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)

Essential arterial hypertension often predisposes patients to prothrombotic state and increased risk of vascular and organ complications. Vital role in regulation of hemostatic processes is played by genetic factors, renin-angiotensin system and disorders of lipid metabolism. Prime genetic factors involved in the process are 4G/5G polymorphism of promoter region coding tissue plasminogen activator inhibitor-1 (PAI-1) and I/D polymorphism for angiotensin converting enzyme (ACE) gene. The aim of work was the evaluation of alterations within fibrinolysis system (estimation of t-PA and PAI-1 levels), fibrinogen concentration (Fb) and ACE activity with regard to co-existent dyslipidemia and features of left ventricle hypertrophy (LVH). Moreover the analysis of influence of 4G/5G PAI and I/D ACE gene polymorphism on intensification of aforementioned alterations among hypertensive patients was performed. Research was carried out in 170 subjects under 40 years old, in two study groups, HT-- hypertensive group--125 patients with previously untreated hypertension without clinical features of ischaemic heart disease and NT--45 normotensive, healthy subjects. HT group has been further divided into four subgroups: DLP (dyslipidemic, n = 51), NLP (normolipidemic n = 74), LVH+ (with features of left ventricle hypertrophy, n = 35), LVH (-) (without features of left ventricle hypertrophy, n = 90). In a whole HT group significantly higher levels of PAI-1, t-PA and Fb were noted in comparison to NT group, considerably more pronounced within DLP rather than NLP subgroups. Moreover, pronounced increase in ACE activity was recorded in DLP and LVH+ subgroups. It has been proved that 4G/4G homozygous subjects of 4G/5G PAI-1 gene polymorphism from HT group tend to present higher levels of PAI-1 and t-PA if contrasted to 4G/4G genotype of NT group, with more distinct effect within DLP subgroup. Carriers of D allele (genotypes I/D, D/D) of I/D ACE gene polymorphism from HT group characterise with significantly higher activity of ACE in contrast to I/I genotype of HT group, with particularly marked effect in DLP and LVH+ subgroups. Basing on above mentioned results it may be concluded that essential hypertension (especially if complicated with dyslipidemia) impairs fibrinolysis, what might be related to renin-angiotensin system activation in lipid metabolism disorders. Deletion alleles of 4G/5G polymorphism (4G allele) and I/D polymorphism (D allele) in patients with hypertension independently modify fibrinolysis towards prothrombotic state with more distinct effect in dyslipidemia. Increased activity of ACE in D allele carriers may predispose to left ventricle hypertrophy.
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PMID:[Plasminogen activator inhibitor-1 (PAI-1) 4G/5G and angiotensin converting enzyme (ACE) I/D gene polymorphisms and fibrinolytic activity in patients with essential hypertension and dyslipidemia]. 1613 May 96

At present, literally no one disputes hyperlipoproteinaemia and dyslipidemia (HLP and DLP) treatment as a rational therapeutic approach in the prevention of cardiovascular diseases (CVD). This approach is in line with the current principles of evidence-based medicine (EBM) and is sufficiently evidenced particularly by the results of large intervention studies. Nevertheless! When the results of the recent studies are critically appraised, these by no means are (mostly, there, obviously, are exceptions) as conclusive as the studies conducted in 1980s and 1990s. Consequently, positive results are being sought in subanalyses, subgroup evaluations and multiple-study metaanalyses. This paper is not intended as a critique of new drugs. These certainly are developed to be safe, effective and well-tolerated. However, the newer studies suffer from a range of issues: the populations studied are already very well managed, it is not possible to compare against placebo and sometimes, let us be honest, the trial design itself is problematic (often it is an uncritical effort to treat as wide as possible range of patients as well as new groups of patients who might not be suitable for the given treatment). Certainly, we should not start disputing the well-evidenced hypotheses and seek alternatives to the long-established arguments and approaches as a consequence to some less convincing studies. We must not overlook the most robust results of statin studies as well as 'positive' studies with other hypolipidemics. There is no doubt that the effect ofstatins on LDL-cholesterol represents a significant move towards cardiovascular disease prevention. Despite this, we currently recognise with increased intensity that this very effective and well-evidenced treatment has its limits and that a high proportion of patients dies or are faced with cardiovascular diseases even though they are treated with a correct dose ofa statin and a target LDL-C level is achieved. This remaining risk (represents more than 50% ofevents) has been termed 'RESIDUAL RISK'. The issue of residual risk is crucial in patients with type 2 diabetes mellitus (DM2T) or in all patients with HDL-C-low DLP. As was repeatedly emphasised, a statin will be a cornerstone of pharmacological treatment of a DLP. However, a question arises what to combine it with. The most convincing data exist for niacin (combination of niacin with laropiprant minimising the incidence of unwanted flushes). We surely should not marginalize other hypolipidemics used mainly in combinations: resin and ezetimibe to treat LDL-C, niacin, fibrates and possibly omega-3-fatty acids to manage the residual risk (HDL and TG). Last but not least we should not forget non-pharmacological treatment as the pivotal treatment approach in all patients.
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PMID:[Hyperlipoproteinaemia and dyslipoproteinaemia II. Therapy: non-pharmacological and pharmacological approaches]. 2084 7

Cardiovascular diseases (CVD) represent a significant health problem in all countries world-wide and in the developed world, including the Czech Republic, in particular. The underlying cause in the majority of CVD patients is atherosclerosis and its complications, respectively. The present paper focuses on prevention and timely treatment of atherosclerosis. Management should be comprehensive and should target the risk factors (RF). Hypertension, hyperlipoproteinaemia and dyslipidemia (HLP and DLP), type 2 diabetes mellitus (T2DM), visceral fat obesity and cigarette smoking are the dominating RFs. Even though all RFs have to be managed simultaneously and it is not possible to focus on just one of them, for the sake of clarity, this paper discusses hypertension and the use of telmisartan, a representative of one the most up-to-date group of antihypertensives. There is a growing evidence that it is not always just a reduction of a specific risk that is important but also the mode of treatment. For example, to reduce a CV risk in a patient with hypertension but also, for example, with metabolic syndrome, it is more beneficial to treat the patient with rennin-angiotensin system (RAS) blocking agents, possibly in a combination with calcium channels antagonists, than to use "traditional" (older) treatment approach with a combination of a beta/blocker and diuretic. Among the RAS-modifying agents, ACE inhibitors and sartans are the most widely used. Among sartans, telmisartan is very well-tolerated and has evidence from a large interventional study for its effect on reducing the CV risk.
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PMID:[Comprehensive management of cardiovascular risk. Focusing on telmisartan]. 2084 16

We shall open our overview of issues related to obesity and hyperlipoproteinemia (HLP) or dyslipidemia with a notoriously known truth (that some are still reluctant to accept): HLP/DLP is not obesity. It is certainly not possible to put an equal sign between subcutaneous fat and the level of plasma lipids and lipoproteins. On the other hand, it is obvious that there is a number of connecting links between HLP/DLP and obesity. These associations on one side and differences on the other are the focus of this review paper. (1) HLP/DLP as well as obesity represent a group of high incidence metabolic diseases (gradually evolving from epidemic to pandemic) that affect several tens of percent of inhabitants. (2) Both HLP/DLP and obesity often occur concurrently, often as a result of unhealthy lifestyle. However, genetic factors are also been studies and it is possible that mutual predispositions for the development of both diseases will be identified. At present, it is only possible to conclude that obesity worsens lipid metabolism in genetically-determined HLP. (3) Both these metabolic diseases represent a risk factor for other pathologies, cardiovascular diseases are the most important common complication of both conditions (central type of obesity only). Concurrent presence of HDL/DLP and obesity is often linked to other diagnoses, such as type 2 diabetes mellitus (DM2T), hypertension, pro-coagulation or pro-inflammatory states; all as part of so called metabolic syndrome. (4) Patients with metabolic syndrome and, mainly, central obesity usually have typical dyslipidemia with reduced HDL-cholesterol (HDL-C) and sometimes hypertriglyceridaemia. Current treatment of HDL/DLP aims to first impact on the primary aim, i.e. LDL-cholesterol (LDL-C), and than influence HDL-C. (5) It seems that the therapeutic efforts in HLP/DLP and obesity will go in the same direction. I will skip the trivial (and difficult to accept by patients) dietary changes. Pharmacotherapy, however, (very scarce with respect to obesity) may bring positive effects on lipids and BMI. Metformin used to be considered as a drug that could improve lipid profile and lead to body weight reduction. Even though larger studies did not provide an unambiguous evidence for this, metformin keeps its position as a first line oral antidiabetic (not only) in patients with T2DM, HLP and obesity. Positive effect on lipids, mainly HDL-C is reported with pioglitazone. This drug, unlike other glitazones, does not bring body weight reduction but at least does not have a negative effect. Other antidiabetics with a positive effect on lipids and body weight include incretins, liraglutid in particular. Liraglutid importantly decreases triglyceride levels and has anorectic effect. Furthermore, metabolic effects of bariatric surgery should not be overlooked. Bariatric surgery brings weight reduction as well as it improves lipid profile and compensation of diabetes mellitus (DM). It should be mentioned here that bariatric surgery has been used for the treatment of HLP as early as 1980s. The results of the 25-year follow up within the POSCH study (ideal bypass indicated for HLP), presented in 2010, confirm a decrease in overall as well as cardiovascular mortality in an operated group, even though patients who did not undergo surgery were significantly more frequently treated with statins.
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PMID:[Dyslipidemia and obesity 2011. Similarities and differences]. 2149 5