title: Cholesterol metabolism differs after statin therapy according to the type of hyperlipemia.
abstract: OBJECTIVE
  Non-cholesterol sterols reflect cholesterol metabolism. Statins reduce cholesterol synthesis usually with a rise in cholesterol absorption. Common hyperlipemias have shown different patterns of cholesterol metabolism. We evaluated whether cholesterol absorption and synthesis may differ after statin therapy in primary hyperlipemias.
  
  
  METHODS
  We determined lipid profile, apoprotein B and serum sterols (lathosterol, sitosterol, campesterol by gas chromatography/mass spectrometry) before and after statins in 80 untreated hyperlipemic patients, 40 with polygenic hypercholesterolemia (PH) and 40 with familial combined hyperlipemia (FCH).
  
  
  RESULTS
  At baseline in FCH lathosterol was significantly higher while campesterol and sitosterol were significantly lower than in PH. After statins, the reduction in LDL-C did not significantly differ between the two groups; in PH there was a significant decrease of lathosterol from 96.1 to 52.6 102 μmol/mmol cholesterol (p=0.0001) with no significant modifications in campesterol and sitosterol; on the opposite, in FCH lathosterol decreased from 117 to 43 102 μmol/mmol cholesterol (p=0.0001) and campesterol and sitosterol significantly increased from 38 to 48 102 μmol/mmol cholesterol (p=0.0001), and from 75 to 86 102 μmol/mmol cholesterol, (p=0.022), respectively. After statin therapy only in FCH Δ-LDL-C showed a significant inverse correlation with Δ-sitosterol and with Δ-campesterol.
  
  
  CONCLUSIONS
  Primary hyperlipemias show different patterns of response to statins: in PH LDL reduction appears completely "synthesis inhibition" dependent, while in FCH LDL decrease appears to be synthesis dependent, partially limited by absorption increase. Studying cholesterol metabolism before and after hypolipemic therapy might be useful in identifying the best tailored treatment.
authors.affiliation: Internal Medicine, Angiology and Atherosclerosis, Department of Clinical and Experimental Medicine, University of Perugia, Italy. glupa@unipg.it
authors.forename: Graziana
authors.initials: G
authors.lastname: Lupattelli
authors.forename: Donatella
authors.initials: D
authors.lastname: Siepi
authors.forename: Stefano
authors.initials: S
authors.lastname: De Vuono
authors.forename: Anna Rita
authors.initials: AR
authors.lastname: Roscini
authors.forename: Federica
authors.initials: F
authors.lastname: Crisanti
authors.forename: Domenico
authors.initials: D
authors.lastname: Covelli
authors.forename: Matteo
authors.initials: M
authors.lastname: Pirro
authors.forename: Elmo
authors.initials: E
authors.lastname: Mannarino
mesh_terms: D000328:Adult; D000368:Aged; D000069059:Atorvastatin; D002784:Cholesterol / Q000031:analogs & derivatives / Q000097:blood*; D008078:Cholesterol, LDL / Q000097:blood; D005260:Female; D008401:Gas Chromatography-Mass Spectrometry; D006538:Heptanoic Acids / Q000494:pharmacology; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology*; D006937:Hypercholesterolemia / Q000188:drug therapy*; D006950:Hyperlipidemia, Familial Combined / Q000188:drug therapy*; D006949:Hyperlipidemias / Q000188:drug therapy*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D010840:Phytosterols / Q000097:blood; D011758:Pyrroles / Q000494:pharmacology; D019821:Simvastatin / Q000494:pharmacology; D012855:Sitosterols / Q000097:blood
chemical_list: D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D010840:Phytosterols; D011758:Pyrroles; D012855:Sitosterols; C021273:campesterol; C025473:gamma-sitosterol; D002784:Cholesterol; D000069059:Atorvastatin; D019821:Simvastatin