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- W4387667090 abstract "Homozygous familial hypercholesterolemia (HoFH) exemplifies that low-density lipoprotein cholesterol (LDL-C) in the absence of additional risk factors is both causal and sufficient to cause and progress atherosclerotic vascular disease and aortic valve stenosis. While for the vast majority of patients with hypercholesterolemia – even those with heterozygous familial hypercholesterolemia (HeFH) [ [1] Katzmann J.L. Lehmann M. Tünnemann-Tarr A. an Haack I. Dressel A. März W. Laufs U. Cutaneous manifestations in familial hypercholesterolaemia. Atherosclerosis. 2021; 333: 116-123https://doi.org/10.1016/j.atherosclerosis.2021.07.007 Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar ] – elevated LDL-C is an imperceptible and invisible contributor to the development of atherosclerosis, in patients with HoFH, the observable cholesterol deposits in the skin and tendons (xanthomas) mirror the parallel pathological processes occurring in the arteries. Patients with HoFH suffer from severely elevated LDL-C from birth due to homozygous (bi-allelic) defects of the LDL receptor, and usually develop atherosclerosis in the first years of life. Those who remain untreated have an average life expectancy of 18 years [ [2] Raal F.J. Pilcher G.J. Panz V.R. van Deventer H.E. Brice B.C. Blom D.J. Marais A.D. Reduction in mortality in subjects with homozygous familial hypercholesterolemia associated with advances in lipid-lowering therapy. Circulation. 2011; 124: 2202-2207https://doi.org/10.1161/CIRCULATIONAHA.111.042523 Crossref PubMed Scopus (290) Google Scholar ]. Therefore, early identification and effective treatment of patients with HoFH is of great importance (see Fig. 1)." @default.
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- W4387667090 date "2023-10-01" @default.
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- W4387667090 title "Liver transplantation for homozygous familial hypercholesterolemia: Cure for a genetic disease?" @default.
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- W4387667090 doi "https://doi.org/10.1016/j.atherosclerosis.2023.117337" @default.
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