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)

Extrarenal calcifications, particularly affecting the cardiovascular system, are common observations which can be a source of serious complications in patients with chronic renal disease, especially those on dialysis. In these patients, cardiovascular disease - myocardial infarction, arrhythmia, calcified valvulopathy, stroke, peripheral ischemic arteriopathy, calciphylaxy, etc. - is the leading cause of death (more than 50%). These complications are closely related to the presence of vascular calcifications (VC) which are much more frequent, severe, and progressive than in the general population. Previously, these calcifications were considered to arise via a passive process within the context of comorbid conditions without specific signs of gravity: high blood pressure, atherosclerosis, aging, diabetes, smoking, dyslipidemia, chronic micro-inflammation, hyperhomocysteinemia, disorders of calcium-phosphorus metabolism. It is now established that VC arise via a complex, probably regulated, active process analogous to the processes leading to bone formation and/or remodeling. New insight provided by a large body of work designed to ascertain the mechanisms underlying the onset of VC has enabled the development of new diagnostic and therapeutic approaches. It is now possible to identify factors clearly favoring the formation of VC: TNF-alpha (which stimulates cell necrosis/apoptosis), CRP, oxidized lipids, AGEs, leptin, inorganic phosphate, high calcium-phosphorus product (CaxPO(4)), calcium, 1,25-OH(2)D(3) and Vitamin D(3), PTHrP (via an intracrine pathway), cyclic AMP, TGF-beta, bone morphogenic protein 2 (BMP2) and factors protective against the formation of VC: magnesium, HDL, inorganic pyrophosphate, albumin, ahsg/fetuin A, osteopontin (OPN), osteoprotegerin (OPG), osteonectin (ON), bone morphogenic protein 7 (BMP7), klotho, PTHrP (via a paracrine pathway), matrix gla protein (MGP), PTH (via Msx2) and vitamin K. In conclusion, until recently, neglected disorders of calcium-phosphorus metabolism are currently recognized as the main actors in the process leading to vascular mediacalcosis in patients with chronic kidney failure.
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PMID:[Origin of the mediacalcosis in kidney failure]. 1934 26

Migraine with aura (MA) is associated with an increased risk of ischemic stroke, especially in young women with vascular risk factors (smoke, contraceptive pill). Patent foramen ovale (PFO) has also been associated with MA. We describe a 41-year-old man, in good health, with MA since 16, familiar history of diabetes, heavy smoker (30 cigarettes/day). Frequency (1-2 attacks/year) and clinical features of migraine have been unchanged since the onset. A few days before our examination he suffered a typical migraine attack. In the following hours, however, the headache became more and more throbbing and the aura symptoms (regressed as usual in 30 min) reappeared and persisted, so he went to an Emergency Department. The CT-scan (without contrast) was normal. The following days he had visual disturbances and spatial disorientation. We found a normal neurological examination and fundus oculi. He referred persisting visual troubles. We prescribed MR + angioMR which confirmed a migrainous infarction and ruled out others pathological conditions. Further tests found out dyslipidemia, hyperhomocysteinemia, impaired glucose tolerance. Transcranial Doppler showed right to left shunting. We also prescribed the screening tests for vasculitis (normal). In our opinion this case highlights the relevance of vascular risk factors in MA complications also in male subjects.
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PMID:Migrainous infarction: association with vascular risk factors in a male subject. 1941 47

Psoriasis is a chronic inflammatory, immune-mediated skin disease affecting 2 to 3% of the general population and may cause significant quality-of-life impairment. Psoriasis and psoriatic arthritis are associated with increased atherothrombotic diseases, including myocardial infarction, deep venous thrombosis, and reduced life span. Both disease-specific and non-disease-specific risk factors are likely to fuel one another in deleterious vicious circles. Disease-specific risk factors are those that are a direct consequence of psoriasis inflammation and include hyperhomocysteinemia, elevated C-reactive protein, elevated blood inflammatory cytokines, and platelet hyperactivity. Non-disease-specific risk factors include insulin resistance/diabetes, obesity, dyslipidemia, hypertension, metabolic syndrome, and habitual tobacco smoking. The presence of cardio-metabolic comorbidities has also relevant implication in the therapy and global approach to patients with psoriasis. Traditional systemic antipsoriatic agents frequently negatively affect cardio-metabolic comorbidities and may have important interactions with drugs commonly used by psoriasis patients. Thus, patients with psoriasis should be treated effectively and encouraged to aggressively correct their modifiable cardiovascular risk factors.
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PMID:Psoriasis and atherothrombotic diseases: disease-specific and non-disease-specific risk factors. 1945

When a decision has been reached to proceed with coronary bypass surgery, this represents a therapeutical option for a partnership between surgical revascularization and an optimized multifaceted medical treatment. We report the guidelines implemented in our department concerning the secondary prevention therapy after coronary bypass surgery. The antiplatelet therapy (and its association with coumadin), the bradycardizing treatments (with a special reference to the approach of unappropriate sinus tachycardia), the specific anti-ischemic therapy, the treatment of dyslipidemia, and the antihypertensive therapy are reviewed as well as the use of additional anti-atheromatous measures, the approach of hyperuricemia and hyperhomocysteinemia, and the oral antidiabetic treatment.
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PMID:[Cardiological medical treatment after coronary bypass surgery]. 1950 49

The higher mortality rate among rheumatoid arthritis (RA) patients in comparison with the general population is largely attributable to cardiovascular (CV) disease, particularly coronary atherosclerosis, but also non-fatal myocardial infarction and heart failure. It may be due to RA-specific risk factors such as hyperhomocysteinemia, disease-related dyslipidemia or vascular inflammation, or morbidity related to high levels of cytokines such as tumour necrosis factor (TNF) and RA medications. Non-steroidal anti-inflammatory drugs (NSAIDs) are among the most important in rheumatology, but many are associated with CV disease. A number of randomised control trials have shown that, although exposure to low doses of corticosteroids for 1-3years does not significantly increase CV risk, longer exposure can increase CV events. The use of disease-modifying antirheumatic drugs (DMARDs), particularly methotrexate, increases homocysteinemia, reduces inflammation and improves lipid profiles, thus reducing the development of atherosclerosis and clinically overt CVD. Although contraindicated in RA patients with severe heart failure, biological agents such as anti-TNF agents delay and even reverse the progression of endothelial dysfunction and atherosclerosis. Tocilizumab leads to changes in lipid profiles without increasing adverse vascular events. The effects on the CV system depend on the drug itself, the dose and the period of exposure, and so CV risk should be evaluated before starting treatment with any drug.
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PMID:The effect of pharmacological therapy on the cardiovascular system of patients with systemic rheumatic diseases. 2067 92

Retinal vein occlusion (RVO) is a disease that is often associated with a variety of systemic disorders including arterial hypertension, diabetes mellitus, dyslipidemia and systemic vasculitis. There are various types of RVO, categorized on the basis of the site of occlusion and on the type of consequent vascular damage. Central retinal vein occlusion (CRVO) is the most clinically relevant type of RVO. In addition to well-known classical risk factors, new thrombophilic factors have been investigated in patients with RVO. Data concerning a number of the parameters remain contradictory; yet, hyperhomocysteinemia and vitamins involved in methionine metabolism appear to play a significant role in the pathogenesis of this disease. Alterations in the fibrinolysis pathway (elevated levels of PAI-1 and Lipoprotein (a)), together with haemorheologic modifications have been recently consistently associated with the disease. Medical treatment includes identification and correction of vascular risk factors. In addition, LMWHs appear to be the best therapeutic approach even if based on a limited number of trials, conducted on a limited number of patients. No data are available on the possible role of antithrombotic strategies in the long-term prevention of recurrent RVO or vascular events.
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PMID:Retinal vein occlusions: a review for the internist. 2159 Apr 40

Much of the decline in stroke incidence and mortality for the past several decades in Western countries has been attributed to better treatment of risk factors. Many epidemiological studies and clinical trials confirmed the importance of managing hypertension. Comparative trials of anti-hypertensive drugs or drug classes have not yielded clear results, but blood pressure variability may play an important role beyond the absolute value of blood pressure. Diabetes therapy remains a conundrum. Although diabetes is clearly a risk factor for ischemic stroke, treatment trials targeting different glycemic goals have not indicated that glucose lowering results in stroke prevention. Trials focused on insulin resistance are ongoing and they may be able to help establish the management of diabetes/impaired glucose tolerance. Evidence for treatment of dyslipidemia has contrasted science to diabetes mellitus. Dyslipidemia has not been strongly or consistently linked to ischemic stroke but the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial showed the impact of statin treatment in stroke prevention. The results of clinical trials investigating dabigatran and rivaroxaban clearly indicate alternative strategies to vitamin K antagonists in stroke prevention for persons with atrial fibrillation. Evidence for stroke prevention by life style modification, treating metabolic syndrome, sleep disordered breathing, lipoprotein (a), hyperhomocysteinemia, and coagulation disorders are also discussed.
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PMID:Treatment of risk factors to prevent stroke. 2171 92

Homocysteine, a sulfur-containing amino acid formed during the metabolism of methionine, exert cytotoxic effects on vascular endothelium. Molecular mechanisms of homocysteine-induced cellular dysfunction include increased inflammatory cytokine expression, altered nitric oxide bioavailability, induction of oxidative stress, activation of apoptosis and defective methylation. Hyperhomocysteinemia is associated with an increased risk of atherosclerotic and thromboembolic disorders, as well as hyperinsulinemia and may partially account for increased risk of cardiovascular disease associated with insulin resistance. Women with PCOS are more likely to develop components of the metabolic syndrome such as disturbances of carbohydrate metabolism, obesity, hypertension and dyslipidemia, which in turn are risk factors for cardiovascular disease. A number of studies confirmed the presence of increased serum homocysteine concentration in PCOS patients and the possible determinants of this observation are still debated. PCOS treatment options can influence homocysteine levels.
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PMID:Homocysteine metabolism in polycystic ovary syndrome. 2179 5

Atherosclerosis, a pathological process that underlies the development of cardiovascular disease, is the primary cause of morbidity and mortality in patients with type 2 diabetes mellitus (T2DM). T2DM is characterized by hyperglycemia and insulin resistance (IR), in which target tissues fail to respond to insulin. Systemic IR is associated with impaired insulin signaling in the metabolic tissues and vasculature. Insulin receptor is highly expressed in the liver, muscle, pancreas, and adipose tissue. It is also expressed in vascular cells. It has been suggested that insulin signaling in vascular cells regulates cell proliferation and vascular function. In this review, we discuss the association between IR, metabolic stress, and atherosclerosis with focus on 1) tissue and cell distribution of insulin receptor and its differential signaling transduction and 2) potential mechanism of insulin signaling impairment and its role in the development of atherosclerosis and vascular function in metabolic disorders including hyperglycemia, hypertension, dyslipidemia, and hyperhomocysteinemia. We propose that insulin signaling impairment is the foremost biochemical mechanism underlying increased cardiovascular morbidity and mortality in atherosclerosis, T2DM, and metabolic syndrome.
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PMID:Insulin resistance, metabolic stress, and atherosclerosis. 2220 99

Psoriasis is a chronic inflammatory skin condition with an increased risk of cardiovascular disease. This risk has been attributed to an association with many independent risk factors including obesity, hypertension, smoking, and dyslipidemia. Psoriasis patients also have lower levels of folate and conversely higher levels of homocysteine, which in itself is a risk factor for cardiovascular disease. It has been postulated that low folate levels in this group may be a direct cause of hyperhomocysteinemia and therefore a treatable risk factor by folate supplementation. This paper looks at the literature published to date on the relationship between psoriasis, homocysteine, and folate levels.
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PMID:A review of psoriasis, a known risk factor for cardiovascular disease and its impact on folate and homocysteine metabolism. 2269 Mar 30


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