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Hirsutism and Virilization PowerPoint Presentation

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Description : Check out this medical presentation on Excessive Hairiness (Hirsutism), which is titled "Hirsutism & Virilization", to know about Hirsutism & Virilization, androgen biosynthesis, androgen types, diagnosis, management and treatment of hirsutism and virilization.

Tags : Excessive Hairiness, Hirsutism, androgen biosynthesis, androgen types, diagnosis, management, treatment

Published on : Jul 07, 2021 | Views : 4042 | Downloads : 23

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Hirsutism & Virilization Dr.Nasrin Saharkhiz Associate professor SBMU,Dept of Ob&Gyn Beckman2019 CHAPTER 40
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To define: Hirsutism & Virilization To learn Androgen biosynthesis Androgen Types To Diagnosis, management & treat hirsutism & Virilization Objectives
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INTRODUCTION Hirsutism is excess terminal hair in a male pattern of distribution. initially by the appearance of midline terminal hair.
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vellus hair is soft, downy, and fine Terminal hair is darker, coarser, and kinkier lanugo hair fine, soft hair of a human fetus
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Origin of excess terminal hair is : Familial pathological
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When a woman is exposed to excess androgens: terminal hair first appears on the: lower abdomen around the nipples next around the chin and upper lip finally between the breasts and on the lower back Usually, a woman with hirsutism also has acne
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VIRILIZATION Virilization is defined as masculinization of a woman and is associated with a marked increase in circulating testosterone. as well as hirsutism
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She first notices: enlargement of the clitoris Then: Temporal balding deepening of the voice involution of the breasts remodeling of the limb–shoulder girdle Over time, she takes on a more masculine appearance
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ANDROGEN PRODUCTION Adrenal glands Ovaries Adipose tissue: (extraglandular production of testosterone from androstenedione)
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Three androgens: 1. Dehydroepiandrosterone (DHEA) 2. Androstenedione 3. Testosterone
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1. Dehydroepiandrosterone (DHEA) a weak androgen secreted principally by the adrenal glands generally measured as dehydroepiandrosterone sulfate (DHEA-S) because of its longer half- life, a more reliable measure.
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2. Androstenedione: a weak androgen secreted in equal amounts by the adrenal glands and ovaries.
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3. Testosterone: A potent androgen secreted by: Adrenal glands Ovaries Adipose tissue from the conversion of androstenedione
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dihydrotestosterone (DHT) an androgen more potent than testosterone This metabolic conversion is the result of the local action of 5α-reductase on testosterone within hair follicles and genital skin This is the basis for constitutional hirsutism
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T Androstenedion DHEA Adrenal cortex Ovary %25 %25 %50 %50 %50 %50 %20 %100 %30 DHEAS
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Ovarian androgen production is regulated by luteinizing hormone (LH) In conditions of sustained or increased LH secretion, androstenedione and testosterone increase.
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When androstenedione production increases, there is a dependent increase in extraglandular testosterone production In obese women: conversion of androstenedione to testosterone is increased. increase in estrone
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Testosterone is the primary androgen that causes increased hair growth,acne, and virilization. bound to a carrier protein—sex hormone binding globulin (SHBG) Bound testosterone is unable to attach to testosterone receptors and is metabolically inactive Only a small fraction(1%–3%) of testosterone is unbound (free)
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Testosterone receptors are scattered throughout the body Hair follicles Sebaceous glands Genital skin Some individuals have increased 5α-reductase within hair follicles, resulting in excessive local production of DHT.
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Excess androgen production causes: PCOS Adrenal disorders Testosterone-secreting tumors Iatrogenic Idiopathic causes
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POLYCYSTIC OVARY SYNDROME The most common cause of androgen excess and hirsutism in women The etiology of this disorder is unknown Genetic predisposition Obesity Other causes of LH excess
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Symptoms of PCOS: Oligomenorrhea or amenorrhea Acne,hirsutism Infertility The disorder is characterized by Chronic anovulation Excess androgen
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Definition of PCOS: Rotterdam cr. Two of the following three: Oligo and/or anovulation Clinical or biochemical signs of hyperandrogenism Hirsuitism, acne, or male pattern balding High serum androgens Polycystic ovaries (by ultrasound) Presence of 12 or more follicles in each ovary, measuring 2-9 mm in diameter, or increased ovarian volume
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It is also important to rule out other endocrine disorders that can mimic PCOS, such as CAH, Cushing syndrome, and hyperprolactinemia
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Obesity In many women with PCOS, obesity seems to be the common factor (seen in 50% of patients) Stein and Levental first described PCOS patients as women with hirsutism, irregular cycles, and obesity Originally called Stein–Levental syndrome PCOS does not currently have obesity as one of its diagnostic criteria
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PCOS is related to obesity by the following mechanism: LH stimulates the theca lutein cells to increase androstenedione production. Androstenedione undergoes aromatization to estrone within adipocytes. estrone has a positive-feedback action on the pituitary secretion of LH With increasing obesity: increased conversion of androstenedione to estrone. there is coincident increased testosterone production, which causes acne and hirsutism
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In obesity: compensatory hyperinsulinemia result in decreased levels of SHBG more bioavailable circulating androgen stimulus to androgen production in the adrenal gland and ovary Insulin have direct hypothalamic effects: abnormal appetite stimulation and gonadotropin secretion
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Hormonal studies in PCOS (1) increased LH:FSH ratio (2) estrone in greater concentration than estradiol (3) androstenedione at the upper limits of normal or increased (4) testosterone at the upper limits of normal or slightly increased
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The unopposed long-term elevated estrogen increase the risk of: Abnormal uterine bleeding Endometrial hyperplasia Endometrial carcinoma
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Metabolic Syndrome (syndrome X): presence of at least three of the following components: • Waist circumference 35 inches or greater • Triglyceride level 150 mg/dL or higher • High-density lipoprotein cholesterol <50 m/dL • Blood pressure 130/85 mm Hg or higher • Fasting glucose level 100 mg/dL or higher
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Approximately 40% of patients with PCOS have impaired glucose tolerance 8% have overt type 2 diabetes mellitus should be screened for diabetes Hypertension is common Increases the risk of cardiovascular disease
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HAIR-AN Syndrome Acanthosis nigricans has been found in a significant percentage of these patients hyperandrogenism insulin resistance A subgroup of patients with PCOS Administration of the insulin-sensitizing agent metformin in these patients also reduces androgen and insulin levels
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Treatment combination oral contraceptives The most common therapy forPCOS weight reduction ovulation induction - Clomiphene citrate - Aromatase inhibitors: letrozole and anastrozole
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Treatment second-line intervention: - exogenous gonadotropins or - laparoscopic ovarian surgery Insulin sensitizers (metformin alone or with clomiphene citrate) to reduce insulin resistance
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Hyperthecosis A more severe form of PCOS androstenedione production may be so great that testosterone , cause: virilization temporal balding clitoral enlargement deepening of the voice, and remodeling at the limb–shoulder girdle
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often refractory to OCP suppression more difficult to successfully induce ovulation in women with this condition.
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OVARIAN NEOPLASMS Sertoli–Leydig Cell Tumors also called androblastoma and arrhenoblastoma secrete testosterone
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OVARIAN NEOPLASMS Uncommon Virilizing Ovarian Tumors Gynandroblastoma Lipid (lipoid) cell tumors Hillar cell tumors
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ADRENAL ANDROGEN EXCESS DISORDERS The most common are: CAH Cushing syndrome Adrenal neoplasms
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CAH caused by enzyme deficiencies result in precursor excess, resulting in androgen excess DHEA is a precursor for androstenedione and testosterone 21-Hydroxylase Deficiency 11β-Hydroxylase Deficiency
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Manifestations of 21-Hydroxylase Deficiency Severe • Newborn female infant • Virilized (ambiguous genitalia), or virilized and has life-threatening salt wasting Mild • Frequently associated with terminal body hair, acne, alterations in menstrual cycles, and infertility • Patients can also have sonographic evidence of polycystic-appearing ovaries
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Manifested at puberty • Adrenarche may precede thelarche • History of pubic hair growth occurring before the onset of breast development may be a clinical clue
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The diagnosis of 21-hydroxylase deficiency measuring 17-OH progesterone during the follicular phase (preferably fasting) In classic 21-hydroxylase deficiency over 2,000 ng/dL In less severe form: -mildly elevated basal levels, 200 ng/dL -increase to usually 1,000 ng/dL in response to ACTH stimulation DHEA-S and androstenedione elevated
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11β-Hydroxylase Deficiency A less common cause of CAH The clinical features: mild hypertension mild hirsutism The diagnosis: increased plasma desoxycorticosterone
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Treatment of CAH Is aimed at restoring normal cortisol levels Non classic CAH: supplementing glucocorticoids Usually, prednisone 2.5 mg daily (or its equivalent) suppresses adrenal androgen production
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Medical therapy for adrenal and ovarian disorders cannot resolve hirsutism. It can only suppress new hair growth. Hair that is present must be controlled by: shaving Bleaching using depilatory agents electrolysis,or laser hair ablation.
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Cushing Syndrome an adrenal disease resulting in adrenal excess Adrenal neoplasm ACTH-producing tumor signs of corticosteroid excess Truncal obesity Moonlike facies glucose intolerance skin thinning with striae osteoporosis proximal muscle weakness hyperandrogenism , menstrual irregularities
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Adrenal Neoplasms rapid increase in hair growth severe acne amenorrhea sometimes, virilization DHEA-S is usually elevated above 6 mg/mL. The diagnosis: computed axial tomography or MRI Adrenal adenomas must be remove surgically
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CONSTITUTIONAL HIRSUTISM after a diagnostic evaluation, there is no explanation for the cause of the disorder By exclusion The hypothesis: have greater activity of 5α- reductase and therefore, more free testosterone
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Treatment 1-primarily androgen blockade Spironolactone 25 to 100 mg/day is the most commonly used flutamide cyproterone acetate finasteride (5 mg orally daily) Eflornithine hydrochloride 13.9% cream for facial use
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Patients taking an androgen receptor or 5α- reductase blocker should be placed on concomitant oral contraceptives
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2-mechanical removal of the excess hair
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IATROGENIC ANDROGEN EXCESS Danazol Progestin-containing oral contraceptives
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