Contraceptivos orais (OC) ou terapia de reposição hormonal

The ESHRE Capri Workshop Group*

Introduction

The following topics related to oral contraceptives (OC) or

hormonal replacement therapy (HRT) were critically discussed

during the workshop: metabolic changes; haemostatic function;

vascular effects; influence on the evolution of the atherosclerotic

plaque; and specific risks and benefits for coronary heart

disease (CHD), venous thromboembolism (VTE) and stroke.

Metabolic changes occuring in women using OC or HRT

Lipids and lipoprotein

Oral contraception

Changes seen in lipids and lipoproteins with combined OC

vary according to the progestogen type and the dose (Godsland

et al., 1990). OC containing low-dose norethisterone or desogestrel

decrease low density lipoprotein (LDL) and increase

high density lipoprotein (HDL) concentrations, as do those

containing gestodene (Crook et al., 1993). Those containing

levonorgestrel and high-dose norethisterone have no effect on

LDL but decrease HDL, particularly HDL2. Most OC increase

triglycerides but this effect is lessened by higher doses of

levonorgestrel (Godsland et al., 1990). The OC-induced

increase in triglycerides is due to increased synthesis rather than

to decreased elimination. Postprandial triglyceride elimination

appears to be increased in OC users. Progestogen-only OC

have minimal effects on lipids and lipoproteins, although there

is a tendency to decrease HDL.

Hormone replacement therapy

With HRT, the changes seen in lipids and lipoproteins depend

both on the types of steroids used, the dose, and their route

of administration. Oral oestrogen therapy improves the lipid

profile by lowering total and LDL cholesterol. It also causes

an increase in HDL, and especially in the HDL2 subfraction

which is thought to confer a degree of cardiovascular protection.

This latter effect appears to be less pronounced with trans-

*A meeting was organized by ESHRE (Capri, September 4–5, 1997)

with financial support from Schering S.p.A. to discuss the above

subjects. The speakers included J.Collins (Hamilton), P.Collins

(London), P.G.Crosignani (Milan), C.La Vecchia (Milan),

P.M.Mannucci (Milan), D.Mishell (Los Angeles), R.Paoletti (Milan),

J.C.Stevenson (London), M.Whitehead (London). The discussants

included G.Benagiano (Rome), E.Diczfalusy (Stockholm), M.Elstein

(Manchester), T.Farley (Geneva), S.Mancuso (Rome), M.Meschia

(Milan), G.Rosano (Rome), S.O.Skouby (Copenhagen) and L.A.J.

Heinemann (Zepernick). This report was prepared by P.G.Crosignani

and B.L.Rubin.

© European Society for Human Reproduction and Embryology 2325

dermal oestradiol than with oral oestrogens (Crook et al.,

1992). The addition of an androgenic progestogen such as

norethisterone does not impede the lowering of LDL by

oestrogen but may blunt or reverse the beneficial increase in

HDL and HDL2. The use of less androgenic C-21 progestogens

such as dydrogesterone does not usually impede the oestrogeninduced

HDL rise (Crook et al., 1997). However, C-21

progestogens do not lower triglycerides whereas androgenic

progestogens do. This can be an important effect when using

conjugated equine oestrogens which increase triglycerides, as

increased triglyceride concentrations may be of particular

importance in the development of CHD in younger women.

Oral oestradiol has little or no effect on triglycerides (Crook

et al., 1997) while transdermal oestradiol actually lowers their

concentrations (Crook et al., 1992). Oral oestradiol also

increases postprandial lipoprotein clearance. Lipoprotein (a)

may be an independent CHD risk marker, and HRT tends to

cause a decrease in this lipoprotein (Soma et al., 1993).

Whether this is actually beneficial remains unknown. There is

also evidence that oestrogens may protect LDL against oxidation,

and again this would be a potentially beneficial effect.

Based