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Hypolipidemic treatment of heterozygous familial hypercholesterolemia: a lifelong challenge

In familial hypercholesterolemia, a defect in low-density lipoprotein receptors causes lifelong two- to threefold elevations in serum low-density lipoprotein-cholesterol levels. This leads to early atherosclerotic changes in infancy. Lifelong hypolipidemic treatment that can be started at a young ag... Full description

Journal Title: Expert review of cardiovascular therapy 2004, Vol.2 (3), p.405-415
Main Author: Vuorio, Alpo F
Other Authors: Kovanen, Petri T , Gylling, Helena
Format: Electronic Article Electronic Article
Language: English
Subjects:
DNA
Quelle: Alma/SFX Local Collection
Publisher: England: Informa Healthcare
ID: ISSN: 1477-9072
Link: https://www.ncbi.nlm.nih.gov/pubmed/15151486
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recordid: cdi_informaworld_taylorfrancis_310_1586_14779072_2_3_405
title: Hypolipidemic treatment of heterozygous familial hypercholesterolemia: a lifelong challenge
format: Article
creator:
  • Vuorio, Alpo F
  • Kovanen, Petri T
  • Gylling, Helena
subjects:
  • atherosclerosis
  • Cholesterol
  • combination therapy
  • Criminal investigation
  • Diagnosis
  • DNA
  • Drug therapy
  • ezetimibe
  • familial hypercholesterolemia
  • Genetic aspects
  • Health aspects
  • Heterozygote
  • hsCRP
  • Humans
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use
  • Hypercholesterolemia
  • Hyperlipoproteinemia Type II - diagnosis
  • Hyperlipoproteinemia Type II - drug therapy
  • Hyperlipoproteinemia Type II - genetics
  • Hypolipidemic Agents - therapeutic use
  • LDL-cholesterol
  • LDL-receptor
  • Low density lipoproteins
  • Mutation - drug effects
  • Mutation - genetics
  • Physiological aspects
  • Receptors, LDL - drug effects
  • Receptors, LDL - genetics
  • Risk factors
  • stanol
  • statin
  • Statins
  • treatment
ispartof: Expert review of cardiovascular therapy, 2004, Vol.2 (3), p.405-415
description: In familial hypercholesterolemia, a defect in low-density lipoprotein receptors causes lifelong two- to threefold elevations in serum low-density lipoprotein-cholesterol levels. This leads to early atherosclerotic changes in infancy. Lifelong hypolipidemic treatment that can be started at a young age is thus greatly needed. Early diagnosis of familial hypercholesterolemia is important, and improved DNA tests for low-density lipoprotein receptor mutations have made it possible to carry out diagnosis at birth. A low saturated-fat, low cholesterol diet can be safely started at 7 months of age. This can be accompanied by dietary stanol esters from 2 years of age. At the age of 10, statin treatment can be safely started. In adults, more aggressive hypolipidemic treatment is required in order to reach the treatment goal for serum low-density lipoprotein-cholesterol levels less than 2.5 mmol/l. This can be achieved by using high doses of statin, or preferably by combining a statin with resin or ezetimibe (Zeita®, Merck and Shering-Plough Pharmaceuticals). Once started, treatment of familial hypercholesterolemia is lifelong.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 1477-9072
fulltext: fulltext
issn:
  • 1477-9072
  • 1744-8344
url: Link


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descriptionIn familial hypercholesterolemia, a defect in low-density lipoprotein receptors causes lifelong two- to threefold elevations in serum low-density lipoprotein-cholesterol levels. This leads to early atherosclerotic changes in infancy. Lifelong hypolipidemic treatment that can be started at a young age is thus greatly needed. Early diagnosis of familial hypercholesterolemia is important, and improved DNA tests for low-density lipoprotein receptor mutations have made it possible to carry out diagnosis at birth. A low saturated-fat, low cholesterol diet can be safely started at 7 months of age. This can be accompanied by dietary stanol esters from 2 years of age. At the age of 10, statin treatment can be safely started. In adults, more aggressive hypolipidemic treatment is required in order to reach the treatment goal for serum low-density lipoprotein-cholesterol levels less than 2.5 mmol/l. This can be achieved by using high doses of statin, or preferably by combining a statin with resin or ezetimibe (Zeita®, Merck and Shering-Plough Pharmaceuticals). Once started, treatment of familial hypercholesterolemia is lifelong.
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languageeng
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subjectatherosclerosis ; Cholesterol ; combination therapy ; Criminal investigation ; Diagnosis ; DNA ; Drug therapy ; ezetimibe ; familial hypercholesterolemia ; Genetic aspects ; Health aspects ; Heterozygote ; hsCRP ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use ; Hypercholesterolemia ; Hyperlipoproteinemia Type II - diagnosis ; Hyperlipoproteinemia Type II - drug therapy ; Hyperlipoproteinemia Type II - genetics ; Hypolipidemic Agents - therapeutic use ; LDL-cholesterol ; LDL-receptor ; Low density lipoproteins ; Mutation - drug effects ; Mutation - genetics ; Physiological aspects ; Receptors, LDL - drug effects ; Receptors, LDL - genetics ; Risk factors ; stanol ; statin ; Statins ; treatment
ispartofExpert review of cardiovascular therapy, 2004, Vol.2 (3), p.405-415
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descriptionIn familial hypercholesterolemia, a defect in low-density lipoprotein receptors causes lifelong two- to threefold elevations in serum low-density lipoprotein-cholesterol levels. This leads to early atherosclerotic changes in infancy. Lifelong hypolipidemic treatment that can be started at a young age is thus greatly needed. Early diagnosis of familial hypercholesterolemia is important, and improved DNA tests for low-density lipoprotein receptor mutations have made it possible to carry out diagnosis at birth. A low saturated-fat, low cholesterol diet can be safely started at 7 months of age. This can be accompanied by dietary stanol esters from 2 years of age. At the age of 10, statin treatment can be safely started. In adults, more aggressive hypolipidemic treatment is required in order to reach the treatment goal for serum low-density lipoprotein-cholesterol levels less than 2.5 mmol/l. This can be achieved by using high doses of statin, or preferably by combining a statin with resin or ezetimibe (Zeita®, Merck and Shering-Plough Pharmaceuticals). Once started, treatment of familial hypercholesterolemia is lifelong.
subject
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16Hyperlipoproteinemia Type II - diagnosis
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20LDL-cholesterol
21LDL-receptor
22Low density lipoproteins
23Mutation - drug effects
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25Physiological aspects
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abstractIn familial hypercholesterolemia, a defect in low-density lipoprotein receptors causes lifelong two- to threefold elevations in serum low-density lipoprotein-cholesterol levels. This leads to early atherosclerotic changes in infancy. Lifelong hypolipidemic treatment that can be started at a young age is thus greatly needed. Early diagnosis of familial hypercholesterolemia is important, and improved DNA tests for low-density lipoprotein receptor mutations have made it possible to carry out diagnosis at birth. A low saturated-fat, low cholesterol diet can be safely started at 7 months of age. This can be accompanied by dietary stanol esters from 2 years of age. At the age of 10, statin treatment can be safely started. In adults, more aggressive hypolipidemic treatment is required in order to reach the treatment goal for serum low-density lipoprotein-cholesterol levels less than 2.5 mmol/l. This can be achieved by using high doses of statin, or preferably by combining a statin with resin or ezetimibe (Zeita®, Merck and Shering-Plough Pharmaceuticals). Once started, treatment of familial hypercholesterolemia is lifelong.
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