In the space of the few years since the publication of the Scandinavian Simvastatin Survival Study (4S) in 1994, cholesterol-lowering treatment and identification of the patients who should receive such therapy has moved from the esoteric practice of a few specialists, viewed by their colleagues with deep suspicion, to occupy a significant and a growing area of mainstream medicine. Many generalists are thus encountering for the first time difficulties posed by patients whose dyslipidaemia refuses to conform to the preconceptions of various national guidelines, which are often an attempt to oversimplify complex metabolic problems. The realisation must increasingly be faced that more knowledge of the pathophysiology of lipoprotein disorders can improve clinical effectiveness. I hope that this short account will prove absorbing, fairly painless and reasonably comprehensive.

This part includes information about common (polygenic) hypercholesterolaemia, familial (monogenic) hypercholesterolaemia, familial combined hyperlipidaemia, hypertriglyceridaemia (moderate and severe), type III hyperlipoproteinaemia, secondary dyslipidaemias and hypolipoproteinaemia (increasingly encountered as the result of more cholesterol testing).

Paul N Durrington
University of Manchester, Manchester, July 2002