Platelet-vessel wall interactions with third-generation oral contraceptives: No evidence of detrimental effects

Because of the association of oral contraceptives (OC) and cigarette smokin g with an increased thrombotic risk, we evaluated thromboxane (TX) and pros tacyclin urinary (u) metabolites, as in vivo indices of platelet-vessel wal l interactions, in women assigned to third generation OC. Twenty-tight wome n (15 smokers) underwent a 6-month trial of 30 mu g ethinylestradiol plus 0 .150 mg desogestrel. Cotinine plasma levels were elevated only in persons c lassified as smokers and serum TXB2 determination confirmed the absence of cyclooxygenase inhibition throughout the study. u-TXB2 and 11-dehydro-TXB2 were higher in smokers than in non-smokers. OC decreased u-11-dehydro-TXB2 both in smokers (from (pg/mu mol creatinine) 35.1 +/- 6.9 to 15.8 +/- 2.8; P <0.025) and non-smokers (from 31.7 +/- 9.8 to 20.6 +/- 4.8, P = N.S.). u- 6-keto-prostaglandin(PG)F-1 alpha excretion, also higher in smokers compare d to non-smokers, was also reduced after OC in smokers (from (pg/mu mol cre atinine) 24.3 +/- 5.2 to 14.8 +/- 2.3; P <0.05). Smokers also had a trend t o higher u-2.3-dinor-6-keto-PGF(1 alpha), marginally reduced by OC. Thus, the OC regimen used here improves - if anything - platelet vessel wal l interactions as assessed by prostanoid production in vivo. The prothrombo tic tendency associated with the use of OC in smokers does not appear to be mediated by changes in platelet-vessel wall interactions.