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  • Plasma lipids are transported in complexes called lipoproteins.
  • Metabolic disorders that involve elevations in any lipoprotein species are termed hyperlipoproteinemias or hyperlipidemias. Hyperlipemia denotes increased levels of triglycerides.
  • The two major clinical sequelae of hyperlipidemias are acute pancreatitis and atherosclerosis. The former occurs in patients with marked hyperlipemia (increased TG). Control of triglycerides can prevent recurrent attacks of this life-threatening disease.
  • Lipoproteins that contain apolipoprotein (apo) B-100 convey lipids into the artery wall. These are low-density (LDL), intermediate-density (IDL), very-low-density (VLDL), and lipoprotein(a) (Lp[a]). Remnant lipoproteins formed during the catabolism of chylomicrons that contain the B-48 protein (apo B-48) can also enter the artery wall, contributing to atherosclerosis. High-density lipoproteins (HDL) exert several antiatherogenic effects. They participate in retrieval of cholesterol from the artery wall and inhibit the oxidation of atherogenic lipoproteins. Low levels of HDL (hypoalphalipoproteinemia) are an independent risk factor for atherosclerotic disease and thus are a target for intervention

National Cholesterol Education Program: Adult Treatment Guidelines:




HIGH (Mg/Dl)

Total Cholesterol

< 200


> 240


< 130


> 160

Hdl: Men

> 40


Hdl: Women

> 50


< 120


> 200


Cause of Hyperlipidemias: Primary And Secondary

Primary hyperlipidemia and treatment:



Diet + single drug

Drug combination

Primary Chylomicronemia (Familial Lipoprotein Lipase Or Cofactor Deficiency; Others)

Chylomicrons, VLDL increased


Dietary management (omega-3 fatty acids, niacin, or fibrate)

Niacin plus fibrate


Familial Hypertriglyceridemia

VLDL increased; chylomicrons may be increased

Omega-3 fatty acids, niacin, or fibrate

Niacin plus fibrate

Familial Combined Hyperlipoproteinemia

VLDL, LDL increased

Omega-3 fatty acids, niacin, or reductase inhibitor

Niacin or fibrate plus reductase inhibitor

Familial Dysbetalipoproteinemia

VLDL remnants, chylomicron remnants increased

Omega-3 fatty acids, fibrate, or niacin

Fibrate plus niacin, or either plus reductase inhibitor

Familial Hypercholesterolemia

LDL increased

Reductase inhibitor, resin, niacin, or ezetimibe

Two or three of the individual drugs

Familial Ligand-Defective

Apo B

LDL increased

Niacin, reductase inhibitor, or ezetimibe

Niacin plus reductase inhibitor or ezetimibe

Lp(A) Hyperlipoproteinemia

Lp(a) increased



Secondary hyperlipidemias:



DM, Alcohol Ingestion, Severe Nephrosis, Estrogens, Uremia, Glucocorticoids Excess, Glycogen Storage Diorders, Acromegaly, Hypopituitarism, Lipodystrophy, Protease Inhibitors

Hypothyroidism, Early Nephrosis, Resolving Lipemia, Anorexia Nervosa, Cholestasis, Hypopituitarism, Glucocorticoids Excess



  1. Statins
    1. Lovastatin                    
    2. Simvastatin      
    3. Pravastatin             
    4. Rosuvastatin              
    5. Atorvastatin
  2. Nicotinic acid
  3. Fibrates
    1. Clofibrate                    
    2. Fenofibrate          
    3. Gemfibrozil
  4. Bile acid binders
    1. Cholestyramine            
    2. Cholesevelam              
    3. Cholistipol
  5. Cholestrol absorption inhibitor
  6. CETP Inhibitors
    1. Torcetrapib


Individual drugs


  1. Statins
    1. Lovastatin            
    2. Simvastatin        
    3. Pravastatin      
    4. Rosuvastatin    
    5. ​Atorvastatin


  1. Inhibit HMG Co reductase, competitively
  2. LDL-R over-expression occurs on liver surface
  3. In LDL receptor defect (Familial hypercholestrolemia), statins do not work
  4. Best given with evening meals


  1. Well absorbed orally
  2. Lovastatin absorption is facilitated by meals
  3. Lovastatin, simvastatin are prodrugs
  4. Pravastatin is hydrophillic; does not enter blood brain barrier
  5. Atorvastatin is most selective
  6. Rosuvastatin is most efficacious, longest acting; half life 24 hours
  7. Pitavastatin, the newest statin is even more effective than rosuvastatin.   
  8. Statins (other properties)
    1. Antiplatelet              
    2. Plaque stabilising        
    3. Anticancer   
    4. Antiproliferatory                  
    5. Anti-osteoporotic


  • Best drugs for lowering LDL cholesterol
  1. Postmenopasal states
  2. Diabetes
  3. Drug induced rise
    1. Thiazdies      
    2. Beta-blockers                
    3. Retinoic acid        
    4. Tacrolimus  
    5. Cyclosporine

Side Effects:

  1. M/C-myalgia
  2. Increase in liver enzymes
  3. Myopathy-rare, due to mitochondrial damage
  4. Rhabdomyolysis-myoglobinuria
  5. Impotence

Drug Interactions:

  1. Lovastatin-NOT given along with nicotinic acid, clofibrate, erythromycin
  2. Erythromycin inhibits metabolism, while clofibrate and nicotinic acid may have additive action
  3. Rosuvastatin + Fenofibrate is safe combination.


  1. Statins are teratogenic, not given in pregnancy, children & lactation
  1. Nicotinic acid
    1. Broadest spectrum
    2. Most efficacious
    3. Lowers:
      1. LDL                      
      2. VLDL                            
      3. Lp (a) 
      4. TAG                  
      5. Total cholesterol          
      6. Fibrinogen
  • Increases:
  1. HDL              
  2. Gastric acid        
  3. Glucose      
  4. Uric acid


  1. Well absorbed                  
  2. Short acting


  • DOC:
  1. Mixed hyperlipidemia
  2. Low HDL dyslipidemia


Side effects

  1. MC side effect-flushing (Other drugs causing flushing as S/E: Mnemonic is VAT)
    1. Vancomycin          
    2. Adenosine            
    3. Tubocurarine
  • Mediated by prostaglandins
  • Treated by aspirin
  1. Hepatitis
  1. Fibrates
    1. Short acting, safer drugs
    2. Well absorbed
    3. Stimulate PPAR-alpha, stimulate LPL, and lower TAG (? Thiozodinediones-stimulate PPAR-gamma)

DOC for:

  1. Dysbetalipidemia (Type II hyperlipoprotenemia)
  2. Hypertriglyceridemia

Side Effects:

  1. GI upset                  
  2. Thrombocytopenia              
  3. C/I: gall bladder disease
  1. Bile Acid Binders:
    1. Inhibit entero-hepatic circulation
    2. Deficient liver, converts cholesterol into bile acids
    3. A statin like mechanism operate & increase LDL expression on liver


  1. Luminal drugs  
  2. Chelating property; bind to many drugs & nutrients in intestinal lumen
  3. Cholestyramine            
  4. Colistipol            
  5. Cholesevelam



  • DOC:
  1. Bile acid diarrhea
  2. Hepatic pruritis
  3. Hyperlipidemia in pregnancy, children & during lactation


  • Diverticulosis


  1. MC-constipation                          
  2. Diarrhea                    
  3. Bloating       
  4. Megaloblastic anemia (chelate B12)            
  5. Bleeding (Chelate Vit K)

Drug Interactions:

  1. Absorption of following can be reduced:  (Mnemonic : DOCTOR)
  2. D-Digoxin                    
  3. O-OCPs                
  4. C-Cimetidine        
  5. T-Theophylline            
  6. O-Oral anticoagulants          
  7. R-Rifampin
    1. MC seen with cholestyramine          
    2. Cholesevelam is safest
  1. Ezitimbe
    1. Cholesterol absorption inhibitor
    2. Luminal drug
    3. More potent than statins
    4. Combined with statins
    5. Increases HDL
    6. Safest lipid lowering drug
  2. CETP Inhibitor:
  • Cholesteryl ester transfer protein (CETP) inhibitors are under active investigation.
  • The first drug in this class, torcetrapib, aroused great interest because it markedly increased HDL and reduced LDL. However, it was withdrawn from clinical trials because it increased cardiovascular events and deaths in the treatment group.
  • Anacetrapib and dalcetrapib are analogs currently in clinical trials.


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