Functional Hypothalamic Amenorrhea: a Stress-Based Disease
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Non Hormonal Management of Menstrual Cylce Irregularities
Journal of Gynecology and Women’s Health ISSN 2474-7602 Review Article J Gynecol Women’s Health Volume 11 Issue 4 - September 2018 Copyright © All rights are reserved by Arif A Faruqui DOI: 10.19080/JGWH.2018.11.555818 Non Hormonal Management of Menstrual Cylce Irregularities Arif A Faruqui* Department of Pharmacology, Clinical Pharmacologist, A 504, Rizvi Mahal, India Submission: August 16, 2018; Published: September 07, 2018 *Corresponding author: Email: Arif A Faruqui, Department of Pharmacology, A 504, Rizvi Mahal Opp. K.B. Bhabha Hospital, Waterfield road Bandra, India, Abstract of bleedingEach month patterns, the endometriumfor example, amenorrhea, becomes inflamed, menorrhagia and the or luminalpolymenorrhea; portion ovarianis shed dysfunctionduring menstruation. for example, Aberrations anovulation in menstrualand luteal physiology can lead to common gynecological conditions, such as heavy or prolonged bleeding. Menstrual dysfunction is defined in terms pathologic process or may predispose a woman to the development of chronic disease. For example, metrorrhagia predisposes to anemia, anddeficiency; the irregular painful menstrual menstruation cycles and associated premenstrual with PCOS syndrome. (see PCOS) Certain can characteristics predispose a woman of menstruation to infertility, can diabetes be a reflection and consequently, of an underlying heart disease. What is it, in this age of life-saving antibiotics, hormonal therapy, surgeries and other seemingly miraculous medical therapies that causes so many individuals to seek therapies outside of conventional medicine? Conventional medicine may be at its best when treating acute crises, but for the treatment of chronic problems it may fall short of offering either cure or healing, leading patients to seek out systems of treatment that they perceive as addressing the causes of their problem, not just the symptoms. -
Androgen Excess in Breast Cancer Development: Implications for Prevention and Treatment
26 2 Endocrine-Related G Secreto et al. Androgen excess in breast 26:2 R81–R94 Cancer cancer development REVIEW Androgen excess in breast cancer development: implications for prevention and treatment Giorgio Secreto1, Alessandro Girombelli2 and Vittorio Krogh1 1Epidemiology and Prevention Unit, Fondazione IRCCS – Istituto Nazionale dei Tumori, Milano, Italy 2Anesthesia and Critical Care Medicine, ASST – Grande Ospedale Metropolitano Niguarda, Milano, Italy Correspondence should be addressed to G Secreto: [email protected] Abstract The aim of this review is to highlight the pivotal role of androgen excess in the Key Words development of breast cancer. Available evidence suggests that testosterone f breast cancer controls breast epithelial growth through a balanced interaction between its two f ER-positive active metabolites: cell proliferation is promoted by estradiol while it is inhibited by f ER-negative dihydrotestosterone. A chronic overproduction of testosterone (e.g. ovarian stromal f androgen/estrogen balance hyperplasia) results in an increased estrogen production and cell proliferation that f androgen excess are no longer counterbalanced by dihydrotestosterone. This shift in the androgen/ f testosterone estrogen balance partakes in the genesis of ER-positive tumors. The mammary gland f estradiol is a modified apocrine gland, a fact rarely considered in breast carcinogenesis. When f dihydrotestosterone stimulated by androgens, apocrine cells synthesize epidermal growth factor (EGF) that triggers the ErbB family receptors. These include the EGF receptor and the human epithelial growth factor 2, both well known for stimulating cellular proliferation. As a result, an excessive production of androgens is capable of directly stimulating growth in apocrine and apocrine-like tumors, a subset of ER-negative/AR-positive tumors. -
Background Briefing Document from the Consortium of Sponsors for The
BRIEFING BOOK FOR Pediatric Advisory Committee (PAC) Prepared by Alan Rogol, M.D., Ph.D. Prepared for Consortium of Sponsors Meeting Date: April 8th, 2019 TABLE OF CONTENTS LIST OF FIGURES ................................................... ERROR! BOOKMARK NOT DEFINED. LIST OF TABLES ...........................................................................................................................4 1. INTRODUCTION AND BACKGROUND FOR THE MEETING .............................6 1.1. INDICATION AND USAGE .......................................................................................6 2. SPONSOR CONSORTIUM PARTICIPANTS ............................................................6 2.1. TIMELINE FOR SPONSOR ENGAGEMENT FOR PEDIATRIC ADVISORY COMMITTEE (PAC): ............................................................................6 3. BACKGROUND AND RATIONALE .........................................................................7 3.1. INTRODUCTION ........................................................................................................7 3.2. PHYSICAL CHANGES OF PUBERTY ......................................................................7 3.2.1. Boys ..............................................................................................................................7 3.2.2. Growth and Pubertal Development ..............................................................................8 3.3. AGE AT ONSET OF PUBERTY.................................................................................9 3.4. -
The Prevalence of and Attitudes Toward Oligomenorrhea and Amenorrhea in Division I Female Athletes
POPULATION-SPECIFIC CONCERNS The Prevalence of and Attitudes Toward Oligomenorrhea and Amenorrhea in Division I Female Athletes Karen Myrick, DNP, APRN, FNP-BC, Richard Feinn, PhD, and Meaghan Harkins, MS, BSN, RN • Quinnipiac University Research has demonstrated that amenor- hormone and follicle-stimulating hormone rhea and oligomenorrhea may be common shut down stimulation to the ovary, ceasing occurrences among female athletes.1 Due production of estradiol.2 to normalization of menstrual dysfunction The effect of oral contraceptives on the within the sport environment, amenorrhea menstrual cycle include ovulation inhibi- and oligomenorrhea tion, changes in cervical mucus, thinning may be underreported. of the uterine endometrium, and motility Key PointsPoints There are many underly- and secretion in the fallopian tubes, which Lean sport athletes are more likely to per- ing causes of menstrual decrease the likelihood of conception and 3 ceive missed menstrual cycles as normal. dysfunction. However, implantation. Oral contraceptives contain a a similar hypothalamic combination of estrogen and progesterone, Menstrual dysfunction is one prong of the amenorrhea profile is or progesterone only; thus, oral contracep- female athlete triad. frequently seen in ath- tives do not stop the production of estrogen. letes, and hypothalamic Menstrual dysfunction is one prong of the Menstrual dysfunction is often associated dysfunction is com- female athlete triad (triad). The triad is a with musculoskeletal and endothelial monly the root of ath- syndrome of linking low energy availability compromise. lete’s menstrual abnor- (EA) with or without disordered eating, men- malities.2 The common strual disturbances, and low bone mineral Education and awareness of the accultur- hormone pattern for density, across a continuum. -
EAU Pocket Guidelines on Male Hypogonadism 2013
GUIDELINES ON MALE HYPOGONADISM G.R. Dohle (chair), S. Arver, C. Bettocchi, S. Kliesch, M. Punab, W. de Ronde Introduction Male hypogonadism is a clinical syndrome caused by andro- gen deficiency. It may adversely affect multiple organ func- tions and quality of life. Androgens play a crucial role in the development and maintenance of male reproductive and sexual functions. Low levels of circulating androgens can cause disturbances in male sexual development, resulting in congenital abnormalities of the male reproductive tract. Later in life, this may cause reduced fertility, sexual dysfunc- tion, decreased muscle formation and bone mineralisation, disturbances of fat metabolism, and cognitive dysfunction. Testosterone levels decrease as a process of ageing: signs and symptoms caused by this decline can be considered a normal part of ageing. However, low testosterone levels are also associated with several chronic diseases, and sympto- matic patients may benefit from testosterone treatment. Androgen deficiency increases with age; an annual decline in circulating testosterone of 0.4-2.0% has been reported. In middle-aged men, the incidence was found to be 6%. It is more prevalent in older men, in men with obesity, those with co-morbidities, and in men with a poor health status. Aetiology and forms Male hypogonadism can be classified in 4 forms: 1. Primary forms caused by testicular insufficiency. 2. Secondary forms caused by hypothalamic-pituitary dysfunction. 164 Male Hypogonadism 3. Late onset hypogonadism. 4. Male hypogonadism due to androgen receptor insensitivity. The main causes of these different forms of hypogonadism are highlighted in Table 1. The type of hypogonadism has to be differentiated, as this has implications for patient evaluation and treatment and enables identification of patients with associated health problems. -
Estrogen Deficiency During Menopause and Its Management: a Current Update V
Review Article Estrogen deficiency during menopause and its management: A current update V. T. Hemalatha1, A. Julius2, S. P. Kishore Kumar3, L. Vijayalakshmi4, Shankar Narayanan1 ABSTRACT Different phases of a woman’s life: Puberty, menses, pregnancy, and menopause have varied influence on her oral health. During the menopause, women go through biological and endocrine changes, particularly in their sex steroid hormone production, affecting their health. Sex hormones strongly influence body fat distribution and adipocyte differentiation. Estrogens and testosterone differentially affect adipocyte physiology, but the importance of estrogens in the development of metabolic diseases during menopause is disputed. Estrogens and estrogens receptor regulate various aspects of glucose and lipid metabolism. Disturbances of this metabolic signal lead to the development of metabolic syndrome and a higher cardiovascular risk in woman. The absence of estrogens is a clue factor in the onset of cardiovascular disease during the menopausal period, which is characterized by lipid profile variations and predominant abdominal fat accumulation. However, influence of the absence of these hormones and its relationship to higher obesity in women during menopause is not clear. This systematic review discusses of the role of estrogens and estrogen receptors in adipocyte differentiation and its various effects and brief discussion on its management. KEY WORDS: Estrogen hormone (estrogens/progestogens) replacement therapy, Menopause, Weight gain INTRODUCTION BODY CHANGES AT MENOPAUSE Menopause occurs when a woman stops ovulating and As we age, our muscles decrease in bulk and our her monthly period (menstruation) stops. metabolism slows down. These changes cancontribute to weight gain around the time of menopause. Other As women age, into their 40s and 50s, there is a tendency physical changes associated with menopause may to gain weight. -
Hypogonadism in Adolescence 173:1 R15–R24 Review
A A Dwyer and others Hypogonadism in adolescence 173:1 R15–R24 Review TRANSITION IN ENDOCRINOLOGY Hypogonadism in adolescence Andrew A Dwyer1,2, Franziska Phan-Hug1,3, Michael Hauschild1,3, Eglantine Elowe-Gruau1,3 and Nelly Pitteloud1,2,3,4 1Center for Endocrinology and Metabolism in Young Adults (CEMjA), 2Endocrinology, Diabetes and Metabolism Correspondence Service and 3Division of Pediatric Endocrinology Diabetology and Obesity, Department of Pediatric Medicine and should be addressed Surgery, Centre Hospitalier Universitaire Vaudois (CHUV), Rue du Bugnon 46, 1011 Lausanne, Switzerland and to N Pitteloud 4Department of Physiology, Faculty of Biology and Medicine, University of Lausanne, Rue du Bugnon 7, Email 1005 Lausanne, Switzerland [email protected] Abstract Puberty is a remarkable developmental process with the activation of the hypothalamic–pituitary–gonadal axis culminating in reproductive capacity. It is accompanied by cognitive, psychological, emotional, and sociocultural changes. There is wide variation in the timing of pubertal onset, and this process is affected by genetic and environmental influences. Disrupted puberty (delayed or absent) leading to hypogonadism may be caused by congenital or acquired etiologies and can have significant impact on both physical and psychosocial well-being. While adolescence is a time of growing autonomy and independence, it is also a time of vulnerability and thus, the impact of hypogonadism can have lasting effects. This review highlights the various forms of hypogonadism in adolescence and the clinical challenges in differentiating normal variants of puberty from pathological states. In addition, hormonal treatment, concerns regarding fertility, emotional support, and effective transition to adult care are discussed. European Journal of Endocrinology (2015) 173, R15–R24 European Journal of Endocrinology Introduction Adolescence is generally defined as the transitional phase (FSH)) (1, 2). -
Current Evaluation of Amenorrhea
Current evaluation of amenorrhea The Practice Committee of the American Society for Reproductive Medicine Birmingham, Alabama Amenorrhea is the absence or abnormal cessation of the menses. Primary and secondary amenorrhea describe the occurrence of amenorrhea before and after menarche, respectively. (Fertil Steril 2006;86(Suppl 4):S148–55. © 2006 by American Society for Reproductive Medicine.) Amenorrhea is the absence or abnormal cessation of the menses complaint. The sexual ambiguity or virilization should be (1). Primary and secondary amenorrhea describe the occurrence evaluated as separate disorders, mindful that amenorrhea is of amenorrhea before and after menarche, respectively. The an important component of their presentation (9). majority of the causes of primary and secondary amenorrhea are similar. Timing of the evaluation of primary amenorrhea EVALUATION OF THE PATIENT recognizes the trend to earlier age at menarche and is therefore History, physical examination, and estimation of follicle indicated when there has been a failure to menstruate by age 15 stimulating hormone (FSH), thyroid stimulating hormone in the presence of normal secondary sexual development (two (TSH), and prolactin will identify the most common causes standard deviations above the mean of 13 years), or within five of amenorrhea (Fig. 1). The presence of breast development years after breast development if that occurs before age 10 (2). means there has been previous estrogen action. Excessive Failure to initiate breast development by age 13 (two standard testosterone secretion is suggested most often by hirsutism deviations above the mean of 10 years) also requires investiga- and rarely by increased muscle mass or other signs of viril- tion (2). -
Androgen Deficiency Diagnosis and Management
4 Clinical Summary Guide Androgen Deficiency Diagnosis and management Androgen deficiency (AD) * Pituitary disease, thalassaemia, haemochromatosis. • Androgen deficiency is common, affecting 1 in 200 men under ** AD is an uncommon cause of ED. However, all men presenting 60 years with ED should be assessed for AD • The clinical presentation may be subtle and its diagnosis Examination and assessment of clinical features of AD overlooked unless actively considered Pre-pubertal onset – Infancy The GP’s role • Micropenis • GPs are typically the first point of contact for men with • Small testes symptoms of AD • The GP’s role in the management of AD includes clinical Peri-pubertal onset – Adolescence assessment, laboratory investigations, treatment, referral • Late/incomplete sexual and somatic maturation and follow-up • Small testes • Note that it in 2015 the PBS criteria for testosterone • Failure of enlargement of penis and skin of scrotum becoming prescribing changed; the patient must be referred for a thickened/pigmented consultation with an endocrinologist, urologist or member of • Failure of growth of the larynx the Australasian Chapter of Sexual Health Medicine to be eligible for PBS-subsidised testosterone prescriptions • Poor facial, body and pubic hair • Gynecomastia Androgen deficiency and the ageing male • Poor muscle development • Ageing may be associated with a 1% decline per year in serum Post-pubertal onset – Adult total testosterone starting in the late 30s • Regression of some features of virilisation • However, men who -
Abnormal Uterine Bleeding: a Management Algorithm
J Am Board Fam Med: first published as 10.3122/jabfm.19.6.590 on 7 November 2006. Downloaded from EVIDENCED-BASED CLINICAL MEDICINE Abnormal Uterine Bleeding: A Management Algorithm John W. Ely, MD, MSPH, Colleen M. Kennedy, MD, MS, Elizabeth C. Clark, MD, MPH, and Noelle C. Bowdler, MD Abnormal uterine bleeding is a common problem, and its management can be complex. Because of this complexity, concise guidelines have been difficult to develop. We constructed a concise but comprehen- sive algorithm for the management of abnormal uterine bleeding between menarche and menopause that was based on a systematic review of the literature as well as the actual management of patients seen in a gynecology clinic. We started by drafting an algorithm that was based on a MEDLINE search for rel- evant reviews and original research. We compared this algorithm to the actual care provided to a ran- dom sample of 100 women with abnormal bleeding who were seen in a university gynecology clinic. Discrepancies between the algorithm and actual care were discussed during audiotaped meetings among the 4 investigators (2 family physicians and 2 gynecologists). The audiotapes were used to revise the algorithm. After 3 iterations of this process (total of 300 patients), we agreed on a final algorithm that generally followed the practices we observed, while maintaining consistency with the evidence. In clinic, the gynecologists categorized the patient’s bleeding pattern into 1 of 4 types: irregular bleeding, heavy but regular bleeding (menorrhagia), severe acute bleeding, and abnormal bleeding associated with a contraceptive method. Subsequent management involved both diagnostic and treatment interven- tions, which often occurred simultaneously. -
Too Much, Too Little, Too Late: Abnormal Uterine Bleeding
Too much, too little, too late: Abnormal uterine bleeding Jody Steinauer, MD, MAS July, 2015 The Questions • Too much (& too early or too late) – Differential and approach to work‐up – Does she need an endometrial biopsy (EMB)? – Does she need an ultrasound? – How do I stop peri‐menopausal bleeding? – Isn’t it due to the fibroids? • Too fast: She’s hemorrhaging—what do I do? • Too little: A quick review of amenorrhea Case 1 A 46 yo G3P2T1 reports her periods have become 1. What term describes increasingly irregular and heavy her symptoms? over the last 6‐8 months. 2. Physiologically, what Sometimes they come 2 times causes this type of per month and sometimes there bleeding pattern? are 2 months between. LMP 2 3. What is the months ago. She bleeds 10 days differential? with clots and frequently bleeds through pads to her clothes. She occasionally has hot flashes. She also has diabetes and is obese. Q1: In addition to a urine pregnancy test and TSH, which of the following is the most appropriate test to obtain at this time? 1. FSH 2. Testosterone & DHEAS 3. Serum beta‐HCG 4. Transvaginal Ultrasound (TVUS) 5. Endometrial Biopsy (EMB) Terminology: What is abnormal? • Normal: Cycle= 28 days +‐ 7 d (21‐35); Length=2‐7 days; Heaviness=self‐defined • Too little bleeding: amenorrhea or oligomenorrhea • Too much bleeding: Menorrhagia (regular timing but heavy (according to patient) OR long flow (>7 days) • Irregular bleeding: Metrorrhagia, intermenstrual or post‐ coital bleeding • Irregular and Excessive: Menometrorrhagia • Preferred term for non‐pregnant bleeding issues= Abnormal Uterine Bleeding (AUB) – Avoid “DUB” ‐ dysfunctional uterine bleeding. -
Male Hypogonadism: Quick Reference for Residents
Male hypogonadism: Quick Reference for Residents Soe Naing, MD, MRCP(UK), FACE Endocrinologist Associate Clinical Professor of Medicine Director of Division of Endocrinology Medical Director of Community Diabetes Care Center UCSF-Fresno Medical Education Program Version: SN/8-21-2017 Male hypogonadism From Harrison's Principles of Internal Medicine, 19e and Up-To-Date accessed on 8-21-2017 Testosterone is FDA-approved as replacement therapy only for men who have low testosterone levels due to disorders of the testicles, pituitary gland, or brain that cause hypogonadism. Examples of these disorders include primary hypogonadism because of genetic problems, or damage from chemotherapy or infection (mump orchitis). However, FDA has become aware that testosterone is being used extensively in attempts to relieve symptoms in men who have low testosterone for no apparent reason other than aging. Some studies reported an increased risk of heart attack, stroke, or death associated with testosterone treatment, while others did not. FDA cautions that prescription testosterone products are approved only for men who have low testosterone levels caused by a medical condition. http://www.fda.gov/Drugs/DrugSafety/ucm436259.htm 2 Hypothalamic-pituitary-testicular axis Schematic representation of the hypothalamic-pituitary- testicular axis. GnRH from the hypothalamus stimulates the gonadotroph cells of the pituitary to secrete LH and FSH. LH stimulates the Leydig cells of the testes to secrete testosterone. The high concentration of testosterone within the testes is essential for spermatogenesis within the seminiferous tubules. FSH stimulates the Sertoli cells within the seminiferous tubules to make inhibin B, which also stimulates spermatogenesis. Testosterone inhibits GnRH secretion, and inhibin B inhibits FSH secretion.