Dyslipidemia

Last Updated on

(Hyperlipidemia)

Dyslipidemia is an increase in plasma cholesterol and / or triglycerides (TG) or a low HDL levels, which contribute to the development of atherosclerosis. The causes may be primary (genetic) or secondary. Diagnosis is by measuring plasma levels of total cholesterol, TG, and individual lipoproteins. The therapy involves adherence to a diet, physical activity and lipid-lowering drugs.

There is no natural boundary between normal and abnormal lipid levels, as the lipid measurement is carried out continuously. However, probably there is a linear relationship between lipid levels and cardiovascular risk, so many people would benefit with “normal” cholesterol levels by lowering further. This reveals itself that there is no numerical definition of dyslipidemia; that term is used for lipid levels, their treatment has proven to be advantageous. The evidence of an advantage is strongest for the lowering of increased low-density Lipoproteinspiegels (LDL). In the total population of proof of an advantage is less pronounced for lowering elevated TG levels or raising low HDL levels.

Dyslipidemia is an increase in plasma cholesterol and / or triglycerides (TG) or a low HDL levels, which contribute to the development of atherosclerosis. The causes may be primary (genetic) or secondary. Diagnosis is by measuring plasma levels of total cholesterol, TG, and individual lipoproteins. The therapy involves adherence to a diet, physical activity and lipid-lowering drugs. There is no natural boundary between normal and abnormal lipid levels, as the lipid measurement is carried out continuously. However, probably there is a linear relationship between lipid levels and cardiovascular risk, so many people would benefit with “normal” cholesterol levels by lowering further. This reveals itself that there is no numerical definition of dyslipidemia; that term is used for lipid levels, their treatment has proven to be advantageous. The evidence of an advantage is strongest for the lowering of increased low-density Lipoproteinspiegels (LDL). In the total population of proof of an advantage is less pronounced for lowering elevated TG levels or raising low HDL levels. However, HDL levels do not always tell a cardiovascular risk before. For example, protect high HDL levels, which are caused by genetic disorders, not against cardiovascular disease, and low HDL levels, which are caused by genetic disorders, do not increase the risk of cardiovascular disease. Although HDL levels predict cardiovascular risk in the general population, an increased risk may be caused more by other factors such as concomitant lipid and metabolic disorders than the HDL level itself. Classification The dyslipidemia was traditionally patterned after the increase of lipids and lipoproteins: classified (phenotyping Fredrickson-see Table lipoprotein (phenotyping Fredrickson)). A more practical system classifies dyslipidemias as primary or secondary, and characterizes them by only an increase in the Cholesteris (pure or isolated hypercholesterolemia) Increases only TGs (pure or isolated hypertriglyceridemia), increases both cholesterol and triglycerides (mixed or combined hyperlipidemias) This system takes into account the specific Lipoproteinstörungen (z. B. low HDL or high LDL) is not, which can lead to disease despite normal TG and cholesterol levels. Lipoprotein (phenotyping Fredrickson) phenotype Increased Increased lipids lipoproteins I chylomicrons IIa TGs LDL cholesterol IIb LDL and VLDL cholesterol and TGs III VLDL and Ch Remnants ylomikron-TG and cholesterol VLDL TGs IV V chylomicrons and VLDL cholesterol and TGs LDL = low-density lipoprotein; TGs = triglycerides; VLDL = very-low-density lipoprotein. Etiology primary (genetic) and secondary causes (the lifestyle question and others) causes contribute in varying degrees to dyslipidemia. For example, the disease occurs where a family history of hyperlipidemia only in the presence of significant secondary causes. Primary causes Primary causes are single or multiple genetic mutations that either an overproduction or impaired degradation of TG and LDL-cholesterol or a reduced production or excessive breakdown of HDL (see Table: Genetic (primary) dyslipidemias) lead. The names of many primary problems are due to an old nomenclature, were discriminated in the lipoproteins according to whether they were after electrophoretic detection and separation in the alpha (HDL) or beta (LDL) band. Genetic (primary) dyslipidemia disease Genetic defect / Mechanism inheritance prevalence Clinical Features Therapy familial hypercholesterolemia LDL receptor defect Reduced LDL clearance co-dominant or complex with multiple genes Occurs worldwide, but is more common among French Canadians, Christian Lebanese and South Africans – Diet lipid-lowering drugs, LDL apheresis (when for homozygotes and heterozygotes severe disease) liver transplantation (homozygotes) Heterozygous: 1/200 to 1/500 tendon xanthomas, corneal arcus, premature coronary heart disease (ages 30-50), responsible for about 5% of myocardial infarction in men <60 years TC: 250-500 mg / dl (7-13 mmol / l) homozygotes: 1.1 million (more common in French Canadians, Christian Lebanese and South Africans) planar and tendon xanthomas and tuberous xanthomas, premature CHD (before age 18) TC> 500 mg / dl (> 13 mmol / l) Family lipoprotein defective Apo B-100 Apo B (defect in the LDL receptor-binding region) reduced LDL-Cle arance Dominant 1/700 xanthomas, corneal arcus, early CHD TC: 250-500 mg / dl (7-13 mmol / l) diet lipid-lowering drugs PCSK9 function increase mutations reinforced degeneration of LDL receptors Dominant Unknown Resembles familial hypercholesterolemia Lipid-lowering diet drugs polygenic hypercholesterolemia Unknown, possibly several defects and mechanisms Variable Often Early CHD TC: 250-350 mg / dl (6.5-9.0 mmol / l) diet lipid-lowering drugs LPL deficiency Endothelial LPL Decreased chylomicron clearance recessive rare, but occurring worldwide failure to thrive (in infants), erupting xanthomas, hepatosplenomegaly, pancreatitis TG:> 750 mg / dl (> 8.5 mmol / l) diet: Total restriction of fat intake with supplementation of fat-soluble vitamins and medium-TGs Gene therapy (approved in the European Union) apo C-II deficiency Apo C-II (causes a functional LPL deficiency) Recessive <1.1 million pancreatitis (some adults), metabolic syndrome (often available) TG:> 750 mg / dl (> 8.5 mmol / l) Diet: total restriction of fat intake with supplementation of fat-soluble vitamins and medium-TGs Familial hypertriglyceridemia Unknown, possibly several defects and mechanisms Dominant 1/100 Usually no symptoms or findings; sometimes hyperuricemia, sometimes early atherosclerosis TG: 200-500 mg / dl (2.3 to 5.7 mmol / l), may be higher depending on the lipid-lowering diet and drinking diet weight loss medications Familial combined hyperlipidemia unknown, possibly more defects and mechanisms Dominant 1 / 50 to 1/100 Early coronary heart disease, accounting for approximately 15% of myocardial infarction in humans <60 years Apo B: disproportionately increased TC: 250-500 mg / dl (6.5 to 13.0 mmol / l) TG: 250- 750 mg / dl (2.8 to 8.5 mmol / l) diet weight loss lipid-lowering drugs Familial dysbetalipoproteinemia Apo E (usually e2 / e2 homozygotes) Decreased Chylomikronen- and VLDL clearance Recessive (more often) or dominant (rare) 1/5000 Worldwide occurring xanthomas (especially tuberös and palmar), yellow palmar lines, early CHD TC: 250-500 mg / dl (6.5 to 13.0 mmol / l) TG: 250-500 mg / dl (2.8 to 5.6 mmol / l) diet lipid-lowering drugs Primary hypoalphalipoproteinemia (familial or not familial) Unknown, may Apo AI, C-III A-IV or Dominant Early About 5% CHD HDL: 15-35 mg / dl Movement HDL-increasing and LDL-lowering drugs Familial apo A / apo C-III deficiency / mutations Apo A or apo C-III Increased HDL catabolism Unknown Rarely corneal opacities, xanthomas, premature CHD (in some people) HDL : 15-30 mg / dl Non Specific familial LCAT deficiency LCAT gene recessive Extremely rare corneal opacities, anemia, kidney failure HDL <10 mg / dl restriction of Fettzufuh r kidney fish eye disease (partial LCAT deficiency) LCAT gene recessive Extremely rare corneal opacities HDL <10 mg / dl unspecific Tangier disease ABCA1 gene recessive Rare Early CHD (in some people), peripheral neuropathy, anemia, corneal clouding, hepatosplenomegaly , orange tonsils HDL: <5 mg / dl diet with low fat Familial HDL deficiency ABCA1 gene Dominant Rare Early CHD diet with low fat Hepatic lipase deficiency Hepatic lipase Recessive Extremely rare Early CHD TC: 250-1500 mg / dL TG: 395-8200 mg / dl HDL: Variable Empirically: diet, lipid-lowering Cerebrotendinous cholesterosis hepatic mitochondrial 27-hydroxylase blockade of bile acid synthesis and conversion of cholesterol to Cho lestanol which accumulates rare recessive cataracts, premature coronary heart disease, neuropathy, ataxia chenodeoxycholic sitosterolemia ABCG5- and ABCG8 gene recessive rare tendon xanthomas, premature CHD restriction of fat intake Gallensäureadsorbenzien ezetimibe Cholesterylesterspeicherkrankheit and Crohn Wolman Lysosomal esterase deficiency Recessive Rare CHD early accumulation of cholesteryl esters and TGs in lysosomes of liver, spleen and lymph nodes may cirrhosis statins enzyme replacement (experimental) = TP ABCA1-binding cassette transporter A1; ABCG5 and 8 = ATP-binding cassette subfamily G members 5 and 8; apo = apoprotein; CHD = coronary heart disease, HDL = high-density lipoprotein; LCAT lecithin-cholesterol acyltransferase =; LDL = low-density lipoprotein; LPL = lipoprotein lipase; MI = myocardial infarction; PCSK9 = proprotein convertase subtilisin-like / kexin type 9; TC = total cholesterol, TG = triglyceride; VLDL = very-low-density lipoprotein. Secondary causes Secondary causes are responsible for all dyslipoproteinemias in adulthood. The most important secondary cause in industrialized countries is the sedentary lifestyle with excessive intake of saturated fat, cholesterol and so-called. Trans fats. Trans fats are polyunsaturated or monounsaturated fatty acids, which hydrogen atoms have been added; they are used in industrially processed food and are as atherogenic as saturated fat. Other common secondary causes are diabetes mellitus alcohol overload Chronic kidney disease hypothyroidism Primary biliary cirrhosis and other cholestatic liver disease drugs such. B. thiazides, ?-blockers, retinoids, highly effective anti-retroviral agents, cyclosporin, tacrolimus, estrogen, progestin and glucocorticoids. Secondary causes of low HDL cholesterol include smoking, anabolic steroids, HIV infection and nephrotic syndrome. Diabetes is a very serious secondary cause because patients often have an atherogenic combination of high TG and high values ??for the fraction of small, dense LDL, and low HDL (diabetic dyslipidemia, hypertriglyceridämisches Hyperapo B). this patients with type 2 diabetes are at particular risk. The combination can be a result of excess weight and / or poor blood sugar control, which increases the amount of circulating free fatty acids (FFAs) and in turn causes increased hepatic VLDL production. TG-rich VLDL transfers the TGs and cholesterol then LDL and HDL, which promotes the formation of TG-rich, small, dense LDL and the reduction of TG-rich HDL. Diabetic dyslipidemia is often significantly worsened by the increased calorie intake and physical inactivity that characterizes the lifestyle of type 2 diabetics. Women with diabetes have this form may be a particular risk for cardiac disease. Symptoms and complaints The dyslipidemia itself usually causes no symptoms, but can lead to symptomatic vascular disease, v. a. for coronary heart disease (CHD), stroke and peripheral artery disease. High TG levels (> 1000 mg / dl [> 11.3 mmol / l]) may cause a pancreatitis. High LDL levels can cause a corneal arcus. Also experience xanthomas of the tendons, z. B. on to the Achilles tendon, elbow, knee and over the metacarpophalangeal joints. Patients with the homozygous form of familial hypercholesterolemia can have the findings described above and plantar or tuberous xanthomas. Planar xanthomas are flat or slightly elevated yellowish spots. Tuberous xanthomas are painless, firm nodules which usually occur on the extensor surfaces of the joints. Patients with a very strong increase in TGs can eruptive xanthomas on the trunk show to back, elbows, buttocks, knees, hands and feet. Patients with rare dysbetalipoproteinemia have palmar and nodular xanthomas. Severe hypertriglyceridemia (> 2000 mg / dL [> 22.6 mmol / L]) give the retinal arteries and veins a creamy white appearance (lipaemia retinalis). Extremely high lipid levels can also be blood plasma look milky. Symptoms paresthesia, dyspnea and confusion may belong. Eruptive xanthoma figure provided by Thomas Habif, M.D. var model = {thumbnailUrl: ‘/-/media/manual/professional/images/eruptive_xanthoma_de.jpg?la=de&thn=0&mw=350’ imageUrl: ‘/-/media/manual/professional/images/eruptive_xanthoma_de.jpg?la = en & thn = 0 ‘, title:’ Eruptive xanthoma ‘description:’ u003Ca id = “v38396171 ” class = “”anchor “” u003e u003c / a u003e u003cdiv class = “”para “” u003e u003cp u003eEruptive Xanthomata are cutaneous manifestations elevated triglyceride u003c / p u003e u003c / div u003e ‘credits’. Figure provided by Thomas Habif

Health Life Media Team

Leave a Reply