Tag Archives: hypercholesterolaemia

Introduction Hypercholesterolaemia, characterised by elevated serum total cholesterol and low-density lipoprotein (LDL), is a crucial factor for atherosclerosis and for the development of cardiovascular diseases (CVD). The hepatic protease proprotein convertase subtilisin/kexin type 9 (PCSK9) targets LDL-receptors for destruction.1,2 Removal of LDL from the blood stream is aided by increased expression of LDL-receptors.3 Statins have been proven to effectively lower LDL-cholesterol (LDL-C) levels and reduce CVD events in many high cardiovascular risk cohorts via 3-hydroxy-3-methylglutaryl coenzyme A (HMG Co-A) reductase inhibition. However, a

Introduction Statins are the gold-standard lipid-lowering therapy based on their efficacy in reducing serum low-density lipoprotein cholesterol (LDL-C) and general tolerability.1 While statins have an extensive body of evidence that have shown them to reduce the risk of cardiovascular (CV) events,2,3 there are concerns around side effects. An increase in cases of treatment-induced comorbidities, such as new-onset diabetes mellitus (NODM) has been observed.4-6 When combined with patient and media concerns, this has led to a reported 50% drop-out rate within 12 months.1 In response, other LDL-C lowering medications have been developed. Proprote

Familial hypercholesterolaemia or not? The importance of considering polygenic hypercholesterolaemia in those with no monogenic cause for familial hypercholesterolaemia (FH), was outlined by Professor Steve Humphries (UCL Institute of Cardiovascular Science, London).1 By looking for the presence of specific high low-density lipoprotein cholesterol (LDL-C), single nucleotide polymorphisms (SNPs) and combining these to generate a SNP-score, those with the most variants can be identified. Professor Steve Humphries Individuals who are in the top five deciles of the SNP-score are highly likely to have a polygenic explanation for their high LDL-C

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FH: improving detection in primary care The launch of the NICE (National Institute of Health and Care Excellence) guidelines for familial hypercholesterolaemia (FH) heralded great optimism for improving detection rates in primary care.1 Even with new research showing that FH is more common than previously thought,2  still around 80% of patients are not recognised. Novel detection approaches are clearly needed. Professor Nadeem Qureshi (University of Nottingham) presented preliminary findings from six GP centres taking part in FAMCHOL (Feasibility of Improving Identification of Familial Hypercholesterolaemia in General Practice: Intervention

Introduction Bile acid sequestrants (BAS) were the first class of lipid-lowering drug to be developed for reducing blood cholesterol levels.1 Now, after their introduction 30 years ago, BAS still continue to command a position in the treatment of hyperlipidaemia.2 How do BAS work? Figure 1. Mode of action of bile acid sequestrants BAS bind to negatively charged bile acids in the intestine and impede their absorption (figure 1). This process depletes the bile acid pool and disrupts the enterohepatic circulation of bile acids, thus, increasing the synthesis of bile acids. Cholesterol is, therefore, diverted to bile acid synthesis, thereby reduc

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