Download PDF
Thromb Haemost 1997; 78(01): 315-326
DOI: 10.1055/s-0038-1657546
Oral contraceptives and thrombotic disease
Schattauer GmbH Stuttgart

Effect of Oral Contraceptives on Haemostasis Variables

C Kluft
Gaubius Laboratory, TNO-PG, Leiden, The Netherlands
,
M Lansink
Gaubius Laboratory, TNO-PG, Leiden, The Netherlands
› Author Affiliations
Further Information

Publication History

Publication Date:
12 July 2018 (online)

  PDF Download  Permissions and Reprints
 

  • References

  • 1 Editorial. Oral contraceptives and thromboembolism. Br Med J 1968; 2: 187-88
    CrossrefPubMedGoogle Scholar
  • 2 Farmer RDT, Preston TD. The risk of venous thromboembolism associated with low oestrogen oral contraceptives. J Obstet Gynecol 1996; 15: 195-200
    PubMedGoogle Scholar
  • 3 Venous thromboembolic disease and combined oral contraceptives: results of international multicentre case-control study. World health organization collaborative study of cardiovascular disease and steroid hormone contraception. Lancet 1995; 346: 1575-1582
    CrossrefPubMedGoogle Scholar
  • 4 Effect different progestagens in low oestrogen oral contraceptives on venous thromboembolic disease. World health organization collaborative study of cardiovascular disease and steroid hormone contraception. Lancet 1995; 346: 1582-1588
    CrossrefPubMedGoogle Scholar
  • 5 Bloemenkamp KW, Rosendaal FR, Helmerhorst FM, Buller HR, Vandenbroucke JP. Enhancement by factor V Leiden mutation of risk of deep-vein thrombosis associated with oral contraceptives containing a third-generation progestagen. Lancet 1995; 346: 1593-1596
    CrossrefPubMedGoogle Scholar
  • 6 Jick H, Jick SS, Gurewich V, Myers MW, Vasilakis C. Risk of idiopathic cardiovascular death and nonfatal venous thromboembolism in women using oral contraceptives with differing progestagen components. Lancet 1995; 346: 1589-1593
    CrossrefPubMedGoogle Scholar
  • 7 Spitzer WO, Lewis MA, Heinemann LAJ, Thorogood M, MacRae KD. Third generation oral contraceptives and risk of venous thromboembolic disorders: An international case-control study. Br Med J 1996; 312: 83-88
    CrossrefPubMedGoogle Scholar
  • 8 Consensus Development Meeting: Metabolic aspects of oral contraceptives of relevance for cardiovascular diseases. Am J Obstet Gynecol 1990; 162: 1335-1337
    CrossrefPubMed
  • 9 Vandenbroucke JP. Epidemiology-Annotation of Esbjerg I Consensus meeting. Gynecol Endocrinol 1996; 10 (Suppl. 02) 5-7
    PubMedGoogle Scholar
  • 10 Vandenbroucke JP. How much of the cardiovascular cardioprotective effect of postmenopausal estrogens is real?. Epidemiology 1995; 6: 207-208
    CrossrefPubMedGoogle Scholar
  • 11 Daly E, Vessey MP, Hawkins MN, Carson JL, Gough P, Marsh S. Risk of venous thromboembolism in users of hormone replacement therapy. Lancet 1996; 348: 922-980
    CrossrefPubMedGoogle Scholar
  • 12 Jick H, Derby LE, Myers MW, Vasilakis C, Newton KM. Risk of hospital admission for idiopathic venous thromboembolism among users of postmenopausal oestrogens. Lancet 1996; 348: 981-983
    CrossrefPubMedGoogle Scholar
  • 13 Grodstein F, Stampfer MJ, Goldhaber SZ, Manson JE, Colditz GA, Speizer FE, Willett WC, Hennekens CH. Prospective study of exogenous hormones and risk of pulmonary embolism in women. Lancet 1996; 348: 983-986
    CrossrefPubMedGoogle Scholar
  • 14 Task force on oral contraceptives-WHO. A multicentre study of coagulation and haemostatic variables during oral contraceptives: variations with four formulations. Br J Obstet Gynecol 1991; 98: 1117-1128
    CrossrefPubMedGoogle Scholar
  • 15 Meade TW, Chakrabarti R, Haines AP, Howarth DJ, North WRS, Stirling Y. Haemostatic, lipid and blood-pressure profiles of women on oral contraceptives containing 50μg or 30μg oestrogen. Lancet 1977; 2: 948-951
    PubMedGoogle Scholar
  • 16 Heinrich J, Schulte H, Assmann G. Oral contraceptives and variables of coagulation and fibrinolysis in an epidemiological study. Gynecol Endocrinol 1993; 7: 55-58
    PubMedGoogle Scholar
  • 17 Jespersen J, Gram J. Increased fibrin formation in blood in women above the age of 30 who are both oral contraceptive users and smokers. Fibrinolysis 1996; 10: 09-13
    PubMedGoogle Scholar
  • 18 Fruzzetti F, Ricci C, Fioretti P. Haemostatis profile in smoking and nonsmoking women taking low-dose oral contraceptives. Contraception 1994; 49 (06) 579-592
    CrossrefPubMedGoogle Scholar
  • 19 Petersen KR, Skouby SO, Jespersen J. Balance of coagulation activity with fibrinolysis during use of oral contraceptives in women with insulin-dependent diabetes mellitus. Int J Fertil Menopausal Stud 1995; 40 (Suppl. 02) 105-111
    PubMedGoogle Scholar
  • 20 Winkler UH, Koslowski S, Oberhoff C, Schindler EM, Schindler AE. Changes of the dynamic equilibrium of hemostasis associated with the use of low-dose oral contraceptives: a controllled study of cyproterone acetate containing oral contraceptives combined with either 35 or 50μg ethinyl estradiol. Adv Contraception 1991; 7 (Suppl. 03) 273-284
    PubMedGoogle Scholar
  • 21 Coata G, Ventura F, Lombardini R, Ciufetti G, Cosmi EV, Di RenzoGC. Effect of low-dose oral triphasic contraceptives on blood viscosity coagulation and lipid metabolism. Contraception 1995; 52: 151-157
    CrossrefPubMedGoogle Scholar
  • 22 Norris LA, Bonnar J. Increased whole blood platelet aggregation in oral contraceptive users can be prevented in vitro by a thromboxane synthetase inhibitor. Gynecol Endocrinol 1996; 10 (Suppl. 02) 153-155
    CrossrefPubMedGoogle Scholar
  • 23 Kluft C. Oral contraceptives and hemostasis. Gynecol Endocrinol 1996; 10 (Suppl. 02) 49-57
    PubMedGoogle Scholar
  • 24 Lebech A-M, Kjaer A, Lebech PE. Metabolic changes during the normal menstrual cycle: A longitudinal study. Am J Obstet Gynecol 1990; 163: 414-416
    CrossrefPubMedGoogle Scholar
  • 25 Blomback M, Eneroth P, Landgren B-M, Lagerstrom M, Anderson O. On the intraindividual and gender variability of haemostatic components. Thromb Haemostas 1992; 67: 70-75
    PubMedGoogle Scholar
  • 26 Larsen LF, Andersen HR, Hansen AB, Andersen O. Variation in risk indicators of cardiovascular disease during the menstrual cycle: an investigation of within-subject variations in glutathione peroxidase, haemostatic variables, lipids and lipoproteins in healthy young women. Scand J Clin Lab Invest 1996; 56: 241-249
    CrossrefPubMedGoogle Scholar
  • 27 Bolis PF, Franchi M, Mariano L, Paganelli AMM. Sampaolo Serial detection of plasma factor XIII levels during the ovalutory cycle and estroprogestative contraception. Clin Exp Obst Gyn 1982; 9: 22-25
    PubMedGoogle Scholar
  • 28 Notelovitz M, Kitchens CS, Khan FY. Changes in coagulation and anticoagulation in women taking low-dose triphasic oral contraceptives: a controlled comparative 12-month clinical trial. Am J Obstet Gynecol 1992; 167: 1255-1261
    CrossrefPubMedGoogle Scholar
  • 29 Reijnen HB, Atsma WJ. Risk is highest during first month of use. Br Med J 1995; 311: 1639
    PubMedGoogle Scholar
  • 30 Poulter NR, Farley TMM, Chang CL, Marmot MG, Meirik O. Safety of combined oral contraceptive pill. Lancet 1996; 347: 547
    PubMedGoogle Scholar
  • 31 Kuhl H. Effects of progestogens on haemostasis. Maturitas 1996; 24: 01-19
    CrossrefPubMedGoogle Scholar
  • 32 Winkler UH. Hemostasis in oral contraception: the role of progestogens. Gynecol Endocrinol 1993; 7: 59-64
    PubMedGoogle Scholar
  • 33 Meade TW, Haines AP, Norht WRS, Chakrabarti R, Howarth DJ, Stirling Y. Haemostatic, lipid and blood-pressure profiles of women on oral contraceptives containing 50μg or 30μg oestrogen. Lancet 1977; 2: 948-951
    PubMedGoogle Scholar
  • 34 Scarabin P-Y, Plu-Bureau G, Zitoun D, Bara L, Guize L, Samama MM. Changes in haemostatis variables induced by oral contraceptives containing 50μg or 30μg oestrogen: absence of dose-dependent effect on PAI-1 activity. Thromb Haemostas 1995; 74: 928-932
    PubMedGoogle Scholar
  • 35 Plu-Bureau G, Amiral J, Guize L, Scarabin P-Y. Safety of combined oral contraceptive pills. Lancet 1996; 347: 549
    CrossrefPubMedGoogle Scholar
  • 36 Prasad RNV, Koh S, Ratnam SS. Effect of three types of combined OC pills on blood coagulation, fibrinolysis and platelet function. Contraception 1989; 39: 369-383
    CrossrefPubMedGoogle Scholar
  • 37 Weinges KF, Wenzel E, Hells ternP, Geurts TBP, Dieben TOM. The effects of two phasic oral contraceptives on hemostasis and platelet function. Adv Contraception 1995; 11: 227-237
    CrossrefPubMedGoogle Scholar
  • 38 Daume E. Influence of modern low-dose oral contraceptives on hemostasis. Adv Contraception 1990; 6: 51-68
    PubMedGoogle Scholar
  • 39 Gevers LeuvenJA, Kluft C, Dersjant-Roorda MC, Harthoom-Lasthuizen EJ, Peters FPAMN, Bemsen MJ, Helmerhorst FM. Changes in coagulation and fibrinolysis variables during use of two oral contraceptives containing the same dose of ethinyl estradiol and either gestodene or desogestrel. Adv Contraception 1990; 6: 69-73
    PubMedGoogle Scholar
  • 40 Bloemenkamp KW, Gevers LeuvenJA, Helmerhorst FM, Dersjant-Roorda MC, de BoerR, Meijer P, Spielman D, Kluft C. In low-dose oral contraceptives containing 20μg or 30μg ethinylestradiol, gestodene is associated with a lower increase in coagulant factor VII than in desogestrel. Gynecol Endocrinol 1996; 10 (Suppl. 02) 145-148
    CrossrefPubMedGoogle Scholar
  • 41 Norris LA, Bonnar J. Estrogen dose and progestogen type: their effect on hemostatid changes in oral contraceptive users. Gynecol Endocrinol 1996; 10 (Suppl. 02) 133-135
    PubMedGoogle Scholar
  • 42 Lox CD. Biochemical effects in women following one year’s exposure to a new triphasic contraceptive-II. Coagulation profiles. Gen Pharmac 1996; 27: 371-374
    PubMedGoogle Scholar
  • 43 Daly L, Bonnar J. Comparative studies of 30Fg ethinyl estradiol combined with gestodene and desogestrel on blood coagulation, fibrinolysis and platelets. Am J Obstet Gynecol 1990; 163: 430-437
    CrossrefPubMedGoogle Scholar
  • 44 Gevers LeuvenJA, Kluft C, Dersjant-Roorda MC, Harthoom-Lasthuizen EJ, de BoerR, Helmerhorst FM. Effects of low dose oral contraceptives differing in progestogen compound on coagulation and fibrinolytic risk variables for venous and arterial thromboembolic diseases. In: Fibrinolysis and disease, molecular and hemovascular aspects of fibrinolysis. Glas-Greenwalt P. ed CRC Press; Chapter 32. 1995: 226-234
    Google Scholar
  • 45 Davies T, Fielhouse G, McNicol GP. The effects of therapy with oestriol succinate and ethinyl oestradiol on the haemostatic mechanism in post-menopausal women. Thromb Haemostas 1976; 35: 403-414
    PubMedGoogle Scholar
  • 46 Kronn U-B, Silfverstolpe G, Tengborn L. The effect of transdermal estradiol and oral conjugated estrogens on haemostasis variables. Thromb Haemostas 1994; 71: 420-423
    PubMedGoogle Scholar
  • 47 Winkler UH, Kramer R, Kwee B, Schindler AE. Östrogensubstitution in der Postmenopause, Blutgerinnung und Fibrinolyse: Vergleicheiner neuartigen transdermalen Östradiol-Behandlung mit der oralen Therapie mit konjugierten Östrogenen. Zentralbl Gynakol 1995; 117: 540-548
    PubMedGoogle Scholar
  • 48 Kluft C. Fibrinolysis risk markers for cardiovascular disease. Gynecol Endocrinol 1993; 7: 45-53
    PubMedGoogle Scholar
  • 49 Collins P, Rosano GMC, Jiang C, Lindsay D, Sarrel PM, Poole-Wilson PA. Hypothesis cardiovascular protection by oestrogen: a calcium antagonist effect?. Lancet 1993; 341: 1264-1265
    CrossrefPubMedGoogle Scholar
  • 50 Mangelsdorf DJ, Thummel C, Beato M, Herrlich P, Schhtz G, Umesono K, Blumberg B, Kastner P, Mark M, Chambon P, Evans RM. The nuclear receptor superfamily: the second decade. Cell 1995; 83: 835-839
    CrossrefPubMedGoogle Scholar
  • 51 Gronemeyer H. Control of transcription activation by steroid hormone receptors. FASEB J 1992; 6: 2524-2529
    CrossrefPubMedGoogle Scholar
  • 52 Pearce D, Yamamoto KR. Mineralocorticoid and glucocorticoid receptor activities distinguished by nonreceptor factors at a composite response element. Science 1993; 259: 1161-1165
    CrossrefPubMedGoogle Scholar
  • 53 Sheikh MS, Shao Z-M, Chen J-C, Hussan A, Jetten AM, Fontana JA. Estrogen receptor negative breast cancer cells transfected with the estrogen receptor exhibit increased RAR gene expression and sensitivity to growth inhibition by retinoic acid. J Cell Biochem 1993; 53: 394-404
    CrossrefPubMedGoogle Scholar
  • 54 Gaub MP, Bellard M, Scheuer I, Chambon P, Sassone-Corsi P. Activation of the ovalbumin gene by the estrogen receptor involves the Fos-Jun complex. Cell 1990; 63: 1267-1276
    CrossrefPubMedGoogle Scholar
  • 55 Beato M, Herrlich P, Schtz G. Steroid hormone receptors: many actors in search of a plot. Cell 1995; 83: 851-857
    CrossrefPubMedGoogle Scholar
  • 56 Farsetti A, Misti S, Citarella F, Felici A, Andreoli M, Fantoni A, Sacchi A, Pontecorvi A. Molecular basis of estrogen regulation of Hageman factor XII gene expression. Endocrinology 1995; 136: 5076-5083
    CrossrefPubMedGoogle Scholar
  • 57 Henrikson KP, Hall ES, Lin Y. Cellular localization of tissue factor and prothrombin in the estrogen-treated immature rat uterus. BiolReprod 1994; 50: 1145-1150
    PubMedGoogle Scholar
  • 58 Lockwood CJ, Krikun G, Papp C, Aigner S, Nemerson Y, Schatz F. Biological mechanisms underlying RU 486 clinical effects: inhibition of endometrial stromal cell tissue factor content. J Clin Endocrinol Metab 1994; 79: 786-790
    PubMedGoogle Scholar
  • 59 Aune B, Oian P, Osterud B. Enhanced sensitivity of the extrinsic coagulation system during ovarian stimulation for in virofertilization. Human Reprod 1993; 8: 1349-1352
    CrossrefPubMedGoogle Scholar
  • 60 Quehenberger P, Kapiotis S, Partan C, Schneider B, Wenzel R, Gaiger A, Speiser W. Studies on oral contraceptive-induced changes in blood coagulation and fibrinolysis and the estrogen effect on endothelial cells. Ann Hematol 1993; 67: 33-36
    CrossrefPubMedGoogle Scholar
  • 61 Harrison RL, McKee PA. Estrogen stimulates von Wiilebrand Factor production by cultured endothelial cells. Blood 1984; 63: 657-665
    PubMedGoogle Scholar
  • 62 Casslen B, Nordengren J, Gustavsson B, Nilbert M, Lund LR. Progesterone stimulates degradation of urokinase plasminogen activator (u-PA) in endometrial stromal cells by increasing its inhibitor and surface expression of the urokinase plasminogen activator receptor. J Clin Endocrinol Metab 1995; 80: 2776-2784
    PubMedGoogle Scholar
  • 63 Miyachi A, Osagu Y, Tahetani Y. Effects of steroid hormones on fibrinolytic system in cultured human endometrial cells. EndocrJ 1995; 42: 57-62
    PubMedGoogle Scholar
  • 64 Lockwood CJ, Krikun G, Papp C, Aigner S, Schatz F. Biological mechanisms underlying the clinical effects of RU486: modulation of cultured endometrial stromal cells plasminogen activator and plasminogen activator inhibitor expression. J Clin Endocrinol Metab 1995; 80: 1100-1105
    PubMedGoogle Scholar
  • 65 Besser D, Verde P, Nagamine Y, Blasi F. Signal transduction and the u-PA/u-PAR system. Fibrinolysis 1996; 10: 215-237
    PubMedGoogle Scholar
  • 66 Ryan TJ, Seeger JI, Kumar SA, Dickerman HW. Estradiol preferentially enhances extracellular tissue plasminogen activators of MCF-7 breast cancer cells. J Biol Chem 1984; 259: 14324-14327
    PubMedGoogle Scholar
  • 67 Dickerman HW, Martinez HL, Seeger JI, Kumar SA. Estrogen regulation of human breast cancer cell line MCF-7 tissue type plasminogen activator. Endocrinology 1989; 125: 492-500
    CrossrefPubMedGoogle Scholar
  • 68 Bulens F. Transcriptional regulation of the human tissue-type plasminogen activator gene. Thesis 1995, Leuven.
    PubMedGoogle Scholar
  • 69 Kooista t, Schrauwen Y, Arts J, Emeis JJ. Regulation of endothelial t-PA synthesis and release. Int J Hematol 1994; 59: 233-255
    PubMedGoogle Scholar
  • 70 Kooistra T, Bosma PJ, Jespersen J, Kluft C. Studies on the mechanism of action of oral contraceptives with regard to fibrinolytic variables. Am J Obstet Gynecol 1990; 163: 404-412
    CrossrefPubMedGoogle Scholar
  • 71 Venkov CD, Rankin AB, Vaughan DE. Identification of authentic estrogen receptor in cultured endothelial cells. A potential mechanism for steroid hormone regulation of endothelial function. Circulation 1996; 94: 727-733
    CrossrefPubMedGoogle Scholar
  • 72 Kim-Schulze S, McGowan KA, Hubchack SC, Cid MC, Martin MB, Kleinman HK, Green GL, Schnaper HW. Expression of an estrogen receptor by human coronary artery and umbilical vein endothelial cells. Circulation 1996; 94: 1402-1407
    CrossrefPubMedGoogle Scholar
  • 73 Caulin-Glaser T, Watson CA, Pardi R, Bender JR. Effects of 17p-estradiol on cytokine-induced endothelial cell adhesion molecule expression. J Clin Invest 1996; 98: 36-42
    CrossrefPubMedGoogle Scholar
  • 74 Stefaneanu L, Kovacs K, Horvath E, Lloyd RV, Buchfelder M, Fahlbusch R, Smyth H. In situ hybridization study of estrogen receptor messenger ribonucleic acid in human adeno-hypophysical cells and pituitary adenomas. J Clin Endocrinol Metab 1994; 78: 83-88
    PubMedGoogle Scholar
  • 75 Koji T, Brenner RM. Localization of estrogen receptor messenger ribonucleic acid in rhesus monkey uterus by nonradioactive in situ hybridization with digoxigenin-labeled oligodeoxy nucleotides. Endocrinology 1993; 132: 382-392
    CrossrefPubMedGoogle Scholar
  • 76 Yamashita S, Korack KS. A modified immunohistochemical procedure for the detection of estrogen receptor in mouse tissues. Histochemistry 1989; 90: 325-330
    CrossrefPubMedGoogle Scholar
  • 77 Kuiper GGJM, Enmark E, Pelto-Huikko M, Nilsson S, Gustafson JA. Cloning of a novel estrogen receptor expressed in rat prostate and ovary. Proc Natl Acad Sci 1996; 93: 5925-5930
    CrossrefPubMedGoogle Scholar
  • 78 Mosselman S, Polman J, Dijkema R. ER: identification and characterization of a novel human estrogen receptor. FEBS Letters 1996; 392: 49-53
    CrossrefPubMedGoogle Scholar
  • 79 Perrot-Applanat M, Cohen-Solal K, Milgrom E, Finet M. Progesterone receptor expression in human saphenous veins. Circulation 1995; 92: 2975-2983
    CrossrefPubMedGoogle Scholar
  • 80 Losordo DW, Kearney M, Kim EA, Jekanowski I, Isner JM. Variable expression of the estrogen receptor in normal and atherosclerotic coronary arteries of premenopausal women. Circulation 1994; 89: 1501-1510
    CrossrefPubMedGoogle Scholar
  • 81 Loskutofff DJ. Regulation of PAI-1 gene expression. Fibrinolysis 1991; 5: 197-206
    PubMedGoogle Scholar
  • 82 Chomiki N, Henry M, Alessi MC, Anfosso F, Juhan-Vague I. Plasminogen activator inhibitor-1 expression in human liver and healthy or atherosclerotic vessel wall. Thromb Haemostas 1994; 72: 44-53
    PubMedGoogle Scholar
  • 83 Thornton AJ, Gelehrter TD. Human hepatocytes express the gene for type I plasminogen activator (PAI-1) in vivo. Fibrinolysis 1995; 9: 09-15
    PubMedGoogle Scholar
  • 84 Shimomura I, Funahashi T, Takahashi M, Maeda K, Kotani K, Nakamura T, Yamashita S, Miura M, Fukuda Y, Takemura K, Tokunaga K, Matsuzawa Y. Enhanced expression of PAI-1 in visceral fat: Possible contributor to vascular disease in obesity. Nature Med 1996; 2: 800-803
    CrossrefPubMedGoogle Scholar
  • 85 Pedersen SB, Fuglsig S, Sjrgren P, Richelsen B. Identification of steroid receptors in human adipose tissue. Eur J Clin Inv 1996; 26: 1051-1056
    CrossrefPubMedGoogle Scholar
  • 86 Karas RH, Patterson BL, Mendelsohn ME. Human vascular smooth muscle cells contain functional estrogen receptor. Circulation 1994; 89: 1943-1950
    CrossrefPubMedGoogle Scholar
  • 87 Freyschuss B, Stavreus-Evers A, Sahlin L, Eriksson H. Induction of the estrogen receptor by growth hormone and glucocorticoids substitution in primary cultures of rat hepatocytes. Endocrinology 1993; 133: 1548-1554
    CrossrefPubMedGoogle Scholar
  • 88 Peirot-Applanat M, Groyer-Picard MT, Garcia E, Lorenze F, Milgrom E. Immunocytochemical demonstration of estrogen and progestrone receptors in muscle cells of uterine arteries in rabbits and humans. Endocrinology 1988; 123: 1511-1519
    CrossrefPubMedGoogle Scholar
  • 89 Abbate R, Pinto S, Rostagno C, Bruni V, Rosati D, Mariani G. Effects of long-term gestodene-containing contraceptive administration on hemostasis. Am J Obstet Gynecol 1990; 163: 424-430
    CrossrefPubMedGoogle Scholar
  • 90 David JL, Demeyer F, Gillian D, Gaspard U. Haemostasis global profile during monophasic oral contraception by norgestimate or desogestrel associated to low-dose ethinyloestradiol Gynecol Endocrinol. 1996; 10 (Suppl. 02) 137-139
    PubMedGoogle Scholar
  • 91 David JL, Gaspard UJ, Gillian D, Raskinet R, Lepot MR. Hemostasis profile in women taking low-dose oral contraceptives. Am J Obstet Gynecol 1990; 163: 420-423
    CrossrefPubMedGoogle Scholar
  • 92 Sabra A, Bonnar J. Hemostatic system changes induced by 50Fg and 30Fg estrogen/progestogen oral contraceptives. Modification of estrogen effects by levonorgestrel. J Reprod Med 1983; 28: 85-91
    PubMedGoogle Scholar
  • 93 Norris LA, Bonnar J. Effect of oestrogen dose on whole blood platelet activation in women taking new low dose contraceptives. Thromb Haemost 1994; 72 (06) 926-930
    Article in Thieme ConnectPubMedGoogle Scholar
  • 94 Schlit AF, Grandjean P, Donnez J, Lavenne E. Large increase in plasmatic ll-dehydroTxB2 levels due to oral contraceptives. Contraception 1995; 51: 053-108
    CrossrefPubMedGoogle Scholar
  • 95 Melis GB, Fruzzetti F, Paoletti AM, Carmassi F, Fioretti P. Fibrinopeptide A plasma levels during low-estrogen oral contraceptive treatment. Contraception 1984; 30: 575-583
    CrossrefPubMedGoogle Scholar
  • 96 Melis GB, Fruzzetti F, Nicoletti I, Ricci C, Lammer P, Atsma WJ, Fioretti P. A comparative study on the effects of a monophasic pill containing desogestrel plus 20μgethinylestradiol, a triphasic combination containing levonorgestrel and a monophasic combination containing gestodene on coagulatory factors. Contraception 1991; 43: 23-31
    CrossrefPubMedGoogle Scholar
  • 97 Fruzzetti F, Ricci C, Nicoletti I, Fioretti P. Clinical and metabolic effects of a triphasic pill containing gestodene. Contraception 1992; 46: 335-347
    CrossrefPubMedGoogle Scholar
  • 98 Winkler UH, Schindler AE, Endrikat J, Dusterberg B. A comparative study of the effects on the hemostatic system of two monophasic gestodene oral contraceptives containing 20μg and 30μg ethinylestradiol. Contraception 1996; 53: 75-84
    CrossrefPubMedGoogle Scholar
  • 99 Winkler UH, Oberhoff C, Bier U, Schindler AE, Gillain D. Hemostatic effects of two oral contraceptives containing low doses of ethinylestradiol and either gestodene or norgestimate: an openrandomized, parallel-group study. Int J Fertil Menopausal Stud 1995; 40: 260-268
    PubMedGoogle Scholar
  • 100 Quehenberger P, Loner U, Kapiotis S, Handler S, Schneider B, Huber J, Speiser W. Increased levels of activated factor VII and decreased plasma protein S activity and circulating thrombomodulin during use of oral contraceptives. Thromb Haemostas 1996; 76 (05) 729-734
    PubMedGoogle Scholar
  • 101 David JL, Demeyer F, Gillian D, Gaspard U. Hemostasis global profile during monophasic oral contraception by norgestimate or desogestrel associated with low-dose ethinylestradiol (preliminary results). Gynecol Endocrinol 1996; 10: 137-139
    CrossrefPubMedGoogle Scholar
  • 102 Petersen KR, Skouby SO, Sidelmann J, Molsted-Pedersen L, Jespersen J. Effects of contraceptive steroids on cardiovascular risk factors in women with insulin-dependent diabetes mellitus. Am J Obstet Gynecol 1994; 171: 400-405
    CrossrefPubMedGoogle Scholar
  • 103 Cachrimanidou A-C, Hellberg D, Nilsson S, von SchoulzB, Crona N, Siegbahn A. Hemostasis profile and lipid metabolism with long-interval use of a desogestrel-containing oral contraceptive. Contraception 1994; 50: 153-165
    CrossrefPubMedGoogle Scholar
  • 104 Jespersen J, Petersen KR, Skouby SO. Effects of newer oral contraceptives on the inhibition of coagulation and fibrinolysis in relation to dosage and type of steroid. Am J Obstet Gynecol 1990; 163: 396-403
    CrossrefPubMedGoogle Scholar
  • 105 Espana F, Gilabert J, Vicente V, Estelles A, Vazques L, Hendl S, Aznar J. Activated protein C: α1-antitrypsin (APC: ±l AT) complex as a marker for in vitro diagnosis of prethrombotic states. Thromb Res 1992; 66 (05) 499-508
    CrossrefPubMedGoogle Scholar
  • 106 Hoem N-O, Johannesen S, Hauge G, Rud AC, Sandem S, Briseid K. Contact activation factors in plasma from women using oral contraceptives-increased levels of factor XII kinin-free high molecular weight kininogen and acetone-activated kallikrein. Thromb Res 1991; 64: 427-434
    CrossrefPubMedGoogle Scholar
  • 107 Norris LA, Bonnar J. The effect of oestrogen dose and progesteron type on haemostatic changes in women taking low dose oral contraceptives. Br J Obstet Gynecol 1996; 103: 261-267
    CrossrefPubMedGoogle Scholar
  • 108 Gevers LeuvenJA, Kluft C, Bertina RM, Hessel LW. Effects of two low-dose oral contraceptives on circulating components of the coagulation and fibrinolytic systems. J Lab Clin Med 1987; 109: 631-636
    PubMedGoogle Scholar
  • 109 Petersen KR, Skouby SO, Sidelmann J, Jespersen J. Different response of the hemostatic system to oral contraception in diabetic and non-diabetic women. Gynecol Endocrinol 1996; 10 (Suppl. 02) 165-167
    PubMedGoogle Scholar
  • 110 Jespersen J, Petersen KR, Skouby SO. Coagulation and fibrinolysis: comparison of two new-dose oral contraceptives. Adv Contraception 1991; 7: 292-296
    PubMedGoogle Scholar
  • 111 Gram J, Munkvad S, Jespersen J. Enhanced generation and resolution of fibrin in women above the age of 30 years using oral contraceptives low in estrogen. Am J Obstet Gynecol 1990; 163: 438-442
    CrossrefPubMedGoogle Scholar
  • 112 Petersen KR, Skouby SO, Sidelmann J, Jespersen J. Assessment of endothelial function during oral contraception in women with insulin-dependent diabetes mellitus. Metabolism 1994; 43: 1379-1383
    CrossrefPubMedGoogle Scholar
  • 113 Pabinger I, Schneider B. and the GTH Study Group on Natural Inhibitors Thrombotic risk women with hereditary antithrombin-, protein C-and protein S-deficiency taking oral contraceptive medication. Thromb Haemostas 1994; 71: 548-552
    PubMedGoogle Scholar
  • 114 Vandenbroucke JP, Koster T, BriNt E, Reitsma PH, Bertina RM, Rosendaal FR. Increased risk of venous thrombosis in oral-contraceptive users who are carriers of factor V Leiden mutation. Lancet 1994; 344: 1453-1457
    CrossrefPubMedGoogle Scholar
  • 115 Kobayashi S, Inoue S, Hosoi T, Ouchi Y, Shiraki M, Orimo H. Associated of bone mineral density with polymorphism of the estrogen receptor gene. J Bone Mineral Res 1996; 11: 306-311
    PubMedGoogle Scholar
  • 116 Green F, Kelleher C, Wilkes H, Temple A, Meade T, Humphries S. A common genetic polymorphism associated with lower coagulation factor VII levels in healthy individuals. Arteriocler Thromb 1991; 11: 540-546
    PubMedGoogle Scholar
  • 117 Meilahn E, Ferrell R, Kiss J, Temple A, Green F, Humphries S, Kuller L. Genetic determination of coagulation factor VIIc levels among healthy middle-aged women. Thromb Haemostas 1995; 73: 623-625
    PubMedGoogle Scholar
  • 118 Basdevant A, Conard J, Pelissier C, Guyene T-T, Lapousterle C, Mayer M, Guy-Grand BDegrelle. Hemostatic and metabolic effects of lowering the ethinyl-estradiol dose from 30μgto 20μgin oral contraceptives containing desogestrel. Contraception 1993; 48: 193-204
    CrossrefPubMedGoogle Scholar
  • 119 Robinson GE, Bounds W, Mackie IJ, Stocks J, Burren T, Machin SJ, Guillebaud J. Changes in metabolism induced by oral contraceptives containing desogestrel and gestodene in older women. Contraception 1990; 42: 263-273
    CrossrefPubMedGoogle Scholar
  • 120 Robinson GE, Burren T, Mackie IJ, Bouds W, Walshe K, Faint R, Guillebraud J, Machin SJ. Changes in haemostasis after stopping the combined contraceptive pill: implications for major surgery. Br Med J 1991; 302: 269-271
    CrossrefPubMedGoogle Scholar
  • 121 Vekemans M, Grippa J, Capel FonduR. The effect of two low-dose contraceptives containing ethinylestradiol and desogestrel or D-norgestrel on blood clotting factors. Curr Ther Res 1987; 42: 1109-1118
    PubMedGoogle Scholar
  • 122 Shaaban MM, Elwan SI, El-Kabsh MY, Farghaly SA, Thabet N. Effect of levonorgestrel contraceptive implants Norplant, on blood coagulation. Contraception 1984; 30: 421-430
    CrossrefPubMedGoogle Scholar
  • 123 Toulon P, Bardin JM, Blumenfeld N. Increased heparin cofactor II levels in women taking oral contraceptives. Thromb Haemostas 1990; 64: 365-368
    PubMedGoogle Scholar
  • 124 Mackie IJ, Segal H, Burren T, Gallimore M, Walshe KJ, Robinson G, Machin SJ. Heparin cofactor II levels are increased by the use of combined oral contraceptives. Blood coagulation and Fibrinolysis 1991; 1: 647-651
    PubMedGoogle Scholar
  • 125 Bonnar J. Coagulation effects of oral contraception. Am J Obstet Gynecol 1987; 157: 1042-1048
    CrossrefPubMedGoogle Scholar
  • 126 Cohen H, Mackie IJ, Walshe K, Gillmer MDG, Machin SJ. A comparison of the effects of two triphasic oral contraceptives on haemostasis. Br J Haemat 1988; 69: 259-261
    CrossrefPubMedGoogle Scholar
  • 127 Fossum S, Hoem N-O, Johannesen S, Korpberget M, Nyland SandemS, Briseid K. Contact factors in plasma from women on oral contraception-significance of factor XI for the measured activity of factor XII. Thromb Res 1994; 74: 477-485
    CrossrefPubMedGoogle Scholar
  • 128 Jespersen J, Kluft C. Increased euglobulin fibrinolytic potential in women on oral contraceptives low in oestrogen-levels of extrinsic and intrinsic plasminogen activators factor XII, and Cl-inactivator. Thromb Haemostas 1985; 54: 454-459
    PubMedGoogle Scholar
  • 129 Kluft C, Los P, Clemmensen I, Brommer EJP, Gevers LeuvenJA, Boks AL, Vellenga E. Quantification of plasma levels of tetranectin-effects of oral contraceptives, pregnancy, treatment with L-asparaginase and liver cirrhosis. Thromb Haemostas 1989; 62: 792-796
    PubMedGoogle Scholar
  • 130 Jespersen J, Kluft C. Individual levels of plasma histidine-rich glycoprotein (HRG) during the normal menstrual cycle and in women on oral contraceptives low in oestrogen. Scand J Clin Lab Invest 1982; 42: 563-566
    CrossrefPubMedGoogle Scholar
  • 131 Omsjo IH, Oian P, Maltau JM, Osterud B. Effects of two triphasic oral contraceptives containing ethinylestradiol plus levonorgestrel or gestodene on blood coagulation and fibrinolysis. Acta Obstet Gynecol Scand 1989; 68: 27-30
    PubMedGoogle Scholar
  • 132 Ball MJ, Ashwell E, Jackson M, Gillmer MDG. Comparison of two triphasic contraceptives with different progestogens: effects on metabolism and coagulation proteins. Contraception 1990; 41: 363-376
    CrossrefPubMedGoogle Scholar
  • 133 Refn H, Kjaer A, Lebech AM, Borggaard B, Schierup L, Bremmelgraard A. Metabolic changes during treatment with two different progestogens. Am J Obstet Gynecol 1990; 163: 374-377
    CrossrefPubMedGoogle Scholar
  • 134 Jespersen J, Kluft C. Inhibition of tissue-type plasminogen activator in plasma of women using oral contraceptives and in normal women during a menstrual cycle. Thromb Haemostas 1986; 55: 388-389
    PubMedGoogle Scholar
  • 135 Malm J, Laurell M, Dählback B. Changes in the plasma levels of vitamin K-dependent proteins C and S and C4b-binding protein during pregnancy and oral contraception. Br J Haemat 1988; 68: 437-443
    CrossrefPubMedGoogle Scholar
  • 136 Osterud B, Robertsen R, Asvang GB, Thijssen F. Resistance to activated protein C is reduced in women using oral contraceptives. Blood Coag Fibr 1994; 5: 853-854
    PubMedGoogle Scholar
  • 137 Olivieri O, Friso S, Manzato F, Guella A, Bernardi F, Lunghi B, Girelli D, Azzini M, Brocco G, Russo G. et at Resistance to activated protein C in healthy women taking oral contraceptives. Br J Haematol 1995; 91: 465-470
    CrossrefPubMedGoogle Scholar
  • 138 Henkes CMA, Bom VJJ, Seinen AJ, van der Meer J. Sensitivity to activated protein C; influence of oral contraceptives and sex. Thromb Haemostas 1995; 73: 402-404
    PubMedGoogle Scholar
  • 139 Sirtori CR, Calabresi L, Franceschini G, Gianfranceschi G, Zoppi F, Winkler S, Bilotta P, Zampetti A. Comparison of the lipoprotein and hemostatic changes after a triphasic and a monophasic low dose oral contraceptive in premenopausal middle-aged women. Atheroclerosis 1990; 84: 203-211
    CrossrefPubMedGoogle Scholar
  • 140 Kloosterboer HJ, van Wayjen RGA, van den Ende A. Effects of three low-dose oral contraceptive combinations on sex hormone binding globulin corticosteroid binding globulin and antithrombin III activity in healthy women: two monophasic desogestel combinations (containing 0.020 or 0.030 mg ethinylestradiol) and one triphasic levonorgestrel combination. Acta Obstet Gynecol Scand 1987; 144: 41-44
    PubMedGoogle Scholar
  • 141 Melissari E, Kakkar VV. The effects of oestrogen administration on the plasma free protein S and C4b-binding protein. Thromb Res 1988; 49: 489-495
    CrossrefPubMedGoogle Scholar