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Cholesterol synthesis inhibitors do not reduce Lp(a) levels in normocholesterolemic patients.

Abstract
Experimental and clinical data suggest that activation of the LDL receptors by the use of HMG CoA reductase inhibitors, in the presence of normal plasma cholesterol levels, may result in a reduction of Lp(a) concentrations. This hypothesis has been tested in an open study on seven subjects with normal cholesterolemia but marked elevations of Lp(a) levels, three of whom received pravastatin and four simvastatin at standard therapeutic doses. While the two drugs caused the expected reduction of plasma total and LDL cholesterol levels, no significant changes in Lp(a) were noted. This study contradicts a prior clinical finding and suggests that HMG CoA reductase inhibitors are unlikely to reduce plasma Lp(a) levels even in the absence of hypercholesterolemia.
AuthorsF Pazzucconi, G Franceschini, G Gianfranceschi, G Campagnoli, C R Sirtori
JournalPharmacological research (Pharmacol Res) 1996 Sep-Oct Vol. 34 Issue 3-4 Pg. 131-3 ISSN: 1043-6618 [Print] Netherlands
PMID9051704 (Publication Type: Clinical Trial, Journal Article, Randomized Controlled Trial, Research Support, Non-U.S. Gov't)
Chemical References
  • Anticholesteremic Agents
  • Lipoprotein(a)
  • Receptors, LDL
  • Cholesterol
  • Lovastatin
  • Simvastatin
  • Pravastatin
Topics
  • Anticholesteremic Agents (pharmacology)
  • Cholesterol (biosynthesis)
  • Female
  • Humans
  • Lipoprotein(a) (blood)
  • Lovastatin (analogs & derivatives, pharmacology)
  • Male
  • Middle Aged
  • Pravastatin (pharmacology)
  • Receptors, LDL (biosynthesis, drug effects)
  • Simvastatin

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