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Hyperlipidemia

The seminar covered the management of hyperlipidemia. It discussed the story of lipids in the body and how chylomicrons, LDL, and HDL transport lipids. High LDL and oxidized LDL can lead to atherosclerosis while HDL removes cholesterol from plaque. Causes of hyperlipidemia include diet, medical conditions, and genetic factors. Treatment involves lifestyle modifications, medical nutrition therapy, and pharmacological options like statins. The goals are to lower LDL, total cholesterol, and triglycerides while raising HDL.

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SEMINAR ON MANAGEMENT OF HYPERLIPIDEMIA. PRESENTED BY MISS PRIYANSHI PATEL DEPARTMENT OF PHARMACOLOGY 17SSRMPH020
INTRODUCTION  Hyperlipidemia is defined as an elevation of one or more of the following: cholesterol, cholesterol esters, phospholipids, or triglycerides.
STORY OF LIPIDS. Chylomicrons transport fats from the intestinal mucosa to the liver In the liver, the chylomicrons release triglycerides and some cholesterol and become low-density lipoproteins (LDL). LDL then carries fat and cholesterol to the body’s cells. High-density lipoproteins (HDL) carry fat and cholesterol back to the liver for excretion.
When oxidized LDL cholesterol gets high, atheroma formation in the walls of arteries occurs, which causes atherosclerosis. HDL cholesterol is able to go and remove cholesterol from the atheroma. Atherogenic cholesterol → LDL, VLDL, IDL
CAUSES OF HYPERLIPIDEMIA  Diet  Hypothyroidism  Nephrotic syndrome  Anorexia nervosa  Obstructive liver disease  Obesity  Diabetes mellitus  Pregnancy  Obstructive liver disease  Acute heaptitis  Systemic lupus erythematousus  AIDS (protease inhibitors)
HEREDITARY CAUSES OF HYPERLIPIDEMIA.  Familial Hypercholesterolemia Codominant genetic disorder, coccurs in heterozygous form Occurs in 1 in 500 individuals Mutation in LDL receptor, resulting in elevated levels of LDL at birth and throughout life High risk for atherosclerosis, tendon xanthomas (75% of patients), tuberous xanthomas and xanthelasmas of eyes.  Familial Combined Hyperlipidemia Autosomal dominant Increased secretions of VLDLs
 Dysbetalipoproteinemia Affects 1 in 10,000 Results in apo E2, a binding-defective form of apoE (which usually plays important role in catabolism of chylomicron and VLDL) Increased risk for atherosclerosis, peripheral vascular disease Tuberous xanthomas, striae palmaris
CHECKING OF LIPIDS.  Nonfasting lipid panel measures HDL and total cholesterol  Fasting lipid panel Measures HDL, total cholesterol and triglycerides LDL cholesterol is calculated: LDL cholesterol = total cholesterol – (HDL + triglycerides/5)
WHEN TO CHECK LIPID PANEL  Two different Recommendations  Adult Treatment Panel (ATP III) of the National Cholesterol Education Program (NCEP) Beginning at age 20: obtain a fasting (9 to 12 hour) serum lipid profile consisting of total cholesterol, LDL, HDL and triglycerides Repeat testing every 5 years for acceptable values  United States Preventative Services Task Force Women aged 45 years and older, and men ages 35 years and older undergo screening with a total and HDL cholesterol every 5 years. If total cholesterol > 200 or HDL <40, then a fasting panel should be obtained Cholesterol screening should begin at 20 years in patients with a history of multiple cardiovascular risk factors, diabetes, or family history of either elevated cholesteral levels or premature cardiovascular disease.
GOALS LDL  < 100 →Optimal  100-129 → Near optimal  130-159 → Borderline  160-189→ High  ≥ 190 → Very High Total Cholesterol  < 200 → Desirable  200-239 → Borderline  ≥240 → High
HDL  < 40 → Low  ≥ 60 → High Serum Triglycerides  < 150 → normal  150-199 → Borderline  200-499 → High  ≥ 500 → Very High
LDL GOALS  0-1 Risk Factors: LDL goal is 160 If LDL ≥ 160: Initiate TLC (therapeutic lifestyle changes) If LDL ≥ 190: Initiate pharmaceutical treatment  2 + Risk Factors LDL goal is 130 If LDL ≥ 130: Initiate TLC If LDL ≥ 160: Initiate pharmaceutical treatment  CHD or CHD Risk Equivalent LDL goal is 100 (or 70) If LDL ≥ 100: Initiate TLC and pharmaceutical treatment
TREATMENT LIFESTYLE MODIFICATIONS  Recommended reasonable and feasible approach to fitness therapy: Exercise programs that include at least 30 minutes of moderate-intensity physical activity [consuming 4-7 kcal/min] 4 to 6 times weekly, with an expenditure of at least 200 kcal/day); suggested activities include brisk walking, riding a stationary bike, water aerobics, cleaning/scrubbing, mowing the lawn, and sporting activities
MEDICAL NUTRITION THERAPY  For adults, a reduced-calorie diet consisting of fruits and vegetables (combined ≥5 servings/day), grains (primarily whole grains), fish, and lean meats is recommended R52. For adults, the intake of saturated fats, trans-fats, and cholesterol should be limited, While LDL-C-lowering macronutrient intake should include plant stanols/sterols (~2 g/ day) and soluble fiber (10-25 g/day) R53. Primary preventive nutrition consisting of healthy lifestyle habits is recommended in all healthy children Tobacco cessation should be strongly encouraged and facilitated
PHARMACOLOGICAL TREATMENT
Other classes are: Niacin (nicotinic acid) Bile acid sequestrants (cholestyramine, colestipol, colesevelam hydrochloride) Microsomal Transfer Triglyceride Protein (MTP) inhibitor (lomitapide) Anti-sense Apolipoprotein B oligonucleotide (mipomersen - subQ injection) Omega-3 fatty acids (icosapent ethyl, omega-3-acid ethyl , esters
STATINS  Recommended as the primary pharmacologic agent For clinical decision making, mild elevations in blood glucose levels and/or an increased risk of new-onset T2DM associated with intensive statin therapy do not outweigh the benefits of statin therapy for ASCVD risk reduction. In individuals within high-risk and very high-risk categories, further lowering of LDL- C beyond established targets with statins results in additional ASCVD event reduction and may be considered Target a reduced LDL-C treatment goal of <70 mg/dL: • Very high-risk individuals with established coronary, carotid, and peripheral vascular disease, or • diabetes, who also have at least 1 additional risk factor, Extreme risk individuals should be treated with statins to target an even lower LDL-C treatment goal of <55 mg/dL
FIBRATES Fibrates should be used to treat severe hypertriglyceridemia (TG >500 mg/dL) Fibrates may improve ASCVD outcomes in primary and secondary prevention when TG concentrations are ≥200 mg/dL and HDL-C concentrations <40 mg/dL
OTHER DRUGS  Omega-3 Fish Oil Prescription omega-3 oil, 2 to 4 g daily, should be used to treat severe hypertriglyceridemia (TG >500 mg/dL). Dietary supplements are not FDA-approved and generally are not recommended for this purpose.  Niacin Niacin therapy is recommended principally as an adjunct for reducing TG Niacin therapy should not be used in individuals aggressively treated with statin due to absence of additional benefits with well-controlled LDL-C
 Bile Acid Sequestrants Bile acid sequestrants may be considered for reducing LDL-C and apo B and increasing HDL-C, but they may increase TG  Cholesterol Absorption Inhibitors Ezetimibe may be considered as monotherapy in reducing LDL-C and apo B, in statin-intolerant individuals. Ezetimibe can be used in combination with statins to further reduce both LDL-C ASCVD risk
 PCSK9 Inhibitors Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors should be considered for use in combination with statin therapy for LDL-C lowering in individuals with FH R70. PCSK9 inhibitors should be considered in patients with clinical cardiovascular disease who are unable to reach LDL-C/non-HDL-C goals with maximally tolerated statin therapy. They should not be used as monotherapy except in statin intolerant individuals
COMBINATION THERAPY Combination therapy of lipid-lowering agents should be considered when the LDL-C /non HDL-C level is markedly increased and monotherapy (usually with a statin) not achieve the therapeutic goal
SPECIAL CONSIDERATION: WOMEN  Women should be evaluated for their ASCVD risk and be treated with pharmacotherapy if lifestyle intervention is insufficient.  Hormone replacement therapy for the treatment of dyslipidemia in postmenopausal women is not recommended
CHILDREN ANS ADOLSCENTS  Recommended for children and adolescents older than 10 years who do not respond sufficiently to lifestyle modification, and Particularly for those satisfying the following criteria LDL-C ≥190 mg/Dl LDL-C ≥160 mg/dL and the presence of 2 or more cardiovascular risk factors, even after vigorous intervention Family history of premature ASCVD (before 55 years of age), Having overweight, obesity, or other elements of the insulin resistance syndrome
FOLLOW UP AND MONITORING  Reassess individuals’ lipid status 6 weeks after therapy initiation and again at 6- week intervals until the treatment goal is achieved  While on stable lipid therapy, individuals should be tested at 6- to 12-month intervals  While on stable lipid therapy, the specific interval of testing should depend on individual adherence to therapy and lipid profile consistency; if adherence is a concern or the lipid profile is unstable, the individual will probably benefit from more frequent assessment
More frequent lipid status evaluation is recommended in situations such as deterioration of diabetes control, use of a new drug known to affect lipid levels, progression of atherothrombotic disease, considerable weight gain, unexpected adverse change in any lipid parameter, development of a new ASCVD risk factor, or convincing new clinical trial evidence or guidelines that suggest stricter lipid goals
 Liver transaminase levels should be measured before and 3 months after niacin or fibric acid treatment initiation because most liver abnormalities occur within 3 months of treatment initiation. Liver transaminase levels should be measured periodically thereafter (e.g. semiannually or annually)  Creatine kinase levels should be assessed and the statin discontinued, at least temporarily, when an individual reports clinically significant myalgias or muscle weakness on statin therapy
Hyperlipidemia