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D. Gudbjartsson, G. Thorgeirsson, P. Sulem, A. Helgadóttir, Arnaldur Gylfason, Jona Saemundsdottir, E. Bjornsson, G. Norddahl, Á. Jónasdóttir, A. Jonasdottir, Hannes Eggertsson, S. Gretarsdottir, G. Thorleifsson, O. Indridason, R. Palsson, F. Jónasson, I. Jónsdóttir, G. Eyjolfsson, O. Sigurdardottir, I. Olafsson, R. Danielsen, Stefán Matthíasson, Snaedis Kristmundsdottir, B. Halldórsson, Á. Hreidarsson, E. Valdimarsson, T. Gudnason, R. Benediktsson, V. Steinthorsdottir, U. Thorsteinsdóttir, H. Hólm, K. Stefánsson (2019)
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Arteriosclerosis, Thrombosis, and Vascular Biology LETTER TO THE EDITOR Response by Björnsson et al to Letter Regarding Article, “Large-Scale Screening for Monogenic and Clinically Defined Familial Hypercholesterolemia in Iceland” Eythór Björnsson, Gudmundur Thorgeirsson, Anna Helgadóttir, Daníel F. Gudbjartsson, Hilma Hólm, Unnur Thorsteinsdóttir, Patrick Sulem, Kári Stefánsson In Response: measurements in our sample, we found extremely high We thank Tromp et al for their interest in our article. molar concentration of lipoprotein(a) (>200 nmol/L) in As the authors mention, we found that the clinical familial 9.3% (n=58 out of 622) of individuals with clinical FH, hypercholesterolemia (FH) phenotype (defined as prob- compared with 4.4% (n=1683 out of 38 426) of those able or definite FH using modified Dutch lipid clinic net- without clinical FH. Thus, it is reasonable to assume that work criteria) was explained by monogenic FH in only about 9% of clinical FH in our study may be explained, about 5% of cases. Tromp et al wonder whether this find- at least in part, by extremely high levels of lipoprotein(a). ing may be related to overestimation of the prevalence Importantly, the cardiovascular risk of these individuals of clinical FH in our study due to: (1) the use of
Arteriosclerosis Thrombosis and Vascular Biology – Wolters Kluwer Health
Published: Jan 23, 2022
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