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Article

Genetic and biochemical analyses in dyslipidemic patients undergoing LDL apheresis.

Journal of clinical apheresis - 1 Oct 2014

Donato Leslie J, Saenger Amy K, Train Laura J, Kotzer Katrina E, Lagerstedt Susan A, Hornseth Jean M, Basu Ananda, Winters Jeffrey L, Baudhuin Linnea M

Abstract excerpt

OBJECTIVE: Familial hypercholesterolemia (FH) can be due to mutations in LDLR, PCSK9, and APOB. In phenotypically defined patients, a subset remains unresponsive to lipid-lowering therapies and requires low density-lipoprotein (LDL) apheresis treatment. In this pilot study, we examined the genoty...

Read the complete abstract on PubMed

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cholesterol, LDL

Share to Hyperlipoproteinemia Type II

Share to Lipoprotein(a)

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Share to Receptors, LDL

Source

Identifiers

PMID: 24420163
DOI: 10.1002/jca.21317

Genes

LDLR
APOB
PCSK9

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-24420163-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

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