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)

A major factor contributing to cardiovascular mortality in type 2 diabetes is dyslipidemia, characterized by low HDL cholesterol and high triglycerides, rather than elevated LDL cholesterol. Lipoprotein lipase (LPL) is the rate-limiting enzyme of triglyceride removal from plasma and has been implicated in atherosclerosis. Since treatment with statins significantly reduces cardiovascular morbidity in diabetes, we analyzed the lipid profile and LPL activities in 61 patients with type 2 diabetes before and 8 weeks after initiation of atorvastatin (40 mg) or placebo treatment. Lipid parameters and LPL activity were unchanged under treatment with placebo. Atorvastatin treatment resulted in a 30% reduction of total and a 45% reduction of LDL cholesterol (6.06 +/- 1.39 mmol/L versus 4.14 +/- 1.27 mmol/L and 4.11 +/- 1.13 mmol/L versus 2.27 +/- 0.89 mmol/L, both P < 0.0001). Triglycerides and VLDL cholesterol were also significantly reduced by statin therapy (2.24 +/- 2.11 mmol/L versus 1.82 +/- 1.46 mmol/L and 1.08 +/- 1.56 mmol/L versus 0.67 +/- 0.66 mmol/L, both P < 0.05). HDL cholesterol was not different between the atorvastatin and the placebo group. Compared to baseline, LPL activity was increased by 25% after atorvastatin treatment (213.0 +/- 28.1 nmol/mL/min versus 171.9 +/- 17.7 nmol/mL/min, P < 0.01). Our data demonstrate that atorvastatin induces a significant improvement of diabetic dyslipidemia and a significant increase of LPL activity. Since low LPL activity indicates an increased cardiovascular risk, the statin-mediated increase in LPL activity may help to explain the reduction of CAD in diabetic patients treated with statins.
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PMID:Atorvastatin improves diabetic dyslipidemia and increases lipoprotein lipase activity in vivo. 1526 89

Prolongation of human life span is considered a tremendous achievement of modern medical sciences. However, it implies simultaneously a quite new challenge relevant to health problems of getting older populations. For elderly people, intensification of physical activity constitutes not only a component of great importance for maintaining a good-quality life, but also for prevention of cardiovascular diseases. The paper presents the state of art of physical training features in relation to physiologic aging processes. Specificity of risk factors of cardiovascular diseases in the elderly, i.e., arterial hypertension, diabetes mellitus, dyslipidemia and obesity, was also discussed. The review of data indicating a beneficial effect of intensified physical activity, both in primary and secondary prevention of CAD in the old population, which is at the highest risk of cardiovascular diseases occurrence, was displayed, either. Finally, some problems and shortcomings encountered in every-day medical practice in the field of introducing and performing cardiac rehabilitation in elderly people were emphasized.
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PMID:[Physical activity as component of cardiovascular disease prevention in elderly people]. 1747 91

The aim of our work was to develop an assay for the determination of angiopoietin-like protein 3 (Angptl3) in human blood, and investigate its levels in healthy volunteers and donors suffer from metabolic syndrome and familiar hypercholesterolemia. We developed and evaluated the sandwich ELISA method for the quantitative determination of human Angptl3 in serum samples. We conducted also the pilot study on individuals with metabolic syndrome or familiar hypercholesterolemia and healthy probands. The following parameters were measured: blood pressure, waist circumference, Angptl3 serum levels, serum cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, insulin, glucose, A-FABP, and BMI and Quicki insulin sensitivity index was calculated. In the study on 93 healthy volunteers we demonstrated that sex or age is not the determinant for Angptl3 serum values. Futhermore, 118 individuals with metabolic syndrome and 200 patients with familiar hypercholesterolemia were tested and it was found that probands with metabolic syndrome or familiar hypercholesterolemia had higher Angptl3 values than healthy individuals from the first study (medians 289.5 vs. 277.1 vs. 224.8 ng/ml, p < 0.01). All of groups did not differ in sex or age. Angptl3 values correlated with the systolic blood pressure, LDL and A-FABP (p < 0.05). No connection of Angptl3 with triglycerides was found (presumably influences of statins, fibrates via PPARs, etc). However, we performed stepwise regression and found A-FABP and Angptl3 serum values as the independent markers for metabolic syndrome presence only (F ratio 29, p < 0.01). Then we adjusted Angptl3 to A-FABP (reputable metabolic syndrome marker) and recognised that Angptl3 is the A-FABP-independent marker. The pilot study supports the hypothesis about the role of Angptl3 as a new class of lipid metabolism modulator. Their values could be a new key predictors of metabolic syndrome. Further research is necessary to confirm our findings in individuals with dyslipidemia, obesity, CAD and different medication in order to assess Angptl3 value as a risk predictor of accelerated atherosclerosis.
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PMID:Angiopoietin-like protein 3: development, analytical characterization, and clinical testing of a new ELISA. 1806 51

Recent research has demonstrated a strong genetic linkage between premature coronary artery disease (pCAD) and dyslipidemia. Genetic variation in lipid metabolism can lead to impediment of lipid anabolism and catabolism, which promotes vascular arterosclerogenesis. Currently, related studies were focused on: (1) Gene mutations related to low density lipoprotein metabolism, such as low density lipoprotein receptor, apolipoprotein B, apolipoprotein E; (2) Gene mutations related to high density lipoprotein metabolism-related genes, such as ATP binding cassette transporter, apolipoprotein A1, lipoprotein lipase; (3) low density lipoprotein receptor-related genes: Adiponectin. These genes had been proved to be cor-related with pCAD. Mutations of these genes can lead to series of genetic disease characterized by pCAD. This review gives a brief summary of the roles of these genes played in the initiation and development of pCAD, providing valuable information to primer prevention and individualized treatment of CAD.
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PMID:[Research progress on the association between genetic variations in lipid metabolism and premature coronary artery disease]. 1855 Apr 87

The cardiovascular disease continuum is a sequence of events, which begins with a host of risk factors consisting of diabetes mellitus, dyslipidemia, hypertension, smoking and visceral obesity. If left untreated, it will inexorably progress to atherosclerosis, CAD, myocardial infarction, left ventricular remodeling, LVH, left ventricular enlargement, and eventually end-stage heart failure and death. Treatment intervention at any stage of its course will prevent or delay its further progression. However, the best results are expected to be achieved when treatment is initiated at the beginning, or at an early stage of its course. A Pub-Med/MEDLINE search was conducted for relevant English language, randomized clinical trials and epidemiologic studies for the years 1995-2009 using the terms, cardiovascular continuum, obesity, hyperlipidemia, diabetes mellitus, hypertension, metabolic syndrome, renal disease, stroke, and blockers of the renin angiotensin system (RAS). A total of 34 pertinent studies were selected for review. This concise review will focus on prevention and the aggressive treatment of the existing cardiovascular risk factors with emphasis on the blockers of RAS, and demonstrate that RAS blockers are the best drugs for its treatment.
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PMID:The treatment of cardiovascular disease continuum: focus on prevention and RAS blockade. 2015 54

Metabolic complications common to the HIV-positive population may increase the risk for cardiovascular disease. Asymptomatic peripheral arterial disease (PAD) is associated with increased cardiovascular risk. The ankle-brachial pressure index (ABI) is a screening tool commonly used for the detection of asymptomatic PAD. The prevalence of asymptomatic PAD based on ABI in HIV-positive patients is unknown. This study was cross-sectional in design and assessed PAD by measuring the systolic ABI as determined by a handheld 8-MHz Doppler probe with the patient at rest in a supine position. A brief medical history including pertinent risk factors was obtained. One hundred and sixty-seven HIV-positive patients were evaluated (97.6% male; mean age 52.0 years; 31.2% current smokers, 29.4% former smokers, 26.3% diabetes mellitus). Asymptomatic PAD (ABI < or = 0.9) was found in four patients (2.4%, 95% CI: 0.3-4.5%). Smoking was a significant predictor of PAD. Patients with a positive test for PAD had at least two major risk factors for the disease including smoking, a history of disease in another vascular bed, dyslipidemia, diabetes, and hypertension. All patients with a positive test for PAD had a high risk (>20%) for cardiovascular disease according to the Framingham risk score. Three of the four patients with positive tests had previously diagnosed vascular disease (CAD, stroke). Three patients presenting with PAD were evaluated and all had a positive ABI. The prevalence of PAD compared to previous studies on PAD in HIV was low and identified only those patients with high cardiovascular risk based on other features. ABI was not useful in detecting occult vascular disease in HIV-positive patients and offers no additional information to that derived from cardiovascular risk stratification.
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PMID:Ankle brachial index screening for occult vascular disease is not useful in HIV-positive patients. 2071 28

Lipoprotein lipase (LPL) plays a central role in dyslipidemia and development of metabolic syndrome. The occurrence of polymorphisms of the LPL gene may result in the disturbance in the lipid metabolism and pathogenesis of CAD. Carriers of X447 allele were reported to have lower triglyceride and higher high-density lipoprotein cholesterol levels as well as a reduced risk of CAD. The patiens with hypertriglicerydemia are carriers of common PLP mutations as Asp9Asn,Asn291Ser, Trp86Arg, Gly188Glu, Pro207Leu, and Asp250Asn. LPL is an interesting enzyme that contributes in a pronounced way to normal metabolism, including insulin action, body weight regulation, energy balance, and atherosclerosis. In this rewiev, the roles of polymorphism LPL and their implications in the control of lipoprotein metabolism and atherosclerosis are discussed, especially in the group of risk developing metabolic syndrome - children with low birth weight (below 2500 g).
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PMID:[Polymorphisms of lipoprotein lipase gene and their participation in metabolic processes]. 2172 17

Management of ischemic heart disease in pregnant women is still difficult, as there is little experience with many of the newer treatments such as clopidogrel. The safety of clopidogrel in pregnancy is unknown, especially in combination with aspirin. Its use during gestation has been described in a few case reports. We describe the case of a 36-year-old woman in her 9th week of pregnancy with a history of chronic hypertension, dyslipidemia and CAD, who required antiplatelet treatment. Clopidogrel and aspirin were administrated until one week before delivery and a healthy child was born at 36 weeks of pregnancy by caesarean section, without any complication.
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PMID:Clopidogrel treatment during pregnancy: a case report and a review of literature. 2184 43

Genetic polymorphism of the endothelial nitric oxide synthase (eNOS) affects the pathogenesis of atherosclerosis and associated with premature coronary artery disease (PCAD). We aimed to explore the association between Glu298Asp polymorphism of the eNOS gene and premature CAD in Egyptians, and the possible interaction between this polymorphism and other risk factors. The study population consisted of 116 patients with PCAD, and 119 controls. Glu298Asp polymorphism (rs1799983) of the eNOS gene was analyzed by polymerase chain reaction (PCR). We found that the TT genotype of the eNOS gene increased the risk of PCAD by 2.6. Hypertension, diabetes, smoking, total cholesterol, triglycerides, LDLc, HDLc and TT genotype of the eNOS gene were independent risk factors for the development of PCAD. We conclude that, the TT genotype of Glu298Asp polymorphism of eNOS gene is an independent risk factor of PCAD in Egyptians. The association of smoking, obesity, dyslipidemia and/or metabolic syndrome with the TT genotype increased the risk of the development of PCAD.
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PMID:Association of endothelial nitric oxide synthase gene polymorphisms with classical risk factors in development of premature coronary artery disease. 2326 19

Hypertriglyceridemia is defined as an abnormal concentration of triglyceride in the blood and has been associated with atherosclerosis, even in the absence of hypercholesterolemia. This case report is of 40-year-old man diagnosed to have hypertriglyceridemia who attended for routine screening in our diagnostic laboratory at Barasat. He was nonsmoker, non-alcoholic, had a reasonable diet with abundant fruits and vegetables, and was on regular exercise. He was not taking any lipid lowering medications. He hailed from Barasat, and was employed in Government sector in Barasat and policeman by profession. His father died at the age of 57 years in a heart attack; but his mother is healthy and now almost 62 years of age, and he has two brothers one elder and another younger to him, both are healthy. His blood pressure was normal, his body-mass index was 27, and his waist circumference was 96 cm and hip circumference was 103. His waist/hip ratio was 0.932. The Biochemical analyses were as follows- Fasting Glucose: 186 mg/dL, Total Cholesterol: 90 mg/dL, Triglycerides: 372 mg/dL, High-density cholesterol: 3.80 mg/dL, Low-density cholesterol: 2.90 mg/dL, VLDL: 83.20 mg/dL, Cholesterol/HDL-C ratio: 23.6:1, LDL-C/HDL-C: 0.07:1. This study revealed the increased prevalence of dyslipidemia to be more prevalent in 31-40 year males, suggesting that this group is at an increased risk of developing CAD leading to young infarcts. Combination lifestyle therapies i.e., enhanced physical activity and dietary modification and therapeutic intervention would help us in the treatment and management of dyslipidemia.
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PMID:Hypertriglyceridemia: a case report from diagnostic laboratory, Barasat, West Bengal, India. 2356 86


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