Type of LDLR mutation and the pharmacogenetics of familial hypercholesterolemia treatment

Pharmacogenomics. 2015;16(15):1743-50. doi: 10.2217/pgs.15.113. Epub 2015 Oct 2.

Abstract

Familial hypercholesterolemia (FH) is an autosomal dominant disease mainly caused by mutations in the low-density lipoprotein receptor (LDLR) gene. FH patients present a wide variability regarding response to drugs and they are usually undertreated. Here, we review studies that evaluated the association between the type of LDLR mutation and the response to lipid-lowering therapy. The main findings were that patients with a null LDLR mutation had: higher baseline LDL-C, higher LDL-C after drug therapy, lower proportion of patients within the LDL-C target value and higher frequencies of CVD. Thus, we conclude that FH patients harboring a null mutation have a trend to an increased risk, even if diagnosis is early established and lipid-lowering treatment instituted. It is suggested that these individuals may benefit from the use of newly approved lipid-lowering agents.

Keywords: LDLR mutation; familial hypercholesterolemia; lipid-lowering therapy; pharmacogenomics; type of mutation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Anticholesteremic Agents / therapeutic use*
  • Humans
  • Hyperlipoproteinemia Type II / drug therapy*
  • Hyperlipoproteinemia Type II / genetics*
  • Mutation / genetics*
  • Pharmacogenetics*
  • Receptors, LDL / genetics*

Substances

  • Anticholesteremic Agents
  • LDLR protein, human
  • Receptors, LDL