Secondary dyslipidaemia after oral contraceptives

Česká verzia

Authors: Soška ^1,2; J. Fiala ³; K. Nebeská ³; D. Hrubá ³
Authors place of work: Oddělení klinické biochemie FN u sv. Anny Brno, přednosta doc. MUDr. Vladimír Soška, CSc. ¹; II. interní klinika Lékařské fakulty MU a FN u sv. Anny Brno, přednosta prof. MUDr. Miroslav Souček, CSc. ²; Ústav preventivního lékařství Lékařské fakulty MU Brno, přednostka prof. MUDr. Zuzana Brázdová, DrSc. ³
Published in the journal: Vnitř Lék 2009; 55(10): 929-933
Category: Original Contributions

Summary

The aim of the study:
To examine changes to blood lipid and lipoprotein levels following introduction of modern oral hormonal contraception agents and to evaluate atherogenic character of this dyslipidemia. Methods, patient sample: Forty four women of the mean age of 22.7 ± 3.5 years, BMI 21.4 ± 2.5 kg/sqm, waste line 71.9 ± 7.1 cm and BP 115.7 ± 12.2/70.1 ± 8.3 mm Hg were included. Total cholesterol, HDL‑cholesterol, LDL‑cholesterol, triglycerides, apolipoprotein A1 and apolipoprotein B levels were assessed before the introduction of contraception and 3 months into the treatment. Results: Following 3 months of treatment, increase in the total cholesterol (4.19 ± 0.80 vs 4.75 ± 0.79 mmol/l; p < 0.001), LDL‑cholesterol (2.10 ± 0.64 vs 2.32 ± 0.66 mmol/l; p = 0.23), HDL‑cholesterol (1.71 ± 0.42 vs 1.90 ± 0.45 mmol/l; p < 0.001), triglycerides (0.85 ± 0.36 vs 1.18 ± 0.50 mmol/l; p < 0.001), apolipoprotein A1 (1.55 ± 0.33 vs 1.88 ± 0.44 g/l; p < 0.001) and apolipoprotein B (0.58 ± 0.15 vs 0.69 ± 0.19 g/l; p < 0.001) levels was observed. The total cholesterol/HDL cholesterol and apolipoprotein B/apolipoprotein A1 ratios have not changed significantly between the two assessments.

Conclusion:
Three‑month treatment with combined hormonal contraception resulted in statistically significantly increased concentrations of triglycerides, total cholesterol, HDL‑cholesterol, LDL‑cholesterol, apolipoprotein A1 and apolipoprotein B. At the same time, total cholesterol/HDL cholesterol and apolipoprotein B/apolipoprotein A1 ratios have not changed significantly and thus hormonal contraception‑induced dyslipidemia should not be regarded as proatherogenic.

Key words:
hormonal contraception – dyslipidemia – apolipoprotein A1 – apolipoprotein B

Zdroje

1. Crosignani PG for the ESHRE Capri Workshop Group. Hormones and cardiovascular health in women. Hum Reprod Update 2006; 12: 483– 497.

2. Dubey RK, Imthurn B, Zacharia LC et al. Hormone replacement therapy and cardiovascular disease: Where went wrong and where do we go from here? Hypertension 2004; 44: 789– 795.

3. Ramakrishnan G, Rana A, Das C et al. Study of low-density lipoprotein receptor regulation by oral (steroid) contraceptives: desogestrel, levonorgestrel and ethinyl estradiol in JEG- 3 cell line and placental tissue. Contraception 2007; 76: 297– 305.

4. Herrington DM, Reboussin DM, Brosnihan KB et al. Effects of estrogen replacement on the progression of coronary-artery atherosclerosis. N Engl J Med 2000; 343: 522– 529.

5. Rossouw JE, Anderson GL, Prentice RL et al. Risks and benefi ts of estrogen plus progestin in healthy postmenopausal women – Principal results from the Women’s Health Initiative randomized controlled trial. JAMA 2002; 288: 321– 333.

6. Hulley SB, Grady D, Bush T et al. for the Heart and Estrogen/ Progestin Replacement Study (HERS) Research Group. Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopauzal women. JAMA 1998; 280: 605– 613.

7. Derry PS. Update on hormones, menopause, and heart disease: evaluating professional responses to the women’s health initiative. Health Care Women Int 2008; 29: 720– 737.

8. Gompel A, Barlow D, Rozenberg S et al. Updating the EMAS 2004/ 2005 clinical recommendations on postmenopausal therapy following the recent publications: WHI and Nurses’ Health Study. Maturitas 2006; 55: 1– 4.

9. Knopp RH, Broyles FE, Cheung M et al. Comparison of the lipoprotein, carbohydrate, and hemostatic effects of phasic oral contraceptives containing desogestrel or levonorgestrel. Contraception 2001; 63: 1–11.10. Tikkanen MJ. Role of plasma lipoproteins in the pathogenesis of atherosclerotic disease, with special reference to sex hormone effects. Am J Obstet Gynecol 1990; 163: 296–304.

11. Stampfer MJ, Willett WC, Colditz GA et al. A prospective study of past use of oral contraceptive agents and risk of cardiovascular diseases. N Engl J Med 1998; 319: 1313–1317.

12. Svačina Š. Vedlejší účinky farmakoterapie na hladinu lipidů. Vnitř Lék 2007; 53: 408–411.

13. Marek J, Hána V, Kršek M. Jak ovlivňují kortikoidy, růstový hormon a estrogeny lipidy a aterosklerózu. Vnitř Lék 2007; 53: 386–390.

14. Wiegratz I, Jung- Hoffmann C, Gross W et al. Effect of two oral contraceptives containing ethinyl estradiol and gestodene or norgestimate on different lipid and lipoprotein parameters. Contraception 1998; 58: 83– 91.

15. Falsetti L, Pasinetti E. Effect of long term administration of an oral- contraceptive containing ethinylestradiol and cyproteron- acetate on lipid- metabolism in women with polycystic-ovary-syndrome. Acta Obstet Gynecol Scand 1995; 74: 56– 60.

16. Gaspard U, Endrikat J, Desager JP et al. A randomized study on the influence of oral contraceptives containing ethinylestradiol combined with drospirenone or desogestrel on lipid and lipoprotein metabolism over a period of 13 cycles. Contraception 2004; 69: 271–278.

17. Shawe J, Lawrenson R. Hormonal contraception in women with diabetes mellitus: special considerations. Treat Endocrinol 2003; 2: 321–330.

18. Klipping C, Marr J. Effects of two combined oral contraceptives containing ethinyl estradiol 20 μg combined with either drospirenone or desogestrel on lipids, hemostatic parameters and carbohydrate metabolism. Contraception 2005; 71: 409–416.

19. Scharnagl H, Petersen G, Nauck M et al. Double-blind, randomized study comparing the effects of two monophasic oral contraceptives containing ethinylestradiol (20 mg or 30 mg) and levonorgestrel (100 mg or 150 mg) on lipoprotein metabolism. Contraception 2004; 69: 105–113.

20. Connelly PW, Stachenko S, MacLean DR et al. The prevalence of hyperlipidemia in women and its association with use of oral contraceptives, sex hormone replacement therapy and nonlipid coronary artery disease risk factors. Can J Cardiol 1999; 15: 419–427.

21. Ridker PM, Glynn RJ, Hennekens CH. C-reactive protein adds to the predictivevalue of total and HDL cholesterol in determining risk of first myocardial infarction. Circulation 1998; 97: 2007– 2011.

22. Middleton J. Effect of analytical error on the assessment of cardiac risk by the high-sensitivity c- reactive protein and lipid screening model. Clin Chem 2002; 48: 1955– 1962.

23. Austin M, Thompson GR, Hulley SB et al. Triglycerides are an independent risk factor for coronary heart disease – A debate. Atherosclerosis 1997; 134: 6.

24. Walldius G, Jungner I, Holme I et al. High apolipoprotein B, low apolipoproteinA- I, and improvement in the prediction of fatal myocardial infarction (AMORIS study): a prospective study. Lancet 2001; 358: 2026– 2033.

25. Barter PJ, Ballantyne CM, Carmena R et al. Apo B versus cholesterol in estimating cardiovascular risk and in quiding therapy: report of the thirty- person/ ten country panel. J Intern Med 2006; 259: 247– 258.

26. Rasouli M, Kiasari AM, Mokhberi V. The ratio of apoB/ apoA1, apoB and lipoprotein(a) are the best predictors of stable coronary artery disease. Clin Chem Lab Med 2006; 44: 1015– 1021.27. Walldius G, Jungner I, Aastveit AH et al. The apoB/ apoA- 1 ratio is better than the cholesterol ratios to estimate the balance between plasma proatherogenic and antiatherogenic lipoproteins and to predict coronary risk. Clin Chem Lab Med 2004; 42: 1355– 1363.