Pharmacology: Hyperlipidemia PC PHPP 515 (IT-I) Fall JACOBS Monday, Oct. 20 4:00 4:50 PM
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1 Pharmacology: Hyperlipidemia PC PHPP 515 (IT-I) Fall 2014 JACOBS Monday, Oct. 20 4:00 4:50 PM Required Reading (via Access Pharmacy) Katzung: Chapters 35 Recommended Reading (via Access Pharmacy) Goodman and Gilman: Chapter 31 1
2 Lecture Outline Lecture Outline: Review of Dietary and Endogenous Lipids Roles of LDL and HDL in atherosclerosis Drugs for Dyslipidemia Ezetimibe Bile Acid Sequestrants Lomitapide Icosapent ethyl Statins Fibrates Niacin Mipomersin 2
3 Overview Dyslipidemia Hyperlipidemia Hyperlipoproteinemia (usually high LDL) Hypercholesterolemia (high cholesterol) Hypertriglyceridemia (high triglycerides) Endogenous Lipids Total Lipids Exogenous (Dietary) Lipids 3
4 Dietary Fats Review Palmitic (16:0) Saturated Fats (rich sources: coconut oil, animal fat) Oleic (18:1) saturated bonds have free rotation 9 10 unsaturated sites have kinks Monounsaturated Fats (rich sources: olive, macadamia oils) Linoleic (18:2) 6 EPA (20:5) 3 Polyunsaturated Fats ( -6 rich sources: veg. oil) ( -3 rich sources: fish) 4
5 Dietary Fats Review Triglycerides Cholesterol (rich sources: animal fat, incl. butter) Cholesterol esters (conjugated to FA so more can be carried in lipoproteins) 5
6 Digestion Food Dietary Fats Review Fat Fat droplets Bile acids cholic acid and chenodeoxycholic acid + Triglycerides (TG) pancreatic lipase Micelles Free fatty acids (FFA) + 2-monoacylglycerides (2-MAG) 6
7 Dietary Fats Review Uptake small intestine epithelium lacteal TG re-synthesis, packaging into chlylomicrons Micelles = Fatty acids + 2-MAG + Cholesterol + Bile acids Chylomicrons NPC1L1 Free cholesterol (FC) 85-90% Triglycerides 5-10% Phospholipids 1-3% Cholesterol esters (CE) 1-2% Apolipoprotein E (Apo E) 1-2% Apolipoproten C2 (Apo C2) 7
8 Dietary Fats Review TG Distribution CD36 peripheral tissues (adipose, muscle) lacteal Lipoprotein Lipase (LPL) FFA Chylomicrons liver capillary *cholesterol-rich Chylomicron remnants* LDLR Cholesterol (+ bile salts) 8
9 HDL Synthesis Dietary Fats Review small intestine epithelium capillary lecithin-cholesterol acyltransferase (LCAT) nascent HDL Apolipoproteins (ApoA1) Free cholesterol (FC) mature HDL FFA + Cholesterol ABCA1 FFA NPC1L1 20% Cholesterol (FC + CE) 20% Phospholipid 5% TG 55% Apolipoprotein A (Apo A-I + Apo A-II) 9
10 Dietary Fats Review VLDL and LDL Synthesis VLDL 50% TG 25% Cholesterol (FC + CE) 25% Apo E + Apo B-100 ILDL Hepatic Lipase (LIPC) LDL Lipoprotein Lipase (LPL) 60% Cholesterol (FC + CE) 10% Phospholipid 30% Apo B-100 FFA FFA CD36 peripheral tissues 10
11 Dietary Fats Review Cellular LDL Uptake LDL peripheral tissues LDLR LDLR Endocytosis LDLR FC + FFA TG LDLR Lipolysis (FC + FFA) Acyl-CoA cholesterol acyltransferase (ACAT) CE Lipid Droplets 11
12 Dietary Fats Review Elimination HDL SCARB1 LDL LDLR cholesterol (+ bile salts) SCARB1 = Scavenger receptor B1 (binds to Apo AII) LDLR = Low density lipoprotein receptor (binds Apo B-100) 12
13 LDLR Dietary Fats Review Summary Dietary Fats Pancreatic Lipase FFA ILDL (TGs + CE) (1:1) LPL FFA NPC100 FC + 2-MAG LDL (CE) VLDL (TGs + CE) (5:1) Small Intestine LCAT HDL (PL + CE) SCARB1 Liver Bile Chylomicrons (TGs + CE) (10:1) (major constituents) LPL FFA Chylomicron Remnants 13
14 Endogenous Fats Review TG Utilization (lipolysis) INSULIN INHIBITS acetyl-coa FFA -Ox acetyl-coa FFA -Ox acetyl-coa FFA -Ox TG DAG MAG Glycerol Hormone sensitive lipase (HSL) MAG lipase (MAGL) 14
15 Endogenous Fats Review FFA Storage (TG synthesis) Glycerol INSULIN STIMULATES GK Phosphate Phospho- Glycerol GPAT LPA AGPAT PA PAP DAG DGAT TG FA CoA Ligase FA-CoA FFA FA CoA Ligase FA-CoA FFA FA CoA Ligase FA-CoA FFA 15
16 Acetyl CoA Endogenous Fats Review Cholesterol Biosynthesis HMG CoA* *3-hydroxy- 3-methylglutaryl coenzyme A RATE-LIMITING STEP HMG-CoA reductase INSULIN STIMULATES Mevalonate 4 steps Geranyl-PP Farnesyl-PP Farnesyl-PP synthase 3 steps Lanosterol 19 steps Cholesterol 16
17 LDL vs. HDL LDL Becomes oxidized and is taken-up by foam cells in atherosclerotic lesions HDL 1. Degrades oxidized lipids 2. Removes cholesterol from macrophages and foam cells 3. Inhibits plaque formation and blood clotting PROMOTES atherosclerotic plaque formation INHIBITS atherosclerotic plaque formation 17
18 Foam Cell Formation Monocyte adhesion migration Endothelium plaque formation cytokine secretion + inflammatory cytokines differentiation Foam Cell lipid oxidation Ox-LDL LDL Macrophage SMC 18
19 LDL Oxidation and Uptake Oxidants (made during inflammation) ONOO- (peroxynitrite) HO (hydroxyl radical) O 2 - (superoxide anion) Enzymes (e.g. MPO) LDL Ox-LDL eat me foam cell membrane Ox-LDL internalization (high in cholesterol) 19
20 Anti-Atherogenic Actions of HDL HDL PON1 Paraoxonase 1 (PON1) Ox-LDL eat me Platelet activating factor acetylhydrolase (PAF-AH) LDL 1. Removal of eat-me signals Several enzymes can remove the eat-me signals on Ox-LDL. PON1 is a component of HDL. PAF-AH is secreted by cells. 20
21 Anti-Atherogenic Actions of HDL 2. Reverse Cholesterol Transport by HDL (out of atherosclerotic plaques, to liver) Ox-LDL CD36 Ox-LDL internalization (high in cholesterol) bile HDL cholesterol esters foam cell 21
22 Anti-Atherogenic Actions of HDL 3. Inhibition of plaque formation and clotting by HDL (effects mediated through gene expression) HDL HDL EDG Receptors (phospholipid-binding) COX-2 (PGI 2 formation) Prostacyclin = anti-clotting) Lipoxygenase (less lipid oxidation) Fibronectin, Collagen (less monocyte adhesion, scarring) 22
23 Ezetimibe Ezetimibe (Zetia ) Ezetimibe + Atorvastatin (Liptruzet ) Ezetimibe + Simvastatin (Vytorin ) Ezetimibe (blocks internalization of the receptor-fc complex) Serum Cholesterol ABCA1 NPC1L1 uptake FFA ABCG5/8 efflux Indications: Hyperlipidemia Familial hypercholesterolemia Sitosterolemia ABCG5 or ABCG8 are mutated in sitosterolemia (familial early onset atherosclerosis) 23
24 Ezetimibe The decrease in serum cholesterol also increases the cellular expression of LDL receptors, and enhances LDL uptake from the serum into peripheral tissues (adipose, skeletal muscle) Lowering serum cholesterol enhances LDL uptake (reduces circulating LDL) LDLR LDLR LDLR Endocytosis LDLR LDLR Lipolysis (FC + FFA) 24
25 Administration ORAL Absorption Rapid, 35-60%* Ezetimibe Metabolism Rapid glucuronidation (80-90% of dose) Serum half-life 22 hr Elimination Mainly fecal (undergoes enterohepatic recycling) as parent drug. Glucuronide is slowly eliminated renally. Drug Interactions: Bile acid sequestrants (cholestyramine) reduces the absorption of ezetimibe (and AUC). Administer ezetimibe at least 2 hours before or at least 4 hours after administration of a bile acid sequestrant. *Varies, some resources list absorption as complete 25
26 Bile Acid Sequestrants Cholestyramine (Prevalite, Questran ) Colesevelam (Welchol ) Colestipol (Colestid ) Apical sodium-dependent bile acid transporter (ABST) Organic solute transporter (OST) Sodium/bile acid cotransporter (NTCP) Enterohepatic recirculation NTCP Hepatocyte BSEP Bile salt export pump (BSEP) Bile acids trapping resin Bile acids Illeum Enterocyte Portal Circulation OST ASBT Excretion 26
27 Bile Acid Sequestrants Administration ORAL (tablet, or granules mixed with liquid) Absorption Not absorbed (hydrophilic, water insoluble resin) Metabolism Not metabolized Excretion Fecal Contraindications Hypersensitivity Adverse effects Minimal (due to non-absorption) Some patients experience GI changes: diarrhea, constipation, or flatulence 27
28 Drug Interactions Bile Acid Sequestrants Decrease the absorption or interfere with the enterhepatic recirculation of MANY other drugs: Penicillin G, Tetracyclines (antibiotics) Barbiturates, Phenytoin, Valproic acid (anticonvulsants) Imipramine, Doxepin (antidepressants) Glimepiride, Glipizide, Glyburide (antidiabetics) Cardiac glycosides: Digoxin Diuretics: Furosemide, Thiazide diuretics Gemfibrozil (Fibrate) Niacin Statins NSAIDs: Ibuprofen, Indomethacin Steroids: Corticosteroids, Estradiol, Progesterones Cyclosporine (immunosuppressant) 28
29 Lomitapide (Juxtapid ) FDA 2012 LDLR LDL FFA CD36 Lomitapide VLDL Inhibit microsomal triglyceride transfer protein (MTP) and block LDL formation Endocytosis FFA CD36 LDLR Lipolysis FFA MTP TGs pre-vldl Microsomes aka ER (site of VLDL synthesis) Lomitapide 29
30 Lomitapide Administration ORAL (tablet, or granules mixed with liquid) Indication Familial hypercholesterolemia Bioavailability 7% (LOW) Metabolism Extensively metabolized in the liver (Major pathway: CYP3A4) Avoid STRONG CYP3A4 inhibitors Serum half-life 40 hr Excretion Urine and feces as inactive metabolites Contraindications Pregnancy, Hepatic impairment, Liver disease Adverse effects High incidence of hepatotoxicity (1/3 of patients) elevation in liver transaminases. 30
31 Icosapent Ethyl Icosapent Ethyl (Ethyl-EPA) (Vascepa ) FDA 2012 De-esterified to FFA in body 3-3 FATTY ACID ANALOG Indication For TG levels in patents with severely high TG levels Effects V-LDL formation by the liver Lipogenesis (new FA formation from Ac-CoA) in the liver -oxidation in liver (FA for energy) Admin: Oral 31
32 HMG CoA RATE-LIMITING STEP HMG-CoA reductase Statins Mevalonate 27 steps Cholesterol Statins (competitive inhibitors) Atorvastatin (Lipitor ) Fluvastatin (Lescol, Lescol-XL ) Lovastatin (Mevacor, Altoprev ) Pitavastatin (Livalo ) Pravastatin (Pravachol ) Rosuvastatin (Crestor ) Simvastatin (Zocor ) 32
33 Indications (FDA) All agents: Hypercholesteremia Statins Some agents: Primary prevention of CV disease in patients with multiple risk factors for CHD, PVD, stroke, or other cerebrovascular disease Secondary prevention of CV events in patients with clinically evident CHD Effects (in patients with high LDL) Big LDL (40-60%*) and total serum cholesterol Moderate HDL (3-15%**) and total Apo AI levels Moderate total Apo B-100 levels (VLDL, IDL, LDL) Moderate serum TGs * BMJ 2003; 326: 1423 **Cardiovasc Drugs Ther 2008; 22(4):
34 Administration ORAL Statins Prodrugs Lovastatin and Simvastatin are prodrugs These are inactive until the lactone ring is hydrolyzed in the liver to the ring-open ( -hydroxy acid) form. Oral Bioavailability: Low Drug ABS AUC Major metabolic pathway Atorvastatin 100% 14% CYP3A4 (active metabolites) Fluvastatin 90% 24% CYP2C9, CYP3A4 Lovastatin 35% <5% CYP3A4 (prodrug) Pitavastatin 50% 50% minor metabolism Pravastatin 34% 17% sulfation (sulfate more active) Rosuvastatin 20% 20% minor metabolism Simvastatin 60-80% <5% CYP3A4 (prodrug) 34
35 Statins Protein Binding High (88-99%) for all statins EXCEPT pravastatin (50%) Serum half-lives (IR) Shorter-lived: Fluvastatin Lovastatin Pravastatin Simvastatin Longer-lived: Atorvastatin Pitavastatin Rosuvastatin 1-3 hr 3-4 hr (active metabolite) 1-3 hr (sulfate more active) 2-3 hr (active metabolite) hr (incl. active metabolites) 12 hr 20 hr Excretion: Mainly in feces (60-90%) Hepatic impairment will increase levels of most statins Renal impairment will increase levels of some statins 35
36 Statins Rank of Potencies highest potency Rosuvastatin high potency Atorvastatin Simvastatin Lovastatin = Pravastatin Fluvastatin low potency lowest potency (rank potency of pitavastatin has not been established) Effect of food Clinically insignificant (administer with or without food) Onset of action: 1-2 weeks Maximal response: 5-6 weeks 36
37 Statins Drug Interactions: Atorvastatin, Lovastatin, Simvastatin: Avoid STRONG CYP3A4 inhibitors (examples: ketoconazole, itraconazole, erythromycin, clarithromycin, HIV protease inhibitors, cyclosporine) Increased risk of myopathy and rhabdomyolysis. (may also fluvastatin, although to a lesser extent) Avoid Grapefruit juice (CYP3A4 inhibitor) Avoid St. John s Wort and other CYP3A4 inducers All Statins: Fibrates, niacin increase risk of myopathy and rhabdomyalosis 37
38 Statins Adverse Effects Rhabdomyalosis (higher risk in elderly patients and females) muscle pain or tenderness weakness elevated CPK Hepatotoxicity Elevation in liver transaminases Dose-dependent 0.5-3% incidence Safety in pregnancy has not been established, so use in pregnant women in contraindicated 38
39 Statins Cardiovascular Benefits INDEPENDENT of LDL-lowering Inhibit monocyte adhesion and migration across the endothelial wall. Inhibit the secretion of proteases (matrix metalloproteinase, MMP) that contribute to plaque rupture. Inhibit the growth of vascular smooth muscle (into and around the atherosclerotic plaque) Inhibit inflammation. Serum levels of C-reactive protein (CRP), a marker of inflammation, are lower in patients taking statins. Elevate HDL levels (partly by increasing Apo AI expression). Beneficial effects of HDL are shown in earlier slides. 39
40 Fibrates Fenofibrate (Tricor, Trilipix, Triglide, other brands, generic) Gemfibrozil (Lopid, generic) Indications (FDA) Hypertriglyceridemia (high serum triglycerides) Effects on serum lipids (in patients with high TGs) Strong serum TG (20-50%) Moderate HDL (10-35%) Moderate LDL (10-30%) Effect on uric acid Fenofibrate (NOT gemfibrozil) increases excretion of uric acid and may be useful in management of hyperuricemia 40
41 Fibrates Bind to nuclear receptor (i.e. ligandactivated transcription factor) PPAR Fenofibrate, Gemfibrozil RXR Gene Expression PPAR expressing cells: Liver Kidney Heart Bone Adipose Gene Expression Changes: Apo AI (Increased HDL) LPL (TG utilization decreased VLDL, LDL) Acyl CoA synthase (FFA breakdown) Cyp7, Cyp12 (Cholesterol breakdown) 41
42 Administration ORAL Fibrates Absorption Fenofibrate, 60% choline salt (Trilipix ), 80% micronized (Antara ), 100% Gemfibrozil, 100% Bioavailability Minor first pass effect. Bioavailability approximates the values for drug absorption listed above Metabolism Fenofibrate is a PRODRUG that is hydrolyzed by esterases to the active metabolite, fenofibric acid. Neither fenofibrate or fenofibric acid are oxidatively metabolized. Fenofibric acid is glucuronidated and excreted in the urine. Gemfibrozil is oxidized in the liver to inactive metabolites, glucuronidated and excreted in the urine. 42
43 Fibrates Efficacy: Although fibrates are effective at reducing TGs, they have not demonstrated significant efficacy in altering cardiovascular mortality in major clinical studies. Adverse Effects GI upset (8-10% of patients) Rhabdomyalosis (higher risk in elderly patients and females) muscle pain or tenderness weakness elevated CPK Although fibrates improve CV end-points (LDL, HDL, TGs) when combined with statins, this combination increases the risk of rhabdomyalosis. The mechanism is unclear. Liver toxicity Fenofibrate (more than gemfibrozil) causes dose-dependent elevations in liver transaminases. 43
44 Niacin Niacin (Nicotinic acid, Vitamin B 3 ) Effects on lipid metabolism Inhibits FFA release from adipose Increases LPL levels Decreases VLDL synthesis How? Unclear. May have to do with sirtuins (e.g. SIRT1) which are transcription factors that control metabolic pathways, and are controlled by NAD+/NADH levels 44
45 Niacin Administration ORAL (IR and ER formulations, Rx and OTC) Absorption Rapid 60-80% Administer WITH food (increases absorption, reduces GI upset) Metabolism Extensive first-pass metabolism. Major metabolite is glycine conjugate, nicotinuric acid (NUA). Serum half-life min Excretion >90% of dose is eliminated renally as parent drug (nicotinic acid) or as primary metabolite, nicotinuric acid 45
46 Adverse Effects Niacin Flushing is a common adverse effect of niacin min Two proposed mechanisms in skin: A. Histidine Histidine Antihistamine (15 min before niacin) decarboxylase (+ NADH cofactor) H Histamine 1 (Vasodilation, Itch) H 2 (Vasodilation) B. Arachidonic acid COX-1 Prostaglandins Vasodilation, Itch NSAIDs (30-60 min before niacin), or Laropiprant (PGD 2 antagonist not approved) 46
47 Other Adverse Effects Niacin Gastrointestinal disturbances (nausea, dyspepsia) Hyperuricemia (worsening of gout) Liver toxicity (avoid use in liver failure, disease or excessive alcohol use) Elevation in blood sugar (10-15%) may cause problems in diabetics Rhabdomyalosis (dose-dependent) Drug Interactions Bile acid sequestrants (reduce niacin absorption) Statins (possible rhabdomyalosis) 47
48 Mipomersin Mipomersin (Kynamro ) FDA 2013 VLDL ILDL Hepatic Lipase (LIPC) LDL TG + Cholesterol + Apo B-100 Mipomersin Apo B-100 antisense oligonucleotide Administration INJ (SQ) Efficacy 20-40% reduction in LDL-C Bioavailability 54-78% Distribution half-life 2-5 hr Metabolism Tissue nucleases Adverse effects Hepatotoxicity (elevated ALT, AST) Steatosis (fatty liver) 48
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