Female and Male Contraception (Trends in Andrology and Sexual Medicine)

Preface
Contents
Part I: Overview on Contraception
1: Birth Control Methods: From Antiquity to the Future
1.1 The Past: Unimaginable Suffering
1.2 The Beginning
1.3 Present: The Contraceptive Paradox
1.4 The Future
1.5 What About Men?
References
2: Medical Eligibility Criteria
2.1 Introduction
2.2 What Are the MEC?
2.3 Development and Updating of the MEC
2.4 Contraceptive Choice
2.5 Effectiveness of Contraception
2.6 Drug Interactions
2.6.1 Conditions that Pose a Significant Risk for Pregnancy
2.6.2 Correct Use of MEC: Practical Considerations
2.6.3 MEC Relate to Use of CHC for Contraception
2.6.4 Different MEC Sometimes Offer Different Guidance
2.6.5 Women with Multiple MEC Conditions
2.7 The List of MEC Conditions Is Not Exhaustive
2.8 MEC Tools and Resources
2.9 Conclusion
References
3: Contraceptive Counselling
3.1 What Is Contraceptive Counselling: Theoretical Background for an Integrated Model
3.2 Step 1: Needs Assessment
3.3 Step 2: Medical and Psychosocial Profile
3.4 Step 3: Individual Benefits
3.5 Step 4: Information, Education, and Empowerment Through Shared Decision-Making (SDM)
3.6 Step 5: Supportive Care
References
4: Contraception and Sexuality
4.1 Introduction
4.2 Findings on Women’s Sexuality Across the Menstrual Cycle
4.3 Combined Oral Contraceptives (COCs) and Female Sexuality
4.4 Vaginal Ring
4.5 Progestin-Only Pill (POP)
4.6 Intrauterine Devices
4.7 Progestin-Only Contraceptive Implant
4.8 Condom
4.9 Conclusion
References
5: Contraceptives and Mood
5.1 Background
5.2 Placebo-Controlled Randomized Trials
5.3 Observational Studies
5.4 What Women Are at Risk for Negative Effects of Hormonal Contraception?
5.5 Mood Symptoms Are Likely Caused by the Progestogen
5.6 Final Conclusions
References
Part II: Female Contraceptives
6: Non-hormonal Contraception
6.1 Male Condoms
6.2 Vaginal Barrier Methods: Female Condoms, Cervical Cap, Diaphragm, and Dental Dam
6.3 Diaphragms, Contoured Diaphragms, and Cervical Caps
6.4 Spermicides
6.5 Fertility Awareness Methods (or Fertility Awareness-Based Methods)
6.5.1 Calendar-Based Methods
6.5.2 Cervical Secretions Monitoring Methods
6.5.3 Basal Body Temperature (BBT)
6.5.4 Combined Fertility Indicator Methods
6.5.5 Digital FABMs
6.6 FABMs and d-FABMs
6.7 Lactational Amenorrhea
Appendix 6.1
References
7: Short-Acting Hormonal Contraception: The Pills, the Patch, and the Rings
7.1 The Beginning
7.2 Early Development of the Estrogen Component
7.3 Progestin Development
7.4 Combined Hormonal Contraception
7.4.1 Administration-Dependent Differences Between Pill, Patches, and Rings
7.4.2 Contraceptive Effectiveness
7.4.2.1 User Dependency
7.4.2.2 Different Regimens of Use
7.4.2.3 Importance of the Progestin Content
7.4.3 Progestin-Only Pills
7.4.4 Low-Dosed Progestin Pills
7.4.5 Medium-Dosed Progestin Pills
7.5 Androgenicity and Anti-androgenicity
References
8: The Advantages of LARC Methods
8.1 Introduction
8.2 Intrauterine Devices (IUD)
8.2.1 The Copper Intrauterine Device (Cu-IUD)
8.2.1.1 Contraceptive Effectiveness
8.2.1.2 Mechanism of Action
8.2.1.3 Use of Cu-IUD Among Nulligravidas and Adolescents
8.2.1.4 Main Reasons for Discontinuation
8.2.1.5 Pregnancy with an IUD In Situ
8.2.2 The Levonorgestrel Intrauterine System (LNG IUS) “Family”
8.2.2.1 The 52 mg LNG IUS
8.2.2.2 The 19.5 mg LNG IUS (Kyleena®)
8.2.2.3 The 13.5 mg LNG-IUS (Jaydess®, Skyla®)
8.2.2.4 Pregnancy with an LNG IUS In Situ
8.2.3 Subdermal Contraceptive Implants
8.2.3.1 Extended Use of Contraceptive Implants
References
9: Venous and Arterial Risks Associated with Combined Hormonal Contraception
9.1 Introduction
9.2 Hormones Used in Contraception
9.2.1 Estrogens
9.2.1.1 Natural Estrogens
9.2.1.2 Synthetic Estrogens
9.2.1.3 Other Estrogen Preparations Used in Hormonal Contraception
9.2.2 Progestogens
9.2.2.1 Natural Progestogens
9.2.2.2 Synthetic Progestogens
9.2.2.3 Progestin Generations
9.3 Venous and Arterial Thrombosis
9.3.1 Coagulation and Thrombosis
9.3.2 Physiologic Effects of Hormones on the Coagulation Cascade
9.3.3 Pharmacologic Effects of Hormones on the Coagulation Cascade
9.3.4 Pharmacologic Risk of Hormones on Arterial Thromboembolic Events
9.4 Important Risk Factors for VTE
9.5 Controversy Regarding Third- and Fourth-Generation Progestins
9.6 Critically Evaluating the Evidence
9.7 Patient-Centered Contraceptive Counseling
9.8 Conclusions
References
10: Non-contraceptive Benefits of Hormonal Methods
10.1 Introduction
10.2 Menstrual and Ovarian Cycle
10.2.1 Dysmenorrhea
10.2.2 Heavy Menstrual Bleeding (HMB)
10.2.3 Dysfunctional Uterine Bleeding
10.2.4 Premenstrual Syndrome (PMS) and Premenstrual Dysphoric Disorder (PMDD)
10.3 Endometriosis and Adenomyosis
10.4 Polycystic Ovarian Syndrome (PCOS), Hirsutism, and Acne
10.4.1 Impact on Acne and Hirsutism
10.4.2 Impact on Metabolic Parameters and Cardiovascular Risk Factors
10.4.3 Impact on Glucose Tolerance
10.4.4 Impact on Venous and Arterial Thromboembolism
10.5 Pelvic Inflammatory Disease (PID)
10.6 Ectopic Pregnancy (EP)
10.7 Bone Mineral Density (BMD)
10.8 Prevention of Cancer
10.8.1 Endometrial Hyperplasia
10.8.2 Endometrial Cancer
10.8.3 Ovarian Cancer
10.8.4 Colorectal Cancer
10.9 Conclusion
References
11: Contraception Cancer Risks and Benefits
11.1 Introduction
11.2 Breast Cancer
11.2.1 Combined Oral Contraceptives
11.2.2 Progestogen-Only Contraceptives
11.2.3 Non-Hormonal Intrauterine Devices
11.2.4 Female Sterilisation
11.3 Cervical Cancer
11.3.1 Combined Oral Contraceptives
11.3.2 Progestogen-Only Contraceptives
11.3.3 Non-Hormonal Intrauterine Devices
11.3.4 Female Sterilisation
11.4 Ovarian Cancer
11.4.1 Combined Oral Contraceptives
11.4.2 Progestogen-Only Contraceptives
11.4.3 Non-Hormonal Intrauterine Devices
11.4.4 Female Sterilisation
11.4.5 High Risk Groups
11.5 Endometrial Cancer
11.5.1 Combined Oral Contraceptives
11.5.2 Progestogen-Only Contraceptives
11.5.3 Non-Hormonal Intrauterine Devices
11.5.4 Female Sterilisation
11.5.5 Women With Lynch Syndrome
11.6 Colorectal Cancer
11.6.1 Combined Oral Contraceptives
11.6.2 Non-Hormonal Intrauterine Devices
11.6.3 Female Sterilisation
11.7 Anal Cancer
11.8 Liver Cancer
11.8.1 Combined Oral Contraceptives
11.8.2 Female Sterilisation
11.9 Other Cancers
11.9.1 Combined Oral Contraceptives
11.10 Net Cancer Effects
11.10.1 Combined Oral Contraceptives
11.10.2 Other Reversible Contraceptives
11.10.3 Female Sterilisation
11.11 Male Sterilisation
11.11.1 Prostate Cancer
11.11.2 Testicular Cancer
References
12: Emergency Contraception
12.1 Introduction
12.2 Historical Methods of EC
12.3 Oral Hormonal Methods
12.3.1 Yuzpe Regimen
12.3.2 LNG
12.3.3 Mifepristone
12.3.4 UPA
12.4 THE Copper-IUCD
12.5 Factors Affecting Efficacy of Hormonal EC
12.5.1 Effect of Obesity
12.5.2 Further Acts of UPSI in the Same Cycle
12.6 Side Effects and Safety
12.7 Care After EC
12.8 Improving Access to EC
References
Part III: Management of Female Contraception Throughout Women’s Lifetime
13: Critical Issues in Adolescent Contraception
13.1 Introduction
13.2 Contextual Factors Significant for Contraceptive Protection
13.3 Critical Biological Issues in Adolescents
13.3.1 Immaturity of Hypothalamic Pituitary Ovarian Axis
13.3.2 Attainment of Peak Bone Mass
13.3.3 Mood and Hormonal Contraception
References
14: Contraception After an Induced Abortion and Childbirth
14.1 Return of Ovulation and Resumption of Sexual Activity
14.1.1 After an Induced Abortion
14.1.2 After Delivery
14.2 Contraception After an Induced Abortion
14.2.1 Surgical Abortion
14.2.2 Changing Landscape of Abortion Care
14.2.3 Medical Abortion and Contraceptive Implants
14.2.4 Medical Abortion and Intrauterine Contraception
14.2.5 Injectable Progestin After Medical Abortion
14.3 Contraception After Childbirth
14.3.1 Can Breastfeeding Be Used as Contraception?
14.3.2 Interpregnancy Interval
14.3.3 Short- and Long-Acting Alternatives in Contraception After Childbirth (SARCs and LARCS)
14.3.3.1 SARC
14.3.3.2 Combined Hormonal Contraception (Pill, Patch, Ring)
14.3.3.3 Progestin-Only Pills (POP)
14.3.3.4 Injectable Progestin Contraception
14.3.3.5 LARC
14.3.3.6 Progestin Implants
14.3.3.7 Intrauterine Contraception
14.3.4 Time of Insertion
14.3.5 Emergency Contraception
14.3.5.1 Oral Options
14.3.5.2 IUD
14.3.6 Service Delivery System and Uptake of Post-Abortal and Postpartum Contraception
References
Suggested Reading
15: Contraception in Perimenopausal Women
15.1 Background of the Perimenopausal
15.2 Contraception After 40 Years
15.3 Future of Hormonal Contraception After 40 Years
References
16: Contraceptive Choice in Women with PCOS
16.1 Background: What Is Polycystic Ovary Syndrome?
16.1.1 Hyperandrogenism
16.1.2 Metabolic Profile in PCOS
16.1.3 Reproductive Features of PCOS
16.2 Rationale for the Use of Hormonal Contraceptives in PCOS
16.2.1 Overview of the Molecules Used in Contraception
16.2.2 General Contraindications of Hormonal Contraceptives
16.2.3 How to Choose the Right Hormonal Contraceptive
16.2.4 Other Non-Contraceptive Benefits of the Combined Oral Contraceptive Pills
16.2.4.1 Sex-Hormone Binding Globulin
16.2.4.2 Testosterone and Free Androgen Index
16.2.4.3 5α-Reductase Activity
16.3 Metabolic Effects of Hormonal Contraceptives and  Cardiovascular Risk
16.3.1 Body Weight
16.3.2 Lipid Profile
16.3.3 Carbohydrate Metabolism
16.3.4 Arterial Pressure
16.3.5 Effects on Hemostasis and the Risk of Thrombosis
16.4 Final Considerations: How to Approach the Patient with PCOS
References
Part IV: Management of Female Contraception in Women with Medical Conditions
17: Contraception and Cardiovascular Diseases
17.1 Preface About International Guidelines Categories
17.2 Hypertension
17.2.1 Definition
17.2.2 Guidelines
17.3 History of High Blood Pressure During Pregnancy
17.3.1 Definition
17.3.2 Guidelines
17.4 History of Ischaemic Heart Disease
17.4.1 Definition
17.4.2 Guidelines
17.5 History of Cerebrovascular Accident
17.5.1 Definition
17.5.2 Guidelines
17.6 Dyslipidaemia
17.6.1 Definition
17.6.2 Guidelines
17.7 Valvular Heart Disease
17.7.1 Definition
17.7.2 Guidelines
17.8 Arrhythmia
17.8.1 Definition
17.8.2 Guidelines
17.9 History of Deep-Vein Thrombosis
17.9.1 Definition
17.9.2 Guidelines
17.10 Thrombogenic Mutations
17.10.1 Definition
17.10.2 Guidelines
17.11 Multiple Risk Factors for Arterial Cardiovascular Disease
17.11.1 Definition
17.11.2 Guidelines
References
18: The Effect of Hormonal Contraceptives on Metabolism
18.1 Introduction
18.2 HC Formulations
18.3 Carbohydrate Metabolism
18.3.1 Estrogens
18.3.2 Progestins
18.3.3 Progestin-Only Contraception
18.3.4 Women with Diabetes
18.3.5 Women with Polycystic Ovary Syndrome
18.4 Lipid Metabolism
18.4.1 Estrogens
18.4.2 Progestins
18.4.3 Progestin-Only Contraception
18.5 Blood Pressure
18.5.1 Estrogens
18.5.2 Progestins
18.6 Body Weight and Composition
18.6.1 Progestin-Only Contraception
18.7 Conclusions
References
19: Contraception in Women with Rheumatologic Disease and After Organ Transplantation
19.1 Rheumatoid Arthritis
19.2 Systemic Lupus Erythematosus (SLE)
19.3 Organ Transplantation
19.4 Hematopoietic Stem Cell Transplantation
References
20: Drug Interactions with Contraceptives
20.1 Drug Interactions: Pharmacological Considerations
20.1.1 Clinical Relevance of Drug–Drug Interactions
20.1.2 Drug–Herbal Interactions
20.2 Hormonal Contraceptives: Pharmacological Classification, Pharmacokinetic Issues and Impact on Drug–Drug Interactions
20.3 Clinically Relevant Drug Interactions Involving HCs
20.3.1 Antiepileptic Agents
20.3.1.1 Effects of Antiepileptic Agents on HCs
20.3.1.2 Effects of HCs on Antiepileptic Agents
20.3.2 Antiretroviral Agents
20.3.2.1 Effects of Antiretroviral Agents on HCs
20.3.2.2 Effects of HCs on Antiretroviral Agents
20.3.3 Antitubercular Agents
20.3.3.1 Effects of Antitubercular Agents on HCs
20.3.3.2 Effects of HCs on Antitubercular Agents
20.3.4 Other Antimicrobials
20.3.4.1 Effects of Antimicrobials on HCs
20.3.4.2 Effects of HCs on Antimicrobials
20.3.5 Antidepressants and Antipsychotics
20.3.5.1 Effects of Antidepressants and Antipsychotics on HCs
20.3.5.2 Effects of HCs on Antidepressants and Antipsychotics
20.3.6 Anticoagulants
20.3.6.1 Effects of Anticoagulants on HCs
20.3.6.2 Effects of HCs on Anticoagulants
20.3.7 Interactions with Herbal Products and Dietary Supplements
20.4 Sources of Information on Drug–Drug Interactions
References
21: Hormonal Contraception and Bone
21.1 Introduction
21.2 Oestrogens and Progestins Used for Contraception
21.2.1 Oestrogens
21.2.2 Progestins
21.3 Clinical Data in Postadolescent Women
21.3.1 Combined Oral Contraceptives Containing Ethinyloestradiol
21.3.1.1 Randomized Controlled Trials
21.3.1.2 Observational Studies
21.3.1.3 Cross-Sectional Studies
21.3.2 Combined Oral Contraceptives Containing 17β-Oestradiol or 17β-Oestradiol Valerate
21.3.3 Combined Oral Contraceptives Containing Oestetrol
21.4 Influence of Low-Dose COCs (15–20 μg EE Daily) on Bone Metabolism
21.4.1 Adult Women
21.4.2 Adolescent Girls
21.5 Nonoral Combined Hormonal Contraceptives
21.5.1 Combined Vaginal Ring
21.5.2 Combined Contraceptive Patch
21.6 Progestin-Only Ovulation Inhibitors
21.6.1 Oral Preparations
21.6.1.1 Classical “Minipill” (30 μg Levonorgestrel per Day)
21.6.1.2 Desogestrel Tablets (0.075 mg per Day)
21.6.2 Hormonal Implants
21.6.2.1 Etonogestrel Implants
21.6.2.2 LNG Implants
21.6.3 Levonorgestrel Intrauterine System (LNG-IUD)
21.6.4 Depot Medroxyprogesterone Acetate (DMPA)
21.6.4.1 DMPA (150 mg i.m.) and DMPA (104 mg s.c.) After Acquisition of Peak Bone Mass
21.6.4.2 Changes in Bone Density and Fracture Rate in Adolescent DMPA Users Before the Acquisition of Peak Bone Mass
21.6.4.3 Use in Women with Increased Risk of Osteoporosis
21.6.5 Norethisterone Enanthate
21.7 Discussion
21.8 Summary
References
Part V: Male Contraception: Current Options and Ongoing Research
22: The Male Role in Family Planning Today
22.1 Introduction
22.2 The Male Role in Contraceptive Decision-Making
22.3 Men’s Knowledge of Contraception
22.4 Men’s Perception of Contraceptive Responsibility
22.5 Male Involvement in Contraception
22.6 Effects of Male Involvement in Family Planning
22.7 Ways to Engage Men in Family Planning Programs
22.8 Conclusions
References
23: Acceptability of Male Hormonal Contraception
23.1 Introductory Considerations
23.2 Acceptability Data from Surveys
23.3 Female Partner’s Perspective and Their Role in Male Hormonal Contraception
23.4 Acceptability Data from Clinical Trials
23.5 Conclusions
References
24: Current Male Contraceptives and Experimental Nonhormonal Contraceptive Research
24.1 Overview of Male Reproductive Physiology
24.2 Currently Available Male Contraceptive Methods
24.2.1 Vasectomy
24.2.2 Condoms
24.2.3 Withdrawal
24.2.4 Experimental Nonhormonal Male Contraceptives
24.2.5 Gossypol
24.2.6 Triptolide
24.2.7 Adjudin
24.2.8 H2-Gamendazole
24.2.9 EPPIN
24.2.10 BRDT Inhibition
24.2.11 Retinoic Acid Receptor Antagonists
24.2.12 Retinoic Acid Biosynthesis Inhibitors
24.2.13 CatSper
24.2.14 Gendarussa
24.2.15 Vas Occlusion Methods
24.3 Conclusions
References
25: Male Contraception: Hormonal Methods
25.1 Introduction
25.2 Physiological Basis of Male Hormonal Contraception
25.3 Experimental Male Hormonal Contraceptives: Efficacy Studies
25.3.1 Androgen-Only MHC Approaches
25.3.1.1 World Health Organization Trials: Short-Acting Testosterone Injections
25.3.1.2 China-Based Trials: Longer-Acting Testosterone Injections
25.3.2 Androgen plus Progestin MHC
25.3.2.1 Australia-Based Trial: Long-Acting Testosterone plus Depot Medroxyprogesterone Acetate
25.3.2.2 WHO/Contraception Research and Development Trial: Long-Acting Testosterone plus Norethisterone
25.4 Studies of Other Potential MHC Regimens
25.4.1 Oral Formulations
25.4.1.1 Oral T plus Cyproterone Acetate
25.4.1.2 Oral Dimethandrolone Undecanoate
25.4.1.3 11β-Methyl-19-Nortestosterone17β-Dodecylcarbonate
25.4.2 Transdermal Formulations
25.4.2.1 Testosterone Gel plus Oral Medroxyprogesterone
25.4.2.2 Transdermal Testosterone plus Nestorone Gel
25.4.3 Injectable and Implantable Regimens Other Than T plus Progestin
25.4.3.1 T plus GnRH Analogs (plus Progestin)
25.4.3.2 7α-Methyl-19-Nortestosterone Subcutaneous Implants
25.5 Possible Mechanisms for Nonuniform Suppression of Spermatogenesis
25.6 Safety, Adverse Events, and Side Effects
25.7 Acceptability of Male Contraception
25.7.1 Method of Delivery Acceptability
25.7.2 Acceptability Related to Suppression Time and Reversibility
25.8 Ethics of Male Contraception
25.9 Barriers to MHC Development
25.9.1 Male-Based Contraceptive Accessibility
25.10 Conclusion
References