considerably higher in obese children than in controls. Also, a positive correlation was found between PAI-1 and TNFalpha levels, and relative BMI, HOMA-IR score, insulin, TG, HDL levels. TGFbeta was inversely correlated only with relative BMI. There was no correlation among three cytokines. In conclusion, childhood obesity contributes to higher PAI-1 and TNFalpha and lower TGFbeta levels. Especially PAI-1 and TNFalpha accompany insulin resistance and dyslipidemia.
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PMID:PAI-1 gene 4G/5G polymorphism, cytokine levels and their relations with metabolic parameters in obese children. 1827 85

Rheumatoid arthritis (RA) is a systemic inflammatory disease that presents not only involvement of joints but also endothelial dysfunction, dyslipidemia, and premature atherosclerosis. The death rate in RA is known to be higher than in the general population and clinical cardiovascular events secondary to atherosclerosis are responsible for the excessive death rate. A better understanding of the mechanisms that take part in the pathogenesis of atherosclerosis in RA patients is needed. Thus, the authors review the role of several factors involved in RA atherosclerosis, including disease activity, new cardiovascular risk factors, dyslipidemia and the association of atherosclerosis with the use of anti-rheumatic drugs, glucocorticoids and anti-tumor necrosis factor (TNF) agents. The role of humoral autoimmunity, namely autoantibodies against heat shock proteins, cardiolipin and beta2-glycoprotein I, and its link with atherosclerosis is also discussed. It is likely that the elucidation of the key mechanisms of atherogenesis in RA may determine a positive impact by reducing cardiovascular morbidity and mortality of these patients.
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PMID:Multiple factors determine the increased prevalence of atherosclerosis in rheumatoid arthritis. 1834 21

An increased amount of adipose tissue or its disproportionate distribution between central and peripheral body regions is related to the development of insulin resistance, type 2 diabetes mellitus, dyslipidemia, atherosclerosis, and coronary artery disease. Until recently, adipose tissue was regarded as a storage depot for lipids. It is now viewed as a hormonally active organ that plays a crucial metabolic role. The most important products of adipose tissue collectively referred to as adipocytokines, include adiponectin, leptin, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), resistin, plasminogen-activating inhibitor-I (PAI-1), and angiotensinogen. These low and medium molecular weight proteins play an important role in the adipose tissue physiology and are believed to be a link between obesity, insulin resistance and endothelial dysfunction. This review describes the metabolic role of two of these proteins, adiponectin and leptin, in relation to insulin sensitivity.
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PMID:Adiponectin and leptin in relation to insulin sensitivity. 1837 Jun 42

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease affecting approximately 1% of the adult general population. Cardiovascular disease is recognized as the leading cause of death in RA patients, accounting for nearly 40% of their mortality. Patients with RA are at a twofold increased risk for myocardial infarction and stroke, with risk increasing to nearly threefold in patients who have had the disease for 10 years or more. Congestive heart failure appears to be a greater contributor to excess mortality than ischemia. This increased cardiovascular disease risk in RA patients seems to be independent of traditional cardiovascular risk factors. Pathogenic mechanisms include pro-oxidative dyslipidemia, insulin resistance, prothrombotic state, hyperhomocysteinemia, and immune mechanisms such as T-cell activation that subsequently lead to endothelial dysfunction, a decrease in endothelial progenitor cells, and arterial stiffness, which are the congeners of accelerated atherosclerosis observed in RA patients. This paper discusses pathogenic mechanisms, effects of methotrexate, tumor necrosis factor antagonists, steroids, and statins, with a perspective on therapy.
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PMID:Rheumatoid arthritis and cardiovascular disease. 1841 67

Adipocytokines, fat tissue derived factors with regulatory properties, are involved in the pathophysiology of atheromatous and metabolic illnesses such as: ischemic heart disease, insulin resistance, obesity, dyslipidemia and diabetes mellitus. Enlargement of visceral adipose tissue depots determines a worse evolution for those complaints. Drugs as angiotensin converting enzyme inhibitors (ACEI), thiazolidinediones (glitazones) or angiotensin-II receptor antagonists, generally associated with the adequate hypolipidemic (statins, fibrates) or antiobesity (orlistat, sibutramine, rimonabant) medication, would increase those adipocytokines with anti-inflammatory and insulin-sensitizing properties (i.e. adiponectin or visfatin), while reducing pro-inflammatory and thrombogenic cytokines (as leptin, tumor necrosis factor [TNF]-alpha, plasminogen activator inhibitor 1 [PAI-1]). Thus, these pharmacologic therapeutic approaches would have a beneficial effect in order to diminish morbidity-mortality and improve the prognosis of patients with said diseases, all of them related to high cardiovascular risk.
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PMID:[Adipocytokines: implications in the prognosis and drug treatment of cardiovascular diseases]. 1845 36

Dyslipidemia, and inflammatory markers: high-sensitivity C-reactive protein (hs-CRP), myeloperoxidase (MPO), lipoprotein associated phospholipase A2(Lp-PLA2), and lipid peroxides (LP) are insufficient to predict the onset, extent, and prognosis of CHD. Lipoxins (LXs), resolvins, and protectins are derived from omega-3 fatty acids: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and omega-6 arachidonic acid in the presence of aspirin; whereas nitrolipids are formed due to the interaction between polyunsaturated fatty acids and nitric oxide (NO). LXs, resolvins, protectins, and nitrolipids are endogenous anti-inflammatory lipid molecules that inhibit production of interleukin-6 (IL-6) and tumor necrosis factor- alpha (TNF-alpha), suppress free radical generation, enhance NO generation; and accelerate tissue repair. Thus, beneficial actions of EPA/DHA and aspirin in CHD could be attributed to the formation of LXs, resolvins, protectins, and nitrolipids and suggest that their plasma levels aid in the prediction and prognosis of CHD.
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PMID:Can endogenous lipid molecules serve as predictors and prognostic markers of coronary heart disease? 1848 92

The metabolic syndrome (MetS) is associated with an increased incidence of diabetes and coronary heart disease. Postprandial lipemia is a prominent feature of dyslipidemia in both type 2 diabetes mellitus and MetS and is also associated with coronary heart disease. Oxidative stress and inflammation are pivotal in all stages of atherosclerosis; however, there is a paucity of data on postprandial oxidative stress and inflammation in subjects with MetS. Thus, the primary aim of this study was to compare the postprandial effects of an energy-dense, high-fat, fast-food-style (FFS) meal with an American Heart Association (AHA)-recommended heart-healthy meal on biomarkers of oxidative stress and inflammation in subjects with MetS. A total of 11 subjects with MetS completed the study. Glucose levels were significantly increased 2 hours after both FFS and AHA diets (P < .0001), and high-density lipoprotein cholesterol levels significantly decreased in FFS diet but not in the AHA diet (P for interaction < .05). Total triglyceride levels significantly increased postprandially only in the FFS meal but not in the AHA meal (P for interaction = .03). Plasma thiobarbituric acid reactive substances and malondialdehyde + hydroxynonenal increased significantly with time in both dietary groups, and the postprandial increase was greater in the FFS diet compared to the AHA diet (P < .0005). Serum high-sensitivity C-reactive protein, interleukin 6, and tumor necrosis factor levels did not change with time or dietary treatment. The postprandial increase in interleukin 1b was significantly higher with the FFS meal, thus resulting in significant differences between both treatments (P for interaction = .03). Thus, in subjects with MetS, consumption of an energy-dense, fatty meal (FFS breakfast) results in increased postprandial oxidative stress compared to a heart-healthy meal (AHA).
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PMID:High-fat, energy-dense, fast-food-style breakfast results in an increase in oxidative stress in metabolic syndrome. 1850 72


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