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Lipids Lipoproteins Cholesterol Dyslipidaemia Classification Atherosclerosis CV Risk Factors Clinical Manifestation |
Dyslipidaemia ClassificationFredrickson (WHO) Classification The Fredrickson classification was the first classification of dyslipidaemias. It was based on the analysis of plasma for various lipoprotein fractions, but took no account of the underlying aetiology of any of the dyslipidaemias. In addition, high-density lipoprotein (HDL) cholesterol levels are not considered in this classification.1 Today it is more common to identify the dyslipidaemias by the particular lipoprotein or apolipoprotein that is abnormal. Once dyslipidaemia has been identified it is important to determine the cause where possible. Dyslipidaemia may be secondary to other disorders or a primary abnormality. Common causes of secondary dyslipidaemia include: diabetes mellitus, the nephrotic syndrome, chronic renal failure, hepatobiliary disease (generally of the obstructive variety) and hypothyroidism. It should be recognized that these cause some but not all dyslipidaemias. For example, diabetes can lead to elevation of triglyceride-rich lipoproteins and reduction of HDL, but does not necessarily increase the levels of LDL. On the other hand, hepatobiliary disease is associated with an increase in the levels of LDL. Of the primary causes of dyslipidaemia, the most severe forms are caused by genetic disorders of lipoprotein metabolism. The most easily identifiable in clinical practice are familial hypercholesterolaemia (FH), polygenic hypercholesterolaemia and familial combined hypercholesterolaemia, all of which increase the risk of premature development of CHD. FH is an autosomal dominant disease with defects in the gene for the LDL receptor. Patients presenting with severe forms of hypercholesterolaemia should undergo family screening to detect other family members for therapy.2 Therapy of these disorders is directed towards aggressive management of hypercholesterolaemia with a LDL-C that depends on the overall coronary risk of the affected person.2 *Adapted from Southern Med J 1995;88:379–391, with permission from Lippincott Williams & Wilkins. References |
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