[Lipids, lipoproteins, arterial accidents and oral contraceptives].

This work reviews lipoprotein metabolism and relationships to atherosclerosis, examines the nature of arterial accidents and lipid modifications that occur with oral contraceptive (OC) use, and assesses the practical consequences for OC prescription. Cholesterol, triglycerides, and phospholipids are not soluble in aqueous milieus, and their transport in plasma is provided by macromolecules comprising a protein part and a lipid part. 5 types of these lipoproteins are distinguished by their relative richness in lipids and protein and by the nature of their proteins. The chylomicrons carry exogenous triglycerides to the peripheral tissues and cholesterol of dietary origin to the liver. Very low density lipoprotein (VLDL) cholesterol is secreted by the liver and transports triglycerides and cholesterol of endogenous origin. Low denisty lipoprotein (LDL) cholesterol originates in the degradation of VLDL cholesterol and transports cholesterol to the cells. High density lipoprotein (HDL) cholesterol is secreted by the liver and intestines or formed in the course of degradation of chylomicrons and VLDL cholesterol. Its role is to carry excess cholesterol in the peripheral tissues to the liver for elimination in the bile. Cholesterol thus follows 2 different pathways in the body: a path from the liver to the peripheral cells, whose markers are LDL and VLDL cholesterol and the plasma apoprotein B, and a path of return of excess cholesterol from the tissues and especially the arteries to the liver, marked by HDL cholesterol and the plasma apoprotein A. Only a proper balance between the 2 flows can prevent an excess of cholesterol in the arteries and the consequent constitution of atherosclerotic lesions. LDL and to a lesser extent VLDL cholesterol are strongly and positively correlated to atherogenic risk, while HDL cholesterol is negatively correlated to risk, independently of other risk factors. Arterial accidents occurring with OC use do not seem to be atheromatous in nature. A study by the Lipid Research Clinics of 2000 OC users and nonusers found that users had higher levels of total cholesterol, of triglycerides, and of LDL and VLDL cholesterol, while the elevation of HDL cholesterol was minimal. The effects of combinations of hormones in OCs depend on their composition. OCs with high or medium doses of estrogen cause an elevation in total cholesterol, triglycerides, and LDL and VLDL cholesterol. HDL cholesterol rises slightly with 19 norsteroids and declines with norgestrel. The ratio of total to HDL cholesterol is on the whole increased. OCs with low estrogen doses induce a decline inHDL cholesterol while the levels of total cholesterol and triglycerides remain unchanged. High dose progestin-only pills induce increases in LDL and decreases in HDL cholestrol. Total cholesterol tends to increases with 19 norsteroids and decline with noregestrel while triglycerides vary slightly. With smaller doses of progestin, less intense effects may be seen. The theoretic atherogenic risk determined by the levels and ratio of total and HDL cholesterol is thus increased with some hormonal combinations. OCs can be prescribed for women with normal lipid balance after a pretreatment lipid profile determination. Lipid balance should be reassessed regularly. OCs are contraindicated in cases of moderate or severe hypercholesterolemia and primary hypo HDLemia. Combined OCs may be used in cases of mild hyperlipoproteinemia in which other contraceptive methods are not possible if regular monitoring is provided.