Влияние двух монофазных оральных контрацептивов, содержащих 30 мкг этинилэстрадиола в комбинации с 2 мг хлормадинона ацетата или 0,15 мг дезогестрела на параметры липидного обмена, гормональные

1. Vessey M, Mant D, Smith A, Yeates D. Oral contraceptives and venous thromboembolism: findings in a large prospective study. Br Med J (Clin Res Ed) 1986; 292: 526.
2. Gerstman B, Piper J, Freiman J et al. Oral contraceptive estrogen and progestin potencies and the incidence of deep venous thromboembolism. Int J Epidemiol 1990; 19: 931–6.
3. Gerstman B, Piper J, Tomita D et al. Oral contraceptive estrogen dose and the risk of deep venous thromboembolic disease. Am J Epidemiol 1991; 133: 32–7.
4. Helmrich S, Rosenberg L, Kaufman D et al. Venous thromboembolism in relation lo oral contraceptive use. Obstet Gynecol 1987; 69: 91–5.
5. Bloemenkamp K, Rosendaal F, Helmerhorst F et al. Enhancement by factor V Leiden mutation of risk of deep-vein thrombosis associated with oral contraceptives containing a third-generation progestagen. Lancet 1995; 346: 1593–6.
6. Jick H, Jick S, Gurewich V et al. Risk of idiopathic cardiovascular death and nonfatal venous thromboembolism in women using oral contraceptives with differing progestagen components. Lancet 1995; 346: 1589–93.
7. Spitzer W, Lewis M, Heinemann L et al. Third generation oral contraceptives and risk of venous thromboembolic disorders: an international case-control study. Transnational Research Group on Oral Contraceptives and the Health of Young Women. BMJ 1996; 312: 83–8.
8. World Health Organization Collaborative Study of Cardiovascular Disease and Steroid Hormone Contraception. Effect of different progestagens in low estrogen oral contraceptives on venous thromboembolic disease. Lancet 1995; 346: 1582–8.
9. Fanner R, Lawrenson R, Todd J et al. A comparison of the risks of venous thromboembolic disease in association with different combined oral contraceptives. Br J Clin Pharmacol 2000; 49: 580–90.
10. Todd J, Lawrenson R, Fanner R et al. Venous thromboembolic disease and combined oral contraceptives: a re-analysis of the MediPlus database. Hum Reprod 1999; 14: 1500–5.
11. Winkler U. Hemostatic effects of third- and second-generation oral contraceptives: absence of a causal mechanism for a difference in risk of venous thromboembolism. Contraception 2000; 62: 11S–20S [discussion 37S–38S].
12. Basdevant A, Conard J, Pelissier C et al. Hemostatic and metabolic effects of lowering the ethinyl-estradiol dose from 30 meg to 20 meg in oral contraceptives containing desogestrel. Contraception 1993; 48: 193–204.
13. O'Brien T, Nguyen T. Lipids and lipoproteins in women. Mayo Clin Proc 1997; 72: 235–44.
14. Skouby S. The rationale for a wider range of progestogens. Climacteric 2000; 3 (Suppl. 2): 14–20.
15. Gaspard UJ. Clinical relevance of plasma lipid changes during use of new low-dose oral contraceptives. Adv Contracept 1991; 7: 180–94.
16. Graff-Iversen S, Hammar N, Thelle D, Tonstad S. Use of oral contraceptives and mortality during 14 years follow-up of Norwegian women. Scand J Public Health 2006; 34: 11–6.
17. Porter J, Jick H, Walker A. Mortality among oral contraceptive users. Obstet Gynecol 1987; 70: 29–32.
18. Vessey M, Painter R. Yeates D. Mortality in relation to oral contraceptive use and cigarette smoking. Lancet 2003; 362: 185–91.
19. Burkman R, Zacur H, Kimball A et al. Oral contraceptives and lipids and lipoproteins: Part I – Variations in mean levels by oral contraceptive type. Contraception 1989; 40: 553–61.
20. Cirkel U, Belkien L, Hanker J et al. Auswirkungen eines chlormadinonazetathaltigen ovulationshemmers auf androgenisierungserscheinungen sowie den leber-und feltsloffwechsel junger frauen. Geburtsh u Frauenheilk 1986; 46: 439–43.
21. Pai MP, Paloucek FP. The origin of the «ideal» body weight equations. Ann Pharmacother 2000; 34: 1066–9.
22. Fotherby K. Twelve years of clinical experience with an oral contraceptive containing 30 micrograms ethinyloestradiol and 150 micrograms desogestrel. Contraception 1995; 51: 3–12.
23. Harvengt C, Desager J, Gaspard U, Lepot M. Changes in lipoprotein composition in women receiving two low-dose oral contraceptives containing ethinylestradiol and gonane progestins. Contraception 1988; 37: 565–75.
24. Godsland I, Crook D, Simpson R et al. The effects of different formulations of oral contraceptive agents on lipid and carbohydrate metabolism. N Engl J Med 1990; 323: 1375–81.
25. Beck P. Malarkey W. Serum prolactin concentrations in women treated with chlormadinone acetate. Am J Obstet Gynecol 1976; 124: 578–81.
26. Curran MP, Wagstaff AJ. Ethinylestradiol/chlormadinone acetate. Drugs 2004; 64: 751–60.
27. Worret I, Arp W, Zahradnik H, Andreas J, Binder N. Acne resolution rates: results of a single-blind, randomized, controlled, parallel phase 111 trial with EE/CMA (Belara) and EE/LNG (Microgynon). Dermatology 2001; 203: 38–44.
28. Charoenvisal C, Thaipisuttikul Y, Pinjarocn S et al. Effects on acne of two oral contraceptives containing desogestrel and cyproterone acetate. Int J Fertil Menopausal Stud 1996; 41: 423–9.
29. Coenen C, Thomas C, Borm G et al. Changes in androgens during treatment with four low-dose contraceptives. Contraception 1996; 53: 171–6.
30. Crook D. Multicenter study of endocrine function and plasma lipids and lipoproteins in women using oral contraceptives containing desogestrel progestin. UK Desogen Study Group. Contraception 1997; 55: 219–24.
31. Katz H, Kempers S, Akin M et al. Effect of a desogestrel-containing oral contraceptive on the skin. Eur J Contracept Reprod Health Care 2000; 5: 248–55.
32. Schramm G, Steffens D. A 12-month evaluation of the CMA-containing oral contraceptive Belara: efficacy, tolerability and anti-androgenic properties. Contraception 2003; 67: 305–12.
33. Coutinho M, Gerstein H, Wang Y, Yusuf S. The relationship between glucose and incident cardiovascular events. A metaregression analysis of published data from 20 studies of 95,783 individuals followed for 12,4 years. Diabetes Care 1999; 22: 233–40.
34. Laakso M. Insulin resistance and coronary heart disease. Curr Opin Lipidol 1996; 7: 217–26.
35. Cachrimanidou A, Hellberg D, Nilsson S et al. Hemostasis profile and lipid metabolism with long-interval use of a desogestrel-containing oral contraceptive. Contraception 1994; 50: 153–65.
36. Coenen C, Thomas C, Bonn G, Holland R. Comparative evaluation of the androgenicity of four low-dose, fixed-combination oral contraceptives. Int J Fertil 1995; 40 (Suppl. 2): 92–7.
37. Meulenberg P, Ross H, Swinkels L, Benraad T. The effect of oral contraceptives on plasma-free and salivary cortisol and cortisone. Clin Chim Acta 1987; 165: 379–85.

________________________________________________

1. Vessey M, Mant D, Smith A, Yeates D. Oral contraceptives and venous thromboembolism: findings in a large prospective study. Br Med J (Clin Res Ed) 1986; 292: 526.
2. Gerstman B, Piper J, Freiman J et al. Oral contraceptive estrogen and progestin potencies and the incidence of deep venous thromboembolism. Int J Epidemiol 1990; 19: 931–6.
3. Gerstman B, Piper J, Tomita D et al. Oral contraceptive estrogen dose and the risk of deep venous thromboembolic disease. Am J Epidemiol 1991; 133: 32–7.
4. Helmrich S, Rosenberg L, Kaufman D et al. Venous thromboembolism in relation lo oral contraceptive use. Obstet Gynecol 1987; 69: 91–5.
5. Bloemenkamp K, Rosendaal F, Helmerhorst F et al. Enhancement by factor V Leiden mutation of risk of deep-vein thrombosis associated with oral contraceptives containing a third-generation progestagen. Lancet 1995; 346: 1593–6.
6. Jick H, Jick S, Gurewich V et al. Risk of idiopathic cardiovascular death and nonfatal venous thromboembolism in women using oral contraceptives with differing progestagen components. Lancet 1995; 346: 1589–93.
7. Spitzer W, Lewis M, Heinemann L et al. Third generation oral contraceptives and risk of venous thromboembolic disorders: an international case-control study. Transnational Research Group on Oral Contraceptives and the Health of Young Women. BMJ 1996; 312: 83–8.
8. World Health Organization Collaborative Study of Cardiovascular Disease and Steroid Hormone Contraception. Effect of different progestagens in low estrogen oral contraceptives on venous thromboembolic disease. Lancet 1995; 346: 1582–8.
9. Fanner R, Lawrenson R, Todd J et al. A comparison of the risks of venous thromboembolic disease in association with different combined oral contraceptives. Br J Clin Pharmacol 2000; 49: 580–90.
10. Todd J, Lawrenson R, Fanner R et al. Venous thromboembolic disease and combined oral contraceptives: a re-analysis of the MediPlus database. Hum Reprod 1999; 14: 1500–5.
11. Winkler U. Hemostatic effects of third- and second-generation oral contraceptives: absence of a causal mechanism for a difference in risk of venous thromboembolism. Contraception 2000; 62: 11S–20S [discussion 37S–38S].
12. Basdevant A, Conard J, Pelissier C et al. Hemostatic and metabolic effects of lowering the ethinyl-estradiol dose from 30 meg to 20 meg in oral contraceptives containing desogestrel. Contraception 1993; 48: 193–204.
13. O'Brien T, Nguyen T. Lipids and lipoproteins in women. Mayo Clin Proc 1997; 72: 235–44.
14. Skouby S. The rationale for a wider range of progestogens. Climacteric 2000; 3 (Suppl. 2): 14–20.
15. Gaspard UJ. Clinical relevance of plasma lipid changes during use of new low-dose oral contraceptives. Adv Contracept 1991; 7: 180–94.
16. Graff-Iversen S, Hammar N, Thelle D, Tonstad S. Use of oral contraceptives and mortality during 14 years follow-up of Norwegian women. Scand J Public Health 2006; 34: 11–6.
17. Porter J, Jick H, Walker A. Mortality among oral contraceptive users. Obstet Gynecol 1987; 70: 29–32.
18. Vessey M, Painter R. Yeates D. Mortality in relation to oral contraceptive use and cigarette smoking. Lancet 2003; 362: 185–91.
19. Burkman R, Zacur H, Kimball A et al. Oral contraceptives and lipids and lipoproteins: Part I – Variations in mean levels by oral contraceptive type. Contraception 1989; 40: 553–61.
20. Cirkel U, Belkien L, Hanker J et al. Auswirkungen eines chlormadinonazetathaltigen ovulationshemmers auf androgenisierungserscheinungen sowie den leber-und feltsloffwechsel junger frauen. Geburtsh u Frauenheilk 1986; 46: 439–43.
21. Pai MP, Paloucek FP. The origin of the «ideal» body weight equations. Ann Pharmacother 2000; 34: 1066–9.
22. Fotherby K. Twelve years of clinical experience with an oral contraceptive containing 30 micrograms ethinyloestradiol and 150 micrograms desogestrel. Contraception 1995; 51: 3–12.
23. Harvengt C, Desager J, Gaspard U, Lepot M. Changes in lipoprotein composition in women receiving two low-dose oral contraceptives containing ethinylestradiol and gonane progestins. Contraception 1988; 37: 565–75.
24. Godsland I, Crook D, Simpson R et al. The effects of different formulations of oral contraceptive agents on lipid and carbohydrate metabolism. N Engl J Med 1990; 323: 1375–81.
25. Beck P. Malarkey W. Serum prolactin concentrations in women treated with chlormadinone acetate. Am J Obstet Gynecol 1976; 124: 578–81.
26. Curran MP, Wagstaff AJ. Ethinylestradiol/chlormadinone acetate. Drugs 2004; 64: 751–60.
27. Worret I, Arp W, Zahradnik H, Andreas J, Binder N. Acne resolution rates: results of a single-blind, randomized, controlled, parallel phase 111 trial with EE/CMA (Belara) and EE/LNG (Microgynon). Dermatology 2001; 203: 38–44.
28. Charoenvisal C, Thaipisuttikul Y, Pinjarocn S et al. Effects on acne of two oral contraceptives containing desogestrel and cyproterone acetate. Int J Fertil Menopausal Stud 1996; 41: 423–9.
29. Coenen C, Thomas C, Borm G et al. Changes in androgens during treatment with four low-dose contraceptives. Contraception 1996; 53: 171–6.
30. Crook D. Multicenter study of endocrine function and plasma lipids and lipoproteins in women using oral contraceptives containing desogestrel progestin. UK Desogen Study Group. Contraception 1997; 55: 219–24.
31. Katz H, Kempers S, Akin M et al. Effect of a desogestrel-containing oral contraceptive on the skin. Eur J Contracept Reprod Health Care 2000; 5: 248–55.
32. Schramm G, Steffens D. A 12-month evaluation of the CMA-containing oral contraceptive Belara: efficacy, tolerability and anti-androgenic properties. Contraception 2003; 67: 305–12.
33. Coutinho M, Gerstein H, Wang Y, Yusuf S. The relationship between glucose and incident cardiovascular events. A metaregression analysis of published data from 20 studies of 95,783 individuals followed for 12,4 years. Diabetes Care 1999; 22: 233–40.
34. Laakso M. Insulin resistance and coronary heart disease. Curr Opin Lipidol 1996; 7: 217–26.
35. Cachrimanidou A, Hellberg D, Nilsson S et al. Hemostasis profile and lipid metabolism with long-interval use of a desogestrel-containing oral contraceptive. Contraception 1994; 50: 153–65.
36. Coenen C, Thomas C, Bonn G, Holland R. Comparative evaluation of the androgenicity of four low-dose, fixed-combination oral contraceptives. Int J Fertil 1995; 40 (Suppl. 2): 92–7.
37. Meulenberg P, Ross H, Swinkels L, Benraad T. The effect of oral contraceptives on plasma-free and salivary cortisol and cortisone. Clin Chim Acta 1987; 165: 379–85.