Svetlana Vujovic1 , Miomira Ivovic1, Milina Tančić-Gajić1, Ljiljana V. Marina1, Marija Barac1, Zorana Arizanovic1, Maja Ivanisevic1, Dragana Rakovic1, Marija Djurović1, Branko Barac1 and Dragan Micić1
(1)
Medical Faculty, Clinic of Endocrinology, Diabetes and Diseases of Metabolism, Clinical Center of Serbia, University of Belgrade, Belgrade, Serbia
Svetlana Vujovic
Email: vujovics@EUnet.rs
18.1 Definition
Climacterium is the phase in women’s life beginning with the first menopausal symptom and cycle irregularities and ending 1 year after the last menstruation. Endocrinological, biological and clinical changes become apparent at that time.
18.2 Etiology
Among many proposed etiological hypothesis, one of the latest is that one of Titus [1]. He explained that a decline in ability to repair DNA double strand damages by homologous recombinant repair during meiosis, due to decline in repair genes BRCA 1, MRE11, Rad 51 and ATM, leads to the accumulation of these damages that contribute to the depletion of ovarian reserve.
18.3 Clinical and Hormonal Changes
Estradiol production in climacterium is very variable. In the beginning of the transition, estradiol levels are 20–30 % higher than in reproductive period. During this time, estradiol levels decrease and reach low levels in menopause. Progesterone level decreases, due to anovulatory cycles, leading to inadequate luteal phase. Menstrual cycles become unpredictable and dysfunctional uterine bleedings occur. Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) are normal at the onset of climacteric period, and then they increase causing menses to cease. In 10 % of women menses abruptly ceases. Anti-Müllerian hormone (AMH), inhibin-A, and inhibin-B decrease during this period indicated decreased ovarian reserve. Many gynecological diseases begin in that period (Table 18.1).
Table 18.1
Hormone-derived gynecological diseases
|
Menorrhagia |
Endometriosis |
|
Metrorrhagia |
Ovarian cysts |
|
Hypermenorrhea |
Benign breast diseases |
|
Myomas |
Endometrial carcinoma |
|
Adenomyosis |
Ovarian carcinoma |
|
Endometrial hyperplasia |
In such a hormonal milieu, typical menopausal symptoms and signs occur: hot flushes, insomnia and sleep disturbances, depression, loss of concentration, irritability, mood swings, gaining weight, painful bones, blood pressure variations, headaches, dry skin, vaginal dryness, and loss of libido inducing sharp decline in the quality of life. All those symptoms and signs vary from women to women. Some women have unremarkable changes, while others have terrible changes inducing unacceptable way of living. The World Health Organization requires from all doctors in the world to offer adequate therapy for women passing from reproductive period to the menopause without symptoms.
18.4 Contraception
Is contraception necessary in the climacterium? In the United States, 38 % of unplanned pregnancies happened in women over 40 years of age, representing similar percentage with that in young women [2]. The live births of mother aged 40 and over doubled from 13 555 (1998) to 26,419 (2008) in the United Kingdom. The latest data confirmed that sterility cannot be assumed until at least at the age of 60 years. So, although a natural decline of fertility occurs from mid-30s, effective contraception is required to prevent an unwanted pregnancy. The age is not a contraindication to any method of contraception.
Contraceptive choice may be influenced by frequency of intercourse, sexual problems, medical conditions, menstrual dysfunctions and wish for noncontraceptive benefits [3]. Depending on wish for having more babies, contraceptive methods can be reversible and permanent (Table 18.2).
Table 18.2
Reversible and permanent contraception
|
Reversible contraception |
|
1. Birth control pills |
|
2. Rings and patches |
|
3. Progestogens: Depo Provera, Mirena |
|
4. Nonhormonal options |
|
Permanent contraception |
|
Sterilization: |
|
A. Tubal ligation – block the tubes with the ring |
|
B. Nonsurgical procedures – small devices are inserted in the fallopian tube where over 3 months, it forms a tissue barrier |
1.
2.
3.
18.5 Contraception and Breasts
COCP decrease the incidence of benign breast disease [11]. Risks of breast carcinoma increase with age, alcohol intake, and body weight. Using COC represents small additional risk which reduces to no risk 10 years after stopping. BRCA 1 and 2 carriers have risks which outweigh benefits. In women with family history of breast carcinoma, usage of COC is unrestricted.
18.6 Ovarian, Endometrial, Cervical, and Colorectal Carcinoma
The risk of developing or dying from ovarian and endometrial carcinoma is reduced with COCP, and the effects last 15 years or more after usage [12, 13]. There is a small increase risk of cervical carcinoma, but benefits overweigh risks. COCP decreases risk of colorectal carcinoma [14].
18.7 COCP, Ischemic Stroke, and Myocardial Infarction
A very small increased risk of ischemic stroke was detected in COCP users. Coronary vascular disease and migraine with aura are contraindications for COCP use. Uncontrolled hypertension may increase the risk of stroke and myocardial infarction in COCP users.
18.8 Nonhormonal Contraception
Copper-bearing intrauterine devices are very often use. During the first 3 months, spotting or irregular bleeding can occur. Efficacy of condom usage is more than 95 %. Nowadays, they represent necessary method not just for the contraception but for the prevention of infective diseases. Spermicides and diaphragm are effective in 92–96%. Non-oil-based lubricants can be used with condoms. For the emergency contraception, progestogen-only pills and progesterone receptor modulators are advised (ulipristal acetate, effects last 120 h).
18.9 Conclusion
The best contraception is the one that is widely indicated, if not contraindicated, after balancing benefits and risks of all strategies. The patients’ needs and preferences are decisive, based on doctors’ advice.
Key Recommendations
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References
1.
Titus S, Li F, Stobezki R, Akula K, Unsal E, Jeong K, Dickler M, Robson M, Moy F, Goswami S, Oktay K (2013) Impairment of BRCA1-related DNA double-strand break repair leads to ovarian aging in mice and humans. Sci Transl Med 5(172ra21):1–12
2.
Baldwin MK, Jensen JT (2013) Contraception during the perimenopause. Maturitas 76(3):235–242. doi:10.1016/j.maturitas.2013.07.009, Epub 2013 Aug 8. Review. PubMedCrossRefPubMed
3.
Faculty of sexual and reproductive health care and clinical guidance (2010) Contraception for women aged over 40 years. http://www.fsrh.org/pdfs/ContraceptionOver40July10.pdf
4.
Jensen JT, Speroff L (2000) Health benefits of oral contraceptives. Obstet Gynecol Clin North Am 27(4):705–721, Review. PubMedCrossRefPubMed
5.
van den Heuvel MW, van Bragt AJ, Alnabawy AK, Kaptein MC (2005) Comparison of ethinylestradiol pharmacokinetics in three hormonal contraceptive formulations: the vaginal ring, the transdermal patch and an oral contraceptive. Contraception 72(3):168–174, PubMedCrossRefPubMed
6.
Royal College of Obstetricians and Gynaecologists (2006) The investigation and management of endometriosis.. http://www.rcog.org.uk/files/rcog-corp/uploaded-files/GT24InvestigationEndometriosis2006.pdf. Accessed 14 May 2010
7.
Frederiksen MC (1996) Depot medroxyprogesterone acetate contraception in women with medical problems. J Reprod Med 41(5 Suppl):414–418, Review. PubMedPubMed
8.
Singh M (2006) Progesterone-induced neuroprotection. Endocrine 29(2):271–274, Review. PubMedCrossRefPubMed
9.
National Institute for Health and Clinical Excellence (NICE) (2005) Long-acting reversible contraception: the effective and appropriate use of long-acting reversible contraception. http://www.nice.org.uk/pdf/CG030fullguideline.pdf. Accessed 14 May 2010
10.
Hudsmith L, Thorne S (2007) Contraception in women with cardiac disease. Womens Health (Lond Engl) 3(6):711–717. doi:10.2217/17455057.3.6.711, PubMedCrossRef
11.
Vessey M (2007) Oral contraceptives and cancer. J Fam Plann Reprod Health Care 33(2):133, PubMedCrossRefPubMed
12.
International Agency for Research on Cancer (IARC) (1999) Hormonal contraception and postmenopausal hormonal therapy (Monographs on the evaluation of carcinogenic risks to humans). Lyons, France: WHO IARC.
13.
Lurie G, Wilkens LR, Thompson PJ, McDuffie KE, Carney ME, Terada KY, Goodman MT (2008) Combined oral contraceptive use and epithelial ovarian cancer risk: time-related effects. Epidemiology 19(2):237–243. doi:10.1097/EDE.0b013e31816334c5, PubMedCrossRefPubMed
14.
Bosetti C, Bravi F, Negri E, La Vecchia C (2009) Oral contraceptives and colorectal cancer risk: a systematic review and meta-analysis. Hum Reprod Update 15(5):489–498. doi:10.1093/humupd/dmp017, Epub 2009 May 4. PubMedCrossRefPubMed