Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0154251 (lipid disorder)
 795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Women are affected by disorders of lipid metabolism in the same way as men. Sex steroids given as oral contraceptives at all doses have clearcut, formulation-specific effects on lipoprotein levels in reproductive-aged women. In estrogen-dominant versus androgenic progestin-dominant formulations, LDL cholesterol levels were unchanged and significantly increased, respectively, and HDL cholesterol was increased and decreased, respectively. The greatest HDL lowering is seen with the most androgenic formulations. Major increases in LDL cholesterol confer risk for cardiovascular disease on this group, so caution is recommended in formulation selection. In general, cardiovascular disease risk in post menopausal women using estrogen is reduced 30 to 70%. Concurrent administration of progestin with post menopausal estrogen appears to reduce the beneficial rise in HDL associated with estrogen administration alone. Cardiovascular disease is likely to be reduced by estrogen in post menopausal women.
Can J Cardiol 1990 May
PMID:Effects of sex steroid hormones on lipoprotein levels in pre- and post menopausal women. 218 17

Hereditary factors play an important role in the etiology and progression of coronary heart disease (CHD), most probably by causing the appearance and the levels of its risk factors. To investigate if there is a correlation between familial hypercholesterolemia and HLA system antigens, 25 subjects of 7 families with familial hypercholesterolemia were compared with 14 normocholesterolemic related subjects. Compared to normocholesterolemic kindreds, the familial hypercholesterolemic subjects have a significant increased HLA-Bw35 antigen and a lack of HLA-A1. Therefore, the correlation found with some HLA system phenotypes improves our knowledge about familial hypercholesterolemia and aids in the identification of subjects affected with this disorder of lipid metabolism, which is one of the most important CHD risk factors.
Clin Cardiol 1986 Apr
PMID:Familial hypercholesterolemia and HLA antigens. 372 44

Familial hypercholesterolemia (FH) is the genetic lipid disorder with a higher risk to develop coronary heart disease (CHD). In the heterozygous patients there are, however, variability in the atherosclerosis age of onset and severity. In recent years, it has been reported elevated levels of Lp(a) in FH, and it is proposed that this lipoprotein contributes to the development of CHD in these patients. This study evaluates the relationship between Lp(a) levels and the presence of CHD in FH. We included 38 patients with heterozygous FH with or without CHD (13 and 25 respectively), and a control group. In comparison to the control group, FH patients had significant elevated levels of Lp(a) (median 8.1 vs 16 mg/dL), and a greater prevalence of hyper Lp(a) (with a cut-off level of 30 mg/dL) (11.4 vs 25.7%). FH patients with CHD had higher levels of Lp(a) than those without CHD (22.8 vs 14.4 mg/dL). A significative negative correlation between age of onset of CHD and Lp(a) levels was found in females. CHD in FH was associated with male gender, older age, higher prevalence of hypertension, higher waist/hip ratios, higher levels of triglycerides and prevalence of hypertriglyceridemia. Our findings suggest that Lp(a) may play a role as an additional risk factor to develop atherosclerosis in FH.
Arch Inst Cardiol Mex
PMID:[Lipoprotein(a) in heterozygote familial hypercholesterolemia]. 772 91

Atherosclerosis is a major cause of death and disability in adults. Recent investigations suggest that although cardiac end-points such as myocardial infarction and strokes mainly occur in middle-age and older subjects, the pathological basis for atherosclerosis begins in childhood. Hypercholesterolemia is one of the most important risk factors for atherosclerosis in adults and elevated cholesterol in children is associated with sub-clinical deposition of lipids in the aorta and coronary arteries. This report summarizes an approach to the diagnosis and treatment of hyperlipidemia in children. Based on guidelines from the National Cholesterol Education Program, children over 2 years of age should be screened for hypercholesterolemia if there is a family history of premature heart disease or hyperlipidemia. Therapy must be individualized. The majority of children with hyperlipidemia should be managed with a low-saturated fat and low-cholesterol diet. Children over 10 years of age with severe elevations of LDL-cholesterol and who come from high-risk families may be considered for more aggressive dietary therapy or medication in some cases. This is especially true for children with inherited disorders of lipid metabolism such as LDL-receptor deficiency. By identifying high-risk children and instituting therapy during childhood it is hoped that premature onset of adult coronary heart disease can be delayed or avoided altogether.
Prog Pediatr Cardiol 2001 Jan
PMID:Management of hyperlipidemia in children. 1122 49

Although molecular cardiology is a relative young discipline, the impact of the new techniques on diagnosis and therapy in cardiovascular disease are extensive. Our insight into pathophysiological mechanisms is rapidly expanding and is changing our understanding of cardiovascular disease radically and irrevocably. Molecular cardiology has many different aspects. In this paper the importance of molecular cardiology and genetics for every day clinical practice are briefly outlined. It is expected that in the genetic predisposition for atherosclerotic disease multiple genes are involved (genetics). The role of only a minority of genes involved in the atherosclerotic process is known. Far less is known about particular gene-gene and gene-environment interactions. In some families disease can be explained mostly by a single, major gene (monogenic), of which the lipid disorder Familial Hypercholesterolemia is an example. In other cases, one or several variations in minor genes (multigenic) contribute to an atherosclerotic predisposition, for instance the lipoprotein lipase gene. Although mutations in this gene influence lipoprotein levels, disease development is predominantly depending on environmental influences. Recently several additional genetic risk factors were identified including elevated levels of lipoprotein (a) [Lp(a)], the DD genotype of angiotensin converting enzyme (ACE), and elevated levels of homocysteine. This illustrates the complexity of genetics in relation to atherosclerosis and the difficulty to assign predictive values to separate genetic risk factors. Furthermore, little attention has been given to protective genes thus far, explaining why some high risk patients are protected from vascular disease. Genetics based treatment or elimination of the genetic risk factor requires complete understanding of the pathogenic molecular basis. Once this requirement is fulfilled, disease management can be strived for, provided that adequate medical management is available. Recent studies suggest that such treatment should be genotype specific, as the genetic makeup can determine the outcome of a pharmacological intervention (pharmacogenetics). Once the trigger for atherosclerosis has initiated disease development, various genes are activated or silenced and contribute to lesion progression. Every stage of lesion development depends on a different gene expression programme (genomics). In this review paper an introduction is provided into genetics, pharmacogenetics and gene expression with respect to atherosclerotic disease.
Int J Cardiol
PMID:Molecular genetics and gene expression in atherosclerosis. 1157 98

Atherosclerosis is currently considered a chronic inflammatory disease combined with a disorder of lipid metabolism and deposition. Risk factors for coronary disease, as well as circulating cytokines, are involved in endothelial activation, leading to an adhesive and dysfunctional endothelium. The CD40 receptor (CD40) and its counterpart, the CD40 ligand (CD40L/CD154), were originally found to regulate T cell-dependent B cell differentiation. Meanwhile, several studies clearly demonstrate that the CD40/CD40L system plays an important role not only in cellular immunity and inflammation, but also in the pathophysiology of atherosclerosis. This is evidenced by the finding that inhibition of CD40/CD40L interaction prevents atherogenesis in animal models. Thus, the regulation of proatherogenic factors including CD40L may provide novel therapeutic options to treat inflammatory disorders such as atherosclerosis.
Can J Cardiol 2004 May 15
PMID:CD40 and vascular inflammation. 1519 19

We tested the hypothesis that gemfibrozil has a differential effect on low-density lipoprotein (LDL) and high-density lipoprotein (HDL) subclass distributions and postprandial lipemia that is different in subjects classified as having LDL subclass pattern A or LDL pattern B who do not have a classic lipid disorder. Forty-three normolipemic subjects were randomized to gemfibrozil (1,200 mg/day) or placebo for 12 weeks. Lipids and lipoproteins were determined by enzymatic methods. The mass concentrations of lipoproteins in plasma were determined by analytic ultracentrifugation and included the S(f) intervals: 20 to 400 (very LDL), 12 to 20 (intermediate-density lipoprotein), 0 to 12 (LDL), and HDL(2) mass (F(1.20) 3.5 to 9.0) and HDL(3) mass (F(1.20) 0 to 3.5). Postprandial measurements of triglycerides and lipoprotein(a) were taken after the patients consumed a 500 kcal/M(2) test meal. Treatment with gemfibrozil, compared with placebo, significantly reduced fasting plasma triglycerides (difference from placebo +/- SE; -50.2 +/- 20.6 mg/dl, p = 0.02), total cholesterol (-16.4 +/- 7.5 mg/dl, p = 0.04), apolipoprotein B (-16.1 +/- 5.5 mg/dl, p = 0.006), very LDL mass of S(f) 20 to 400 (-50.8 +/- 24.1 mg/dl, p = 0.02), S(f) 20 to 60 (-17.5 +/- 8.5 mg/dl, p = 0.05), S(f) 60 to 100 (-16.2 +/- 8.1 mg/dl, p = 0.05), and increased peak S(F) (0.48 +/- 0.27 Svedberg, p = 0.08). Gemfibrozil reduced the postprandial triglyceride level significantly at 3 (p = 0.04) and 4 (p = 0.05) hours after the test meal. A significantly different subclass response to gemfibrozil was observed in those with LDL pattern A versus B. Those with LDL pattern B had a significantly greater reduction in the small LDL mass S(f) 0 to 7 (p = 0.04), specifically regions S(f) 0 to 3 (p = 0.009) and S(f) 3 to 5 (p = 0.009). In conclusion, normolipemic subjects with either predominantly dense or buoyant LDL respond differently to gemfibrozil as determined by the changes in LDL subclass distribution. Thus, treatment with gemfibrozil may have additional antiatherogenic effects in those with LDL pattern B by decreasing small dense LDL that is not apparent in those with pattern A.
Am J Cardiol 2005 Nov 01
PMID:Gemfibrozil reduces small low-density lipoprotein more in normolipemic subjects classified as low-density lipoprotein pattern B compared with pattern A. 1625 95

Five lines of evidence justify comprehensive lipoprotein management over aggressive low-density lipoprotein (LDL) lowering alone in most cases of cardiovascular disease (CVD) prevention. First, lipoprotein lipid transport consists of a single, recycling system involving very-low-density lipoprotein, LDL, and high-density lipoprotein (HDL). Single lipid interventions affect all lipoprotein classes to varying degrees. These effects can be expanded by using different drug classes in combination. Second, observational studies support the unitary nature of lipoprotein risk. A family of curves describes increasing CVD risk from increasing LDL as other risk factors are present. Conversely, a family of curves describes increasing CVD risk from decreasing levels of HDL in mirror image to LDL. The LDL and HDL risks are additive. Third, clinical trials that raise HDL and lower triglyceride ameliorate CVD, as does lowering LDL. Lowering LDL prevents heart disease, but by only 22%-36% with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor therapy. Studies indicate that better CVD prevention is obtained when drugs for triglyceride and HDL reduction are combined with LDL reduction. Fourth, HDL and its apolipoprotein (apo), apo A-I, as well as apo A-I analogues, decrease atherosclerosis. Each modality decreases atherosclerosis in animal models, and apo A-I Milano acutely decreases human coronary luminal stenosis. Apo A-I analogues have similar promise. Fifth, combined hyperlipidemia is the most common lipid disorder, has the strongest risk for CVD, and combines elevated LDL, hypertriglyceridemia, and low HDL. This condition requires the comprehensive treatment approach described above. In conclusion, 5 lines of evidence justify comprehensive diet and drug treatment for combined hyperlipidemia and, at lesser LDL elevations, the atherogenic dyslipidemias of obesity, diabetes mellitus, and the metabolic syndrome.
Am J Cardiol 2008 Apr 17
PMID:Comprehensive lipid management versus aggressive low-density lipoprotein lowering to reduce cardiovascular risk. 1837 42

Accumulation of lipids inside the cell is primarily caused by disorders of lipid metabolism. S-adenosylmethionine synthetase (SAMS) produces SAM, an important methyl donor in various phospholipid methyltransferase reactions catalysed by phosphoethanolamine N-methyltransferase (PMT-1). A gel-based, quantitative proteomic analysis of the RNA interference (RNAi)-mediated inactivation of the pod-2 gene, which encodes acetyl-CoA carboxylase, showed a substantial down-regulation of SAMS-1. Consequently, RNAi of either sams-1 or pmt-1 caused a significant increase in lipid droplet size in the intestine of Caenorhabditis elegans. Lipid droplets exhibited increased triacylglycerol (TG) and decreased phosphatidylcholine (PC) levels, suggesting a reciprocal relationship between TG and PC regulation. These lipid-associated phenotypes were rescued by choline feeding. Among the five fat metabolism-related genes examined, two genes were highly induced by inactivation of sams-1 or pmt-1: pod-2 and stearoyl-CoA desaturase (fat-7). Thus, both SAMS-1 and PMT-1 were shown to contribute to the homoeostasis of TG and PC levels in C. elegans, which would provide an important survival strategy under harsh environmental conditions.
 ...
PMID:Contribution of sams-1 and pmt-1 to lipid homoeostasis in adult Caenorhabditis elegans. 2138 45

We evaluated preventive cardiology education in United States cardiology fellowship programs and their adherence to Core Cardiovascular Training Symposium training guidelines, which recommend 1 month of training, faculty with expertise, and clinical experience in cardiac rehabilitation, lipid disorder management, and diabetes management as a part of the prevention curricula. We sent an anonymous survey to United States cardiology program directors and their chief fellow. The survey assessed the program curricula, rotation structure, faculty expertise, obstacles, and recommended improvements. The results revealed that 24% of surveyed programs met the Core Cardiovascular Training Symposium guidelines with a dedicated 1-month rotation in preventive cardiology, 24% had no formalized training in preventive cardiology, and 30% had no faculty with expertise in preventive cardiology, which correlated with fewer rotations in prevention than those with specialized faculty (p = 0.009). Fellows rotated though the following experiences (% of programs): cardiac rehabilitation, 71%; lipid management, 37%; hypertension, 15%; diabetes, 7%; weight management/obesity, 6%; cardiac nutrition, 6%; and smoking cessation, 5%. The program directors cited "lack of time" as the greatest obstacle to providing preventive cardiology training and the chief fellows reported "lack of a developed curriculum" (p = 0.01). The most recommended improvement was for the American College of Cardiology to develop a web-based curriculum/module. In conclusion, most surveyed United States cardiology training programs currently do not adhere to basic preventive cardiovascular medicine Core Cardiovascular Training Symposium recommendations. Additional attention to developing curricular content and structure, including the creation of an American College of Cardiology on-line knowledge module might improve fellowship training in preventive cardiology.
Am J Cardiol 2012 Jul 01
PMID:Current status of preventive cardiology training among United States cardiology fellowships and comparison to training guidelines. 2248 64


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