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Familial hypercholesterolaemia is underdiagnosed and undertreated in the general population: guidance for clinicians to prevent coronary heart disease: consensus statement of the European Atherosclerosis Society.
Nordestgaard, BG, Chapman, MJ, Humphries, SE, Ginsberg, HN, Masana, L, Descamps, OS, Wiklund, O, Hegele, RA, Raal, FJ, Defesche, JC, et al
European heart journal. 2013;(45):3478-90a
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Abstract
AIMS: The first aim was to critically evaluate the extent to which familial hypercholesterolaemia (FH) is underdiagnosed and undertreated. The second aim was to provide guidance for screening and treatment of FH, in order to prevent coronary heart disease (CHD). METHODS AND RESULTS Of the theoretical estimated prevalence of 1/500 for heterozygous FH, <1% are diagnosed in most countries. Recently, direct screening in a Northern European general population diagnosed approximately 1/200 with heterozygous FH. All reported studies document failure to achieve recommended LDL cholesterol targets in a large proportion of individuals with FH, and up to 13-fold increased risk of CHD. Based on prevalences between 1/500 and 1/200, between 14 and 34 million individuals worldwide have FH. We recommend that children, adults, and families should be screened for FH if a person or family member presents with FH, a plasma cholesterol level in an adult ≥8 mmol/L(≥310 mg/dL) or a child ≥6 mmol/L(≥230 mg/dL), premature CHD, tendon xanthomas, or sudden premature cardiac death. In FH, low-density lipoprotein cholesterol targets are <3.5 mmol/L(<135 mg/dL) for children, <2.5 mmol/L(<100 mg/dL) for adults, and <1.8 mmol/L(<70 mg/dL) for adults with known CHD or diabetes. In addition to lifestyle and dietary counselling, treatment priorities are (i) in children, statins, ezetimibe, and bile acid binding resins, and (ii) in adults, maximal potent statin dose, ezetimibe, and bile acid binding resins. Lipoprotein apheresis can be offered in homozygotes and in treatment-resistant heterozygotes with CHD. CONCLUSION Owing to severe underdiagnosis and undertreatment of FH, there is an urgent worldwide need for diagnostic screening together with early and aggressive treatment of this extremely high-risk condition.
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Role of fibrates in reducing coronary risk: a UK Consensus.
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Current medical research and opinion. 2004;(2):241-7
Abstract
This paper presents the consensus reached by a panel of experts on the role of fibrates in reducing coronary heart disease (CHD). The emphasis is on the application of these agents in clinical practice. Evidence that low levels of high-density lipoprotein cholesterol (HDL-C) play a major role in the development of CHD, plus the roles of lifestyle modification and statin treatment in raising HDL-C, are briefly reviewed. Current thinking on single agent and combination therapies with fibrates is discussed with particular relevance to patients with low baseline HDL-C- whether receiving statins or not - and those with features of the metabolic syndrome. Recommendations on the practical use of fibrates are made in the light of recently published international guidelines on HDL-C management and the relevant evidence base.
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UK Food Standards Agency cis-monounsaturated fatty acid workshop report.
Sanderson, P, Gill, JM, Packard, CJ, Sanders, TA, Vessby, B, Williams, CM
The British journal of nutrition. 2002;(1):99-104
Abstract
The UK Food Standards Agency convened a group of expert scientists to review current research investigating the optimal dietary intake for n-9 cis-monounsaturated fatty acids (MUFA). The aim was to review the mechanisms underlying the reported beneficial effects of MUFA on CHD risk, and to establish priorities for future research. The issue of optimal MUFA intake is contingent upon optimal total fat intake; however, there is no consensus of opinion on what the optimal total fat intake should be. Thus, it was recommended that a large multi-centre study should look at the effects on CHD risk of MUFA replacement of saturated fatty acids in relation to varying total fat intakes; this study should be of sufficient size to take account of genetic variation, sex, physical activity and stage of life factors, as well as being of sufficient duration to account for adaptation to diets. Recommendations for studies investigating the mechanistic effects of MUFA were also made. Methods of manipulating the food chain to increase MUFA at the expense of saturated fatty acids were also discussed.