Does diabetes cause hyperlipidemia


Az előadások a következő témára: "Dyslipidemia és atherosclerosis"— Előadás másolata: 1 Dyslipidemia és atherosclerosis Dr. Pallós Júlia klinikai farmakológus — Cholesterol is also an important component of all cell membranes and is required for proper nervous system function. The relationship between high cholesterol levels and increased risk for coronary heart disease CHD is well known.

However, raised LDL cholesterol has been shown to be most strongly associated with the development of atherosclerosis and the risk of CHD. An in-depth family history of CHD and other atherosclerotic diseases should be an integral part of risk assessment. CHD risk is greater in males, in the elderly, and in individuals with a closely related family member with CHD. Also, the impact of any risk factor is intensified with increasing age.

When diabetes mellitus and hypertension occurred together, the incidence of MI was eight-fold greater than in subjects without any risk factors. If dyslipidaemia was also present, a further two-fold increase in risk was observed.

These data confirm both the independent risk associated megelőző cukorbetegség kezelésében diabetes mellitus and the synergistic interaction that diabetes has with other common risk factors for coronary heart disease. Am Heart J ;— Adapted from Am Heart J ;—, with permission from Elsevier. Assmann G, Schulte H. This is caused by the production of a number of vasoactive substances, including prostaglandins, does diabetes cause hyperlipidemia, and nitric oxide NO.

References Weissberg PL. Atherosclerosis involves more than just lipids: Plaque dynamics.

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Eur Heart J. Ross R. The pathogenesis of atherosclerosis: A perspective for the s. Coronary plaque rupture and erosion may result in thrombus does diabetes cause hyperlipidemia within coronary arteries. If blood flow is completely obstructed, either due to a thrombus or by a large atherosclerotic plaque, myocardial infarction MI may occur. If damage to the myocardium is very severe, the result may be congestive heart failure or even sudden cardiac death.

A stroke may also be caused by formation of a thrombus or embolus, arterial rupture, or hemorrhage of the cerebral arteries stopping the oxygen supply to parts of the brain.

It can lead to permanent damage to the brain, disability, and sudden death.

These include an aching or cramping pain caused by insufficient oxygen reaching the muscles in the legs. Due to the risk of blood clots with PAD, risk of death from heart attack and stroke is increased. Dallas, Texas: American Heart Association, American Heart Association, Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded?

Castelli WP. Epidemiology of coronary heart disease: the Framingham Study. Am J Med. Stamler J et al. Ezért a plazmában szállítófehérjékhez apolipoproteinek kötődnek foszfolipidekkel együtt. Ezt a speciális komplexumot nevezik lipoproteinnek. Cholesterol reduction yields clinical benefit: impact of statin trials.

Dyslipidemia és atherosclerosis - ppt letölteni

National Health and Nutrition Examination Survey. Arch Intern Med. Available at: Accessed October 25, Gould AL, et al.

Qinna: oj. Biala, H.

LDL cholesterol has been shown to be strongly associated with the development of atherosclerosis and the risk of CHD events in patients with and without established CHD. While this applies to women as well as men, the general level of CV risk is lower in premenopausal women. This modification is apparent especially when total cholesterol and LDL cholesterol are only moderately elevated. Prevention of coronary heart disease in clinical practice: recommendations of the Second Joint Task Force of European and other societies on coronary prevention.

Wood D et gel kezelésében trofikus fekélyek a cukorbetegségben. This effect is independent of LDL cholesterol and other risk factors. Concentrations of HDL cholesterol tend to be low when triglycerides are high. Wood D, et al.

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Recent data suggest elevated triglycerides are an independent CHD risk factor. Intensified LDL-lowering drug therapy should be administered first, followed by nicotinic acid or fibrate treatment if necessary. Non-high-density lipoprotein cholesterol level as a predictor of cardiovascular disease mortality.

Arch Intern Med ; 1. More aggressive therapy of dyslipidemia is needed to attain NCEP goals. Results of the primary care L-TAP survey showed that hypercholesterolemia treatment is suboptimal, particularly among patients in higher risk groups.

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Culpability can be related to failings by patients and their physicians as well as to limitations of currently available drugs. The most important reason, however, is that hypercholesterolemia is often underdiagnosed and either untreated or undertreated. Interpatient variability marks the response to statins, and some individuals may experience hepatotoxic effects or elevated muscle enzymes.

Tolerability-limiting adverse effects of nicotinic acid include flushing, gastrointestinal events, and pruritus. Bile acid-binding resins are poorly palatable and produce gastrointestinal side effects. Because of their LDL-C—lowering efficacy, they are able to achieve LDL-C treatment goals in the majority of patients, regardless of their risk category.

Statins are also remarkably safe as will be described below.

These drugs are not as effective in lowering LDL-C and cause bothersome side effects which make patient compliance a problem. However, they are effective in reducing CHD risk and in the majority of patients can be successfully taken. If patients require additional treatment to achieve their secondary treatment goal defined by non-HDL-C, several approaches can be chosen.

Statin therapy or other LDL-C—lowering regimens may be intensified, or triglyceride-lowering drugs may be added to the regimen.

Bile acid—binding resins interrupt the enterohepatic circulation of bile acids, increasing the synthesis of new bile acids and the expression of LDL receptors. Importantly, statin therapy has not been associated with an increase in noncardiovascular events. These data demonstrate that statins improve the quality of life by reducing nonfatal events and also lengthen life by reducing total mortality.

Effect of statins on risk of coronary disease: a meta-analysis of randomized controlled trials. Reductase inhibitor monotherapy and stroke prevention. Effect of simvastatin on ischemic signs and symptoms in the Scandinavian Simvastatin Survival Study 4S.

Common side effects include headache, upset stomach, fatigue, flu-like symptoms, and myalgia without changes in creatine kinase [CK]. Whether statin-induced elevations in liver enzymes constitute true hepatotoxicity has not been determined. Cases of serious liver dysfunction or failure are exceedingly rare and not clearly related to statin therapy.

Enzymes will frequently return to normal by reducing doses or even with continuation of therapy. If an elevation persists, discontinuation of therapy for a short period until levels return to normal is advised. Statin therapy may then be reinitiated. Very rare cases of rhabdomyolysis, myoglobinuria, acute renal necrosis, and death have been reported. The incidence of myopathy appears related to the systemic blood concentration of the statin. Myopathy is most likely to occur with higher doses, in does diabetes cause hyperlipidemia with renal impairment, when a statin is combined with a fibrate, when a drug interfering with the metabolism of the statin is given concurrently e.

All patients started on statins should be instructed to report immediately muscle symptoms or brown urine and to have CK measured. If myopathy is present or strongly suspected, the statin should be discontinued immediately.

The time course for these antiatherosclerotic effects of statins ranges from days to years. Within weeks to months after beginning statin therapy, endothelial function of coronary arteries is restored.

Concurrent with this or following by just a few months is a reduction in inflammatory markers, such as high-sensitivity C-reactive protein. These effects appear to coincide with the reduction in ischemic events demonstrated after about 18 months of statin therapy. After several years of therapy i. These changes coincide somewhat with stabilization of vulnerable atherosclerotic plaque during which the lipid-rich core of plaque is replaced with connective tissue and matrix. This risk is enhanced with high statin doses, in the presence of renal insufficiency, in older patients, and whenever drugs that may interfere with statin metabolism are given concurrently.

Click here to view. We thank patients at the UAB gout clinic for asking us the question whether gout is associated with other hearing illness which prompted us to perform this study. Footnotes Contributors: JAS designed the study, developed study protocol, reviewed analyses and wrote the first draft of the paper.

To minimize the muscle side effects when combining any of these drugs with a statin, the following suggestions are made. If adding a triglyceride-lowering drug to the statin, give preference to fish oils or niacin, as the risk of myopathy appears low.

Dyslipidemia és atherosclerosis

If a fibrate is to be added, fenofibrate is preferred over gemfibrozil, since there may be a lower risk of myopathy. Use the lowest effective dose of both the statin and fibrate to achieve treatment goals e.

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Dose the fibrate in the morning and the statin in the evening note that this suggestion is based on theoretical considerations and not on any evidence that this recommendation will reduce the incidence of muscle toxicity. Avoid or cautiously use statins in patients who have compromised renal function as is often found in elderly patients or hepatic function including alcoholics.

Hyperlipidemia in pregnancy in: Orvosi Hetilap Volume Issue 19 ()

Assure that no other drugs are or will be used concurrently that could interfere with the metabolism of the statin. Obtain a baseline CK level and repeat it mustármag diabetes kezelése the course of therapy if the patient reports muscle symptoms. Teach the patient to recognize and report muscle weakness, tenderness, or pain and be prepared to evaluate patients who experience these symptoms.

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The mechanism of action of fibrates is very complex and not entirely understood. Their agonist effect on these receptors down-regulates the apo C-III gene and up-regulates genes for apo A-I, fatty acid transport protein, fatty acid oxidation, and possibly lipoprotein lipase.

The effects on lipoprotein lipase and apo C-III which inhibits lipoprotein lipase enhance the catabolism of triglyceride-rich lipoproteins, whereas increased fatty acid oxidation reduces formation of VLDL triglycerides.

Fibrates are generally well tolerated in most patients. GI complaints are the most common side effects. All drugs in this does diabetes cause hyperlipidemia appear to increase the lithogenicity of bile and increase the likelihood of cholesterol gallstones.

Additionally, the fibrates are highly bound to serum albumin and may displace warfarin, increasing its anticoagulant effects. Since fibrates are excreted primarily by the kidneys, caution should be observed in patients with renal failure. Myopathy has been observed particularly when combined with a statin.

More comment will be given to this issue in slide Helsinki Heart Study: primary-prevention trial with gemfibrozil in does diabetes cause hyperlipidemia men with dyslipidemia.

Safety of treatment, changes in risk factors, and incidence of coronary heart disease. Prevention of the angiographic progression of coronary does diabetes cause hyperlipidemia vein-graft atherosclerosis by gemfibrozil after coronary bypass surgery in men with low levels of HDL cholesterol.