Antihyperlipidemic Drugs Munir Gharaibeh, MD, PhD, MHPE
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1 Antihyperlipidemic Drgs Mnir Gharaibeh, MD, PhD, MHPE School of Medicine, The University of Jordan November, 2017
2 Antihyperlipidemic Drgs Hyperlipidemias. Hyperlipoproteinemias. Hyperlipemia. Dyslipidemias Hypercholestrolemia.
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8 Niacin Nicotinic Acid or Vitamin B3, is one of the oldest drgs. Water- solble B-complex vitamin, fnctions only after conversion to NAD or NADP+ Nicotinamide. Niacin has hypolipidemic effects only in large doses. Affects all lipid parameters: Best agent to increase HDL-C(35-40%). Lowers triglycerides (35-45%). Decreases LDL-C prodction(20-30%). Redces fibrinogen levels. Increases plasminogen activator, 8
9 Mechanism of Action: Niacin In adipose tisse, inhibits the lipolysis of triglycerides by inhibiting adipocyte adenylyl cyclase, which redces transport of free fatty acids to the liver and decreases hepatic triglyceride synthesis. May also inhibit a rate limiting enzyme of triglyceride synthesis, diacylglycerol acetyltransferase 2. Redction of triglyceride synthesis redces hepatic VLDL and conseqently LDL. Inhibits intracelllar lipase in adipose tisses leading to decreased FFA flx to the liver. Completely absorbed, peaks within 1hr, half-life is abot 1 hr, so need to be given by twice or thrice 9 daily administration.
10 Toxicity: Niacin Harmless ctaneos vasodilation and sensation of warmth, can be prevented by NSAIDS. Prrits, rashes, dry skin or mcs membranes (acanthosis nigricans). Nasea, vomiting, abdominal discomfort, diarrhea. Elevations in transaminases and possible hepatotoxicity. Inslin resistance and hyperglycemia. Hyperricemia and got. Cardiac arrhythmias. 10 Amblyopia, blrring of vision.
11 Acanthosis Nigricans 11
12 Fibrates or Fibric Acid Derivatives or PPARs Activators Clofibrate, Gemfobrozil. Fenofibrate. Bezafibrate. Activate PPAR- α (Peroxisome Proliferator Activated Receptor- α) which stimlates fatty acid oxidation, increases LPL synthesis, and redces expression of apo C-III, and increases apoa-i and apoa-ii expression. Increase lipolysis of lipoprotein triglyceride via LPL. Decrease levels of VLDL and LDL. Moderately increase HDL. Also Mnir Gharaibeh, have MD, PhD, MHPE anticoaglant and fibrinolytic Oct activities. Drgs of choice in severe hypertriglyceridemia.
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14 Fibrates Toxicity: Rashes, rticaria, hair loss, headache, GIT symptoms, impotence, and anemia. Myalgia, fatige, myopathy and rhabdomyolysis. (Breakdown of mscle fibers reslting in the release of mscle fiber contents (myoglobin) into the blood stream). Risk of cholesterol gallstones. Interacts with statins, levels of both drgs will increase. Used with cation in renal failre. 14 Elevated transaminases or alkaline phosphatase.
15 Bile Acid Binding Resins Colestipol. Chlestyramine. Colesevelam. These are large polymeric anionic- exchange resins, insolble in water, which bind the negatively charged bile acids in the intestinal lmen and prevent their reabsorption leading to depletion of bile acid pool and increased hepatic synthesis. Conseqently, hepatic cholesterol content is decreased, stimlating the prodction of LDL receptors. This leads to increased LDL clearance and lowers LDL-C levels. However, this effect is partially offset by the enhanced cholesterol synthesis cased by preglation of HMG-CoA redctase. May increase triglyceride levels. 15
16 Idications: Bile Acid Binding Resins Lower LDL as mch as 25%, bt will case GI side effects. Relieve prrits in cholestasis. Digitalis toxicity, can bind digitoxin and enhance its excretion. 16
17 Toxicity: Bile Acid Binding Resins Probably the safest drgs, since they are not absorbed from the intestine becase of their large size. Maximal doses are effective bt case side effects. Gritty sensation is npleasant bt can be tolerated. Constipation and bloating. Heartbrn. Malabsorption of Vitamin K. Gall stones. Impaired absorption of many drgs( digitalis, propranolol, thiazides, warfarin, folic acid, statins, aspirin.etc).. 17
18 Competitive Inhibitors of HMG-CoA Redctase Statins Mevastatin Simvastatin Lovastatin Pravastatin Flvastatin Atorvastatin. Rosvastatin. 18
19 Competitive Inhibitors of HMG-CoA Redctase Statins Most commonly prescribed drgs worldwide. Isolated from a mold Penicillin citrinm, Modified derivatives and distinct synthetic componds. Most effective in lowering LDL. 19
20 Statins Competitively inhibit the early rate- limiting enzyme in de novo synthesis of cholesterol (3- hydroxy-3methylgltaryl coenzyme A redctase). This reslts in increased expression of the LDL receptor gene. Redced free cholesterol in hepatocytes activates a protease which will cleave membrane- bond SREBPs which will be translocated to the ncles to enhance trasncription of LDL receptors. Increased nmber of LDL receptors will increase removal of LDL-C from the blood ths lowering of LDL-C. Also can redce LDL levels by enhancing the removal of LDL precrsors (VLDL and IDL) and by 20 decreasing hepatic VLDL prodction.
21 Statins Higher doses can redce triglyceride levels cased by elevated VLDL levels. Some (simvastatin and rosvastatin) can raise HDL-C levels. Decrease oxidative stress and vasclar inflammation by enhancing NO prodction. Redce platelet aggregation. 21
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23 Toxicity: Statins Toxicity is dose-related, associated with advanced age, hepatic or renal dysfnction, small body size, associated diseases, hypothyroidism and concomitant drgs. Elevation of transaminases, intermittent and not associated with strong evidence of liver failre. Elevation of creatine kinase (CK) activity. Rhabdomyolysis, casing myoglobinria and renal injry and failre or even death. It is extremely rare (less than one in 10,000 people). 23 Lps-like disorder and peripheral neropathy.
24 Common Side Effects to Statins Headache Difficlty sleeping Flshing of the skin Mscle aches, tenderness, or weakness (myalgia) Drowsiness Dizziness Nasea and/or vomiting Abdominal cramping and/or pain Bloating and/or gas Diarrhea Constipation Rash Statins also carry warnings that memory loss, mental confsion, high blood sgar, and type 2 diabetes are possible side effects. It is Oct important to remember that statins may also interact with other medications.
25 Pharmacogenetics of Statins Statins are good example of the principles of pharmacogenetics. This is becase they are metabolized by the CYP enzyme system, which is a sbject to individal genetic differences. These differences will be exhibited for their: Therapetic Response Side Effects. 25
26 Inhibitors of Sterol Absorption Ezetimibe: Can redce LDL. Inhibitor of NPC1L1, a specific transport process in jejnal brsh border. Redces cholesterol absorption and reabsorption by 54%, precipitating a compensatory increase in cholesterol synthesis. Redces cholesterol delivery to the liver by the chylomicron remnants. This will stimlate the expression of the hepatic genes reglating the LDL receptor expression leading to enhanced LDL-C clearance from the plasma(15-20%). Action is complementary to statins(60% rection in LDL-C).. Can Mnir Gharaibeh, case MD, PhD, allergic MHPE Oct-17 reactions, reversible impairment 26 of liver fnction tests and myopathy.
27 Inhibitors of Cholesteryl Ester Transfer Protein Torcetrapib: withdrawn Anacetrapib. Dalcetrapib CETP is a plasma glycoprotein synthesized by the liver that mediates the transfer of cholesteryl esters from HDL to triglyceriderich lipoproteins and LDL in exchange for a molecle of triglyceride. Can Mnir Gharaibeh, increase MD, PhD, MHPE HDL levels by % Oct in hmans.
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