Amenorrhea: Volume 10: Frontiers in Gynecological Endocrinology

Contents
1: Müllerian Malformations and Their Treatments
1.1 Introduction
1.2 Prevalence
1.3 Etiopathology
1.4 Classification Systems
1.5 Clinical Manifestations
1.6 Diagnostic Methods
1.7 Treatment
1.7.1 Which Classification Is Better for Patient Management?
1.7.2 Congenital Uterine Malformations by Experts (CUME): Definitions 2018
1.8 Controversies
1.8.1 Uterovaginal Anastomosis for Cervical Agenesis
1.8.2 Surgery of Septate Uterus by Different Definitions
1.8.3 Cervical Septum Preservation and Resection
1.8.4 Blind Hemivagina
1.9 Challenges and Ongoing and Further Studies
1.10 Discussion
References
2: Adolescent Amenorrhea: New Aspects of an Old Problem
2.1 Why Should Amenorrhea Be Considered as a “Vital” Sign?
2.2 Who Should Be Evaluated for Amenorrhea?
2.3 How Should Adolescent Amenorrhea Be Evaluated?
2.4 What Are the Causes of Adolescent Amenorrhea?
2.4.1 Endocrine Defects Within the Hypothalamic-Pituitary-Ovarian Axis (Table 2.1)
2.4.1.1 Hypogonadotropic Hypogonadism
Congenital Hypogonadotropic Hypogonadism
Acquired Hypogonadotropic Hypogonadism
2.4.1.2 Hypergonadotropic Hypogonadism
Gonadal Dysgenesis
Defects in Testosterone Production
Androgen Resistance Disorders
Complete Androgen Insensitivity Syndrome (CAIS)
5aR Deficiency
2.4.2 Genetic Defects of Ovary
2.4.2.1 X Chromosome
2.4.2.2 Autosomal Gene Mutations
2.4.3 Metabolic Disorders
2.4.4 Autoimmune Diseases
2.4.5 Infections
2.4.6 Iatrogenic Causes (Radiotherapy, Chemotherapy)
2.4.7 Mullerian Defects
2.4.8 Environmental Factors (Lifestyle, Endocrine Disruptors)
2.4.9 Idiopathic
2.5 Treatment
2.6 Conclusions
References
3: Amenorrhea in Eating Disorders
3.1 Introduction
3.2 Anorexia Nervosa
3.2.1 Physical Signs of AN
3.3 Functional Hypothalamic Amenorrhea
3.3.1 Endocrine Disturbances
3.4 Medical Consequences of Hypothalamic Amenorrhea
3.5 Management of Hypothalamic Amenorrhea
3.6 Treatment of AN
3.7 Bulimia Nervosa
3.7.1 Physical Signs of BN
3.8 Menstrual Disturbances in BN
3.9 Association Between Bulimia and PCOS
3.9.1 Antiandrogenic Treatment
3.10 Management of Amenorrhea in BN
3.11 Treatment of BN
3.12 Conclusion
References
4: The New Forms of Functional Hypothalamic Amenorrhoea
4.1 Special Profiles of Functional Hypothalamic Amenorrhoea (FHA)
4.2 The Crosstalk Between Body and Central Nervous System on Endocrine and Metabolic Homeostasis
4.3 Adaptation to Low Energy Availability (LEA) and to Persistent Psychological and Physical Stress
4.4 Diagnostic Workup
4.5 Special Clinical Situations in the Framework of FHA
References
5: Exercise and Stress-Related Amenorrhea
5.1 Introduction
5.2 Menstrual Dysfunctions in Athletes
5.3 Training, Stress, and Altered Neuroendocrine Control of Reproduction
5.4 Neuroendocrine Mechanisms of Stress-Induced Impairment of Reproductive Function
5.5 Neuroendocrine Mechanism of Hypothalamic Amenorrhea
5.6 Metabolic Signals as Stressors in Hypothalamic Amenorrhea
5.7 Resolution of FHA
5.8 Conclusive Remarks
References
6: Sexual Dysfunction in Functional Hypothalamic Amenorrhea
6.1 Introduction
6.2 Sexual Function and FHA: Modulation of the Neuroendocrine System
6.3 Sexual Function and FHA: The Importance of Mood
6.4 Sexual Function and FHA: Expanding Our Understanding on the Role of Other Possible Mediators
6.5 Conclusions
References
7: Endocrine Gland Disorder-Related Amenorrhoea
7.1 Introduction
7.2 Pituitary Tumours
7.2.1 Hyperprolactinaemia
7.2.2 Acromegaly
7.2.3 Cushing’s Disease
7.3 Thyroid Disorders
7.3.1 Hypothyroidism
7.3.2 Hyperthyroidism
7.4 Adrenal Gland Disorders
7.4.1 Non-classical Congenital Adrenal Hyperplasia Due to 21 Hydroxylase Deficiency
7.4.2 Non-classical Congenital Adrenal Hyperplasia Due to 11-Beta-Hydroxylase Deficiency
7.4.3 Addison’s Disease
7.5 Conclusions
References
8: Polycystic Ovarian Syndrome
8.1 Introduction
8.2 Etiology
8.2.1 Genetic Factors
8.2.2 Environmental Factors
8.3 Pathophysiology
8.4 Diagnostic Criteria and Different Phenotypes
8.4.1 Diagnostic Criteria
8.4.2 Phenotypes
8.5 Evaluation
8.5.1 Menstrual Irregularity
8.5.2 Hyperandrogenism
8.5.2.1 Clinical Hyperandrogenism
8.5.2.2 Biochemical Hyperandrogenism
8.5.3 PCOM
8.5.4 Other Biochemical Characteristics
8.6 Differential Diagnosis
8.7 Health Risks
8.7.1 Metabolic Health Risks
8.7.1.1 Weight Gain and Obesity
8.7.1.2 Impaired Glucose Tolerance (IGT): Type 2 Diabetes Mellitus (T2DM)
8.7.1.3 Dyslipidemia
8.7.1.4 Insulin Resistance
8.7.1.5 Metabolic Syndrome
8.7.1.6 Nonalcoholic Fatty Liver Disease (NAFLD)
8.7.1.7 Sleep Apnea
8.7.2 Cardiovascular Health Risks
8.7.3 Gynecological Health Risks
8.7.3.1 Endometrial Cancer
8.7.3.2 Pregnancy Complications
8.7.3.3 Infertility
8.7.4 Psychosocial Health Risks
8.8 Treatment
8.8.1 Metabolic Abnormalities
8.8.2 Menstrual Irregularity: Endometrial Protection
8.8.3 Hyperandrogenism
8.8.4 Ovulation Induction and Fertility
8.8.4.1 Weight Loss
8.8.4.2 Letrozole
8.8.4.3 Clomiphene Citrate
8.8.4.4 Metformin
8.8.4.5 Exogenous Gonadotropins
8.8.4.6 Laparoscopic Ovarian Drilling
8.8.4.7 Assisted Reproduction Technology (ART)
8.8.4.8 Other Treatments
8.9 PCOS in Adolescents
8.10 PCOS in Postmenopausal Women
8.11 Discussion and Future Perspectives
References
9: Amenorrhea Associated with Contraception and the Postpartum Period
9.1 Introduction
9.2 Breastfeeding Effects on Ovulation
9.3 Counselling
9.4 Contraceptive Methods (Table 9.1)
9.4.1 Lactational Amenorrhea Method (LAM)
9.4.2 Surgical Methods
9.4.3 Barrier Methods and Local Chemicals
9.4.4 Intrauterine Device (IUD)
9.5 Hormonal Therapies
9.5.1 Estroprogestinic (EP) Contraception
9.5.2 Progestogen-Only Contraception (POC)
9.6 Conclusions
References
10: Amenorrhea in Oncological Patients
10.1 Introduction
10.2 Etiologies and Pathogenesis
10.2.1 Gonadotoxicity of Anticancer Treatments
10.3 Prognostic Factors
10.4 Chemotherapy-Induced Ovarian Failure
10.5 Radiotherapy-Induced Ovarian Failure
10.5.1 Predicting Age of Ovarian Failure After Radiation
10.6 Prophylactic Menstrual Suppression
10.7 Menstrual Suppression
10.7.1 Gonadotropin-Releasing Hormone Agonists
10.7.2 Progestin-Only Therapy
10.7.3 Combined Hormonal Contraceptives
10.7.4 Emergent Treatment of Acute Uterine Bleeding
10.8 Fertility Preservation Strategies
10.8.1 Oocyte and Embryo Cryopreservation
10.8.2 Ovarian Tissue Cryopreservation
10.8.3 Ovarian Transposition and Gonadal Shielding During RT
10.8.4 Need to Reduce Gonadotoxicity: Medical Gonadoprotection
10.8.5 Life After Treatment
References
11: Premature Ovarian Insufficiency
11.1 Introduction
11.2 Definition of POI
11.3 Prevalence of POI
11.4 Etiology of POI
11.5 Pathogenesis of POI
11.6 Clinical Symptoms and Signs
11.6.1 Early Symptoms and Signs
11.6.2 Late Symptoms and Signs
11.7 Complications of Untreated POI
11.7.1 Cardiovascular Diseases
11.7.2 Metabolic Changes
11.7.3 Osteoporosis
11.7.4 Cognitive Health and Brain Function
11.7.5 Urogenital Function and Sexuality
11.7.6 Infertility
11.8 Diagnosis of POI
11.9 Differential Diagnosis
11.10 Therapy of POI
11.10.1 Cardiovascular Effects
11.10.2 Metabolic Effects
11.10.3 Osteoporosis
11.10.4 Brain Effects
11.10.5 Sexuality
11.10.6 Infertility
11.11 Risks of HRT and POI
11.11.1 Breast Cancer
11.11.2 Stroke, Venous Thromboembolism
11.11.3 Endometriosis
11.11.4 Migraine
11.11.5 Fibroids
11.12 Conclusion
References
12: Menopause Is a Natural Condition: Does It Require to Be Corrected? For Whom and for How Long?
12.1 Signs and Symptoms of Menopause
12.2 When to Start Menopause Hormone Therapy?
12.3 Benefits and Risks of Hormone Therapy
12.3.1 Cardiovascular System and Metabolism
12.3.2 Central Nervous System
12.3.3 Bone
12.3.4 Cancer
12.4 Tailoring Treatment According to Age and Risk Factors
12.5 How Long Should the Therapy Be Continued?
12.6 The Effects of Discontinuation
References