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Harangi et al. Vessel Plus 2017;1:91-5 Vessel Plus
DOI: 10.20517/2574-1209.2017.08
www.vpjournal.net
Case Report Open Access

LDL apheresis or PCSK9 inhibition?

Sometimes we have to combine them

Mariann Harangi, Lilla Juhász, Bíborka Nádró, József Balla, György Paragh
Department of Internal Medicine, University of Debrecen Faculty of Medicine, H-4032 Debrecen, Hungary.

Correspondence to: Dr. Mariann Harangi, Department of Internal Medicine, University of Debrecen Faculty of Medicine, Nagyerdei krt. 98, H-4032
Debrecen, Hungary. E-mail: mharangi@hotmail.com

How to cite this article: Harangi M, Juhász L, Nádró B, Balla J, Paragh G. LDL apheresis or PCSK9 inhibition? Sometimes we have to combine
them. Vessel Plus 2017;1:91-5.
Dr. Mariann Harangi is an Associate Professor at Department of Internal Medicine at University of Debrecen,
Faculty of Medicine, Hungary. She is specialized in treatment of primary and secondary lipid disorders with
particular focus on familial hypercholesterolemia and statin intolerance. She is the General Secretary of the
Hungarian Atherosclerosis Society.

ABSTRACT
Article history: This study presents the case of a female patient with severe heterozygous familial
Received: 26-03-2017 hypercholesterolemia. Despite the combined maximum dose oral treatment with rosuvastatin
Accepted: 18-04-2017 and ezetimibe, we found markedly elevated lipid parameters. Therefore, we indicated monthly
Published: 27-06-2017 selective low density lipoprotein (LDL) apheresis treatment using the Direct Adsorption of
Lipoproteins system. After more than 2 years the lipid levels of the patients were still above the
Key words: therapeutic goals. Finally, we completed the treatment by the inhibitor evolocumab biweekly.
Low density lipoprotein apheresis, Further LDL cholesterol (LDL-C) reduction was achieved resulting in lipid parameters on
PCSK9 inhibition, goals. However, administration of evolocumab without LDL apheresis could not reduce the
familial hypercholesterolemia, LDL-C below 2.5 mmol/L. We concluded that both LDL apheresis and proprotein convertase
low-density lipoprotein, subtilisin/kexin type 9 (PCSK9) inhibitor treatments were effective and well tolerated. None of
lipoprotein(a) them alone would be enough to achieve lipid goals in this patient. However, the combination of
these potent treatments may normalize the lipid levels and prevent cardiovascular complications.

INTRODUCTION phenotype include LDLR (low-density lipoprotein
receptor), APOB (apolipoprotein B-100), and PCSK9
Familial hypercholesterolemia (FH) is perhaps the (proprotein convertase subtilisin/kexin type 9).
[2]
most common single-gene variant causing premature The FH phenotype is based on family history, LDL
morbidity and mortality. Heterozygous FH affects cholesterol (LDL-C) levels, and presence of physical
about 1 in 200 people. Genetic loci involved in FH findings such as xanthomas, xanthelasma and corneal
[1]
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