Recall by genotype and cascade screening for familial hypercholesterolemia in a population-based biobank from Estonia

Genet Med. 2019 May;21(5):1173-1180. doi: 10.1038/s41436-018-0311-2. Epub 2018 Oct 1.

Abstract

Purpose: Large-scale, population-based biobanks integrating health records and genomic profiles may provide a platform to identify individuals with disease-predisposing genetic variants. Here, we recall probands carrying familial hypercholesterolemia (FH)-associated variants, perform cascade screening of family members, and describe health outcomes affected by such a strategy.

Methods: The Estonian Biobank of Estonian Genome Center, University of Tartu, comprises 52,274 individuals. Among 4776 participants with exome or genome sequences, we identified 27 individuals who carried FH-associated variants in the LDLR, APOB, or PCSK9 genes. Cascade screening of 64 family members identified an additional 20 carriers of FH-associated variants.

Results: Via genetic counseling and clinical management of carriers, we were able to reclassify 51% of the study participants from having previously established nonspecific hypercholesterolemia to having FH and identify 32% who were completely unaware of harboring a high-risk disease-associated genetic variant. Imaging-based risk stratification targeted 86% of the variant carriers for statin treatment recommendations.

Conclusion: Genotype-guided recall of probands and subsequent cascade screening for familial hypercholesterolemia is feasible within a population-based biobank and may facilitate more appropriate clinical management.

Keywords: cascade screening; familial hypercholesterolemia; genomics-guided disease management; population-based biobank; recall by genotype.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apolipoprotein B-100 / genetics
  • Biological Specimen Banks
  • Estonia / epidemiology
  • Female
  • Genotype
  • Humans
  • Hyperlipoproteinemia Type II / diagnosis*
  • Hyperlipoproteinemia Type II / epidemiology*
  • Hyperlipoproteinemia Type II / genetics*
  • Male
  • Mass Screening / methods*
  • Mutation
  • Proprotein Convertase 9 / genetics
  • Receptors, LDL / genetics
  • Sequence Analysis, DNA

Substances

  • APOB protein, human
  • Apolipoprotein B-100
  • LDLR protein, human
  • Receptors, LDL
  • PCSK9 protein, human
  • Proprotein Convertase 9