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Thromb Haemost 1999; 82(03): 1164-1170
DOI: 10.1055/s-0037-1614347
Letters to the Editor
Schattauer GmbH

Platelet-vessel Wall Interactions with Third-generation Oral Contraceptives: No Evidence of Detrimental Effects

Franca Fruzzetti
2   From the Department of Obstetrics and Gynecology, the University of Pisa, and C.N.R. Institute of Clinical Physiology, Pisa, Italy
,
Daniela Giannessi
1   C.N.R. Institute of Clinical Physiology, Pisa, Italy
,
Cabiria Ricci
2   From the Department of Obstetrics and Gynecology, the University of Pisa, and C.N.R. Institute of Clinical Physiology, Pisa, Italy
,
Walter Bernini
1   C.N.R. Institute of Clinical Physiology, Pisa, Italy
,
Roberto Puntoni
1   C.N.R. Institute of Clinical Physiology, Pisa, Italy
,
Andrea Riccardo Genazzani
2   From the Department of Obstetrics and Gynecology, the University of Pisa, and C.N.R. Institute of Clinical Physiology, Pisa, Italy
,
Raffaele De Caterina
1   C.N.R. Institute of Clinical Physiology, Pisa, Italy
› Author Affiliations
Further Information

Publication History

Received 26 May 1998

Accepted 26 April 1999

Publication Date:
09 December 2017 (online)

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Summary

Because of the association of oral contraceptives (OC) and cigarette smoking with an increased thrombotic risk, we evaluated thromboxane (TX) and prostacyclin urinary (u) metabolites, as in vivo indices of platelet-vessel wall interactions, in women assigned to third generation OC. Twenty-eight women (15 smokers) underwent a 6-month trial of 30 μg ethinylestradiol plus 0.150 mg desogestrel. Cotinine plasma levels were elevated only in persons classified 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/μmol 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)F1α excretion, also higher in smokers compared to non-smokers, was also reduced after OC in smokers (from (pg/μmol creatinine) 24.3 ± 5.2 to 14.8 ± 2.3; P <0.05). Smokers also had a trend to higher u-2,3-dinor-6-keto-PGF1α, marginally reduced by OC.

Thus, the OC regimen used here improves – if anything – platelet vessel wall interactions as assessed by prostanoid production in vivo. The prothrombotic tendency associated with the use of OC in smokers does not appear to be mediated by changes in platelet-vessel wall interactions.

Key words

Oral contraceptive - ethinylestradiol - desogestrel - platelets - thromboxane - prostacyclin - urinary prostanoids - platelet-vessel wall interactions
 

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