Publications by authors named "Sibbeliene E van den Bosch"
Purpose: Familial hypercholesterolemia (FH) leads to elevated low-density lipoprotein cholesterol levels, which increases the risk of premature atherosclerotic cardiovascular disease (ASCVD). Since the first functional and morphologic changes of the arterial wall occur in childhood, treatment should start early in childhood to mitigate the elevated risk of ASCVD. Pediatricians play an important role in the detection and care of children with FH.
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- - The study investigates the knowledge and practice of familial hypercholesterolaemia (FH) care among Dutch general practitioners (GPs) to address underdiagnosis and undertreatment of the condition, which can lead to early cardiovascular disease.
- - An online questionnaire revealed that while a majority of GPs rated their familiarity with FH positively, many lacked accurate understanding of key FH concepts, with 58.4% scoring low on knowledge questions.
- - Findings show that despite better familiarity and guideline awareness in the Netherlands compared to other regions, significant knowledge gaps remain, highlighting the need for improved education and global collaboration in FH understanding.
Article Synopsis
- Familial hypercholesterolemia is a genetic condition that causes high LDL cholesterol levels from birth, increasing the risk of heart disease.
- Early screening and treatment in children can significantly lower the chances of developing premature cardiovascular issues.
- Recent advancements in cholesterol-lowering therapies have made familial hypercholesterolemia manageable, with studies showing favorable outcomes and cost-effectiveness for early interventions.
Familial hypercholesterolemia (FH) is one of the most common genetically inherited disorders in the world. Children with severe heterozygous FH (HeFH), i.e.
View Article and Find Full Text PDFFamilial hypercholesterolemia (FH) is a hereditary disorder that causes severely elevated low-density lipoprotein (LDL-C) levels, which leads to an increased risk for premature cardiovascular disease. A variety of genetic variants can cause FH, namely variants in the genes for the LDL receptor (), apolipoprotein B (), proprotein convertase subtilisin/kexin type 9 (), and/or LDL-receptor adaptor protein 1 (). Variants can exist in a heterozygous form (HeFH) or the more severe homozygous form (HoFH).
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