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Severe hypertriglyceridemia is primarily polygenic.

Jacqueline S Dron1, Jian Wang2, Henian Cao2

  • 1Robarts Research Institute, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada; Department of Biochemistry, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada.

Journal of Clinical Lipidology
|November 24, 2018
PubMed
Summary
This summary is machine-generated.

Genetic factors significantly influence hypertriglyceridemia (HTG). This study reveals that common genetic variants, indicated by a high polygenic risk score, are the primary driver of HTG, while rare variants also contribute.

Keywords:
Copy-number variants (CNVs)Familial chylomicronemia syndrome (FCS)Hypertriglyceridemia (HTG)MonogenicNext-generation sequencing (NGS)PolygenicPolygenic risk scoreRare variantsSingle-nucleotide polymorphism (SNP)

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Area of Science:

  • Genetics
  • Molecular Biology
  • Cardiovascular Disease

Background:

  • Hypertriglyceridemia (HTG) is a complex trait characterized by elevated plasma triglyceride levels.
  • The genetic underpinnings of HTG, encompassing both monogenic and polygenic factors, remain incompletely understood.

Purpose of the Study:

  • To comprehensively characterize the genetic profiles of individuals with severe HTG.
  • To quantify the contributions of genetic determinants and molecular factors to severe HTG.

Main Methods:

  • Conducted targeted next-generation sequencing of 73 genes and 185 SNPs related to dyslipidemia in two independent cohorts (n=563).
  • Screened for rare variants in key genes (LPL, APOC2, GPIHBP1, APOA5, LMF1).
  • Utilized a polygenic risk score to evaluate the impact of common variant accumulation.

Main Results:

  • Combined analysis of 563 Caucasian patients revealed significant genetic susceptibility to HTG compared to controls (OR 5.77).
  • 32.0% of patients exhibited an extreme accumulation of common variants (high polygenic risk), and 14.4% carried heterozygous rare variants.
  • Only 1.1% of patients had biallelic rare variants, indicating monogenic HTG.

Conclusions:

  • This study provides the most in-depth evaluation of genetic determinants for severe HTG to date.
  • The predominant genetic feature in severe HTG is the accumulation of common variants (polygenic HTG, 46.3%), with rare variants contributing in a subset of patients.
  • Monogenic HTG due to biallelic rare variants is rare (1.1%).