REPRODUCTIVE ENDOCRINOLOGY

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1 REPRODUCTIVE ENDOCRINOLOGY dr. Judit Tőke SEMMELWEIS UNIVERSITY 2nd Department of Medicine

2 Outline Male hypogonadism Polycystic ovarian syndrome Disorders of sexual differentiation Primary and secondary amenorrhoea

3 MALE HYPOGONADISM

4 Male hypogonadism Primary Testicular causes T, LH, FSH Secondary Hypothalamic- Pituitary causes T, LH, FSH Peripherial hormonal resistance T norm, LH, FSH Decrease in one or both function of testes: Sperm production Testosterone production

5 Time of onset Clinical symptoms of male hypogonadism Prepubertal * delayed or lacking puberty Adult * within weeks: weakness fatigue low libido * within years: loss of hair decreased muscle mass decreased BMD * infertility * gynecomastia * normocytic anaemia

6 Diagnosis of male hypogonadism Laboratory testing Serum total testosterone * production: Leydig cells under stimulation of LH * 95-98%: bounded to SHBG (high affinity)* albumin (low affinity) * normal range (fasting, 8-10 AM): ng/dl Guideline: clinical signs + low T at two occasion = diagnosis of male hypogonadism Testosterone Therapy in Men With Hypogonadism: An Endocrine Society* Clinical Practice Guideline, J Clin Endocrinol Metab, May 2018, 103(5):1 30 Serum free testosterone * 2-5% of total T * responsible for biological activity LH, FSH * differentiate primary and secondary causes * SHBG * high: hyperthyroidism, liver disease, aging * low: hypothyroidism, obesity, GH excess, glucocorticoids, anabolic steroids, nephrotic sy

7 Diagnosis of male hypogonadism Semen analysis males with infertility Normal semen: Parameter Value Volume 2-6 ml Viscosity Liquefaction in 1 hr ph 7-8 Count > million/ml Motility > 40 % Moving forward > 32 % Morphology 60 % normal

8 Male hypogonadism Primary Testicular causes T, LH, FSH Secondary Hypothalamic- Pituitary causes T, LH, FSH Peripherial hormonal resistance T norm, LH, FSH Decrease in one or both function of testes: Sperm production Testosterone production

9 Causes of primary hypogonadism CONGENITAL ANOMALIES 1. Klinefelter syndrome (47XXY, 48XXXY, 46XY/ 47XXY mosaicism) * 1:1000 male birth * small, firm testes * severly subnormal sprem count infertility * decreased virilisation * increased length of long bones (legs, arms) * LH, FSH : testicular aromatase estradiol gynecomastia * predisposition to develop diseases: chronic bronchitis, TE diseases, germ cell tumors, NHL, SLE, breast cancer 2. Cryptorchidism * testes are in the abdominal cavity or in the inguinal canal and cannot be manipulated manually to within the scrotum by the age of one year (severly) subnormal sprem count 3. Disorders in androgen biosynthesis

10 Causes of primary hypogonadism ACQUIRED DISEASES 1. Infections Mumps orchitis * painful swelling of testes atrophy of testes (damage of seminiferous tubules) * mumps vaccine!!! 2. Radiation Treatment of leukaemia 3. Chemotherapy alkylating agents (cyclophosphamide, chlorambucil, cisplatin, carboplatin, busulfan) 4. Ketokonazol 5. Glucocorticoids 6. Testicular torsion 7. Chronic diseases: cirrhosis, chronic renal failure, HIV 8. Idiopathic

11 Male hypogonadism Primary Testicular causes T, LH, FSH Secondary Hypothalamic- Pituitary causes T, LH, FSH Peripherial hormonal resistance T norm, LH, FSH Decrease in one or both function of testes: Sperm production Testosterone production

12 Causes of secondary hypogonadism CONGENITAL ANOMALIES Isolated hypogonadotrop hypogonadism As a part of CPHD Congenital GnRH deficinency Impaired expression of transcription factors: * Kallmann syndrome * LHX3, LHX4 * Prader-Willi syndrome * HESX-1 Gonadotropin subunit mutation * PROP-1 * beta subunit of LH * beta subunit of FSH ACQUIRED DISEASES Hypothalamus (GnRH ) Stalk Pituitary (LH, FSH ) Suppression on LH, FSH Damage to gonadotroph cells Tumors Tumors Hyperprolactinaemia Tumors Infiltrative diseases Infiltrative diseases GnRH analogs (LH T ) Infiltrative diseases Piuitary apoplexy Piuitary apoplexy Glucocorticoid excess Piuitary apoplexy, trauma Trauma Trauma Anorexia nervosa Hypophysistis

13 Male hypogonadism Primary Testicular causes T, LH, FSH Secondary Hypothalamic- Pituitary causes T, LH, FSH Peripherial hormonal resistance T norm, LH, FSH Decrease in one or both function of testes: Sperm production Testosterone production

14 Androgen insensivity syndrome

15 Testosterone action Testosterone aromatase 5α-reductase Testosterone DHT Estradiol Action on: * external genitalia (prostate gland) * sexual hair development Action on: * bone

16 Treatment of male hypogonadism Testosterone treatment Only for males with hypogonadism! Only for testosterone deficiency NOT for impaired spermatogenesis! GOAL: restoration of normal serum testosterone concentration Desired effects of T treatment Adverse effects of T treatment Virilisation (induction or maintenance) Prostate disorders (BPH) Increasing libido Acne Improving BMD Sleep apnea Improving mood and cognitive function Erythrocytosis Increasing muscle strength Increasing fat-free mass

17 Treatment of male hypogonadism Testosterone treatment Choice of regimen T: well absorbed from the intestine, rapidly metabolize in the liver oral use is not convenient Long-acting injections (im) Extra-long-acting injections (im) Transdermal gels Testosterone enanthate Testosterone undecanoate (Nebido) Testim 1% Testosterone cypionate AndroGel 1% and 1.62 % Contraindications: - prostate, breast cancer - PSA > 4 ug/l or 3 ug/l for high-risk patients - Hct > 50% - untreated severe sleep apnea - uncontrolled heart failure - AMI or stroke in the last 6 months

18 Treatment of male hypogonadism Fertility induction in males with secondary hypogonadism Initial treatment hcg: has the biological activity of LH with longer half-life in the circulation Leydig cells T production 3 times a week 2000 IU im Adding FSH after serum T maintained in the normal range and sperm count is still abnormal human menopausal gonadotropin (hmg) or recombinant FSH 3 times a week 75 IU im. Pulsatile GnRH in patient with hypothalamic disease

19 POLICYSTIC OVARIAN SYNDROME

20 Pathophysiology of PCOS Heritable factors: Intrauterine factors: Postnatal factors: Maternal PCOS Congenital virilisation Obesity Polycystic ovarian morphology Hyperandrogenemia Intrauterin malnutrition Insulin resistance Hyperinsulinism Gene variants of genes encoding: Hypothalamus: GnRH pulses steroidogenic enzymes, sex hormone-binding globulin, androgen receptor, transcription factors gonadotropins and gonadotropin receptors Pituitary: LH excess Ovarian theca cells: androgen production Luteinized granulosa cells: oligo-, anovulation

21 Epidemiology: 5-12 % of women Menstrual dysfunction Clinical symptoms of PCOS Menstrual irregularity: Hyperandrogenism Clinical signs: oligomenorrhoea ( 9 menstrual periods / year) OR amenorrhoea ( no menstrual periods 3 consecutive months) typically begins in teenage years acne male-pattern hair loss hirsutism

22 Hirsutism Definition: excess of terminal hair (thick, pigmented) in a male distribution Assessment: Ferriman-Gallwey score > 8

23 Epidemiology: 5-12 % of women Menstrual dysfunction Clinical symptoms of PCOS Menstrual irregularity: Hyperandrogenism Clinical signs: Laboratorical results: oligomenorrhoea ( 9 menstrual periods / year) OR amenorrhoea ( no menstrual periods 3 consecutive months) typically begins in teenage years acne male-pattern hair loss hirsutism elevated concentrations of serum androgens Polycystic ovaries (TVUS) Obesity % of patients with PCOS Insulin resistance % of both lean and obese patients Non-alcoholic steatohepatitis (NASH) Mood disorders depression, anxiety

24 Diagnosis of PCOS Laboratory testing 1. Serum total testosterone ULN in women: ng/dl or nmol/l if serum total T > 150 ng/dl search for ovarian or adrenal androgen-producing tumors 2. Serum 17-hydroxy-progesterone on the 3rd day of menstrual period at 8 AM ULN: 200 ng/ml to rule out late-onset CAH: Synacthen-test if 60 min 17OHP > 1000 ng/ml after 250 ug corticotropin iv late-onset CAH Tests to rule out other causes of oligo-, amenorrhoea: - Prolactin - TSH - hcg LH:FSH ratio is NOT indicated to calculate!!!!!!

25 Diagnosis of PCOS Rotterdam criteria 2003 Two out three of the following criteria: 1. Oligo-, anovulation 2. Hyperandrogenism (clinical and/or laboratorical signs) 3. Polycystic ovaries on TVUS Confirmation: Rule out other causes: thyroid disease, late-onset CAH, androgen-pruducing adrenal/ovarien tumor, hyperprl

26 Further investigations after diagnosis of PCOS Cardiometabolic risk assessment: 1. BMI, blood pressure measurement 2. Fasting lipid profile 3. 75g ogtt ONLY for screening IGT or T2DM not for measuring insulin resistance!!! 4. Insulin resistance assessment is NOT the part of the diagnosis of PCOS!!!! Non-alcoholic fatty liver disease

27 Treatment options of PCOS 1. Combined oral contraceptive pills (COCs): estrogen + progestin At least 30 ug ethynil-estradiol + progestin with antiadrogenic effect: drospirenone or norgestimate suppress hypothalamic-pituitary-ovarian axis suppress ovarian androgen production Indication: a) irregular menstrual cycle b) hirsutism, acne Contraindication: history of VTE 2. Progestine alone (medroxy-progesterone acetate) direct inhibits endometrial proliferation Indication: irregular menstrual cycle alone 3. Cosmetic options for hirsutism eflornithine hydrochloride (Vaniqua cream) / laser therapy 4. Treatment of obesity and insulinresistance with PCOS Physical activity and metformin or thazolidinediones if T2DM is present

28 DISORDERS OF SEXUAL DIFFERENTIATION

29 Differentiation of internal genital ducts SRY protein Anti-Müllerian Hormon (AMH) produce: Sertoli cells Testosterone produce: Leydig cells In the absence of AMH In the absence of testosterone

30 Disorders of sexual development (DSD) DSD: congenital discrepancy between external genitalia, gonadal, and chromosomal sex Manifestations bilateral cryptorchidism scrotal or perineal hypospadias clitoromegaly: clitoral width >6 mm or clitoral length >9 mm posterior labial fusion: anogenital ratio >0.5 phenotypic female appearance with a palpable gonad (with or without inguinal hernia) hypospadias with a unilateral nonpalpable gonad

31 Different degrees of virilisation in females (Prader) White PC, Speiser PW, Endocrine Reviews 21(3): , 2000

32 Disorders of sexual development (DSD) DSD: congenital discrepancy between external genitalia, gonadal, and chromosomal sex Classification 46, XY DSD Undervirilised male Congenital adrenal hyperplasia (17α-hydroxylase deficiency) Abnormal testicular activity: gonadal dysgenesis Abnormal androgen synthesis Abnormal androgen response (androgen insensivity) 46, XX DSD Virilised female Congenital adrenal hyperplasia (21-hydroxylase deficinency) Gestational hyperandrogenism Sex choromsome DSD Turner-syndrome (45,X) Klinefelter-syndrome (47,XXY)

33 Congenital adrenal hyperplasia 21-hydroxylase deficiency Lab results: 17-OH-P - newborn screening!! Androstenedione ACTH Cortisol (and) aldosterone PRA

34 Congenital adrenal hyperplasia 21-hydroxylase deficiency 95 % of all CAH Genetic defects of CYP21A2 gene encoding 21-hydroxylase enzyme Autosomal recessive disorder Clinical phenotypes: Female newborn with classic CAH (salt-wasting and simple virilisating) Male with salt-wasting CAH on 7 to 14 th day of life Male with non-classic CAH (early virilisation) at age of 2 to 4 years Late-onset CAH: early pubarche mentrual irregularity and hisrutism in young women Treatment: hydrocortisone (and) fludrocortisol replacement

35 PRIMARY AND SECONDARY AMENORRHOEA

36 Primary amenorrhoea Secondary amenorrhoea Primary amenorrhoea = absence of menses at age 15 years = absence of menses > 3 consecutive months Secondary amenorrhoea (exclude pregnancy!!) Hypothalamic-, and pituitary disease Isolated GnRH deficiency (ie Kallman-syndrome) Hyperprolactinemia Infiltrative diseaes and tumors Infiltrative diseaes and tumors Untreated severe systemic illness (celiac disease, T1DM, IBD) Untreated severe systemic illness (celiac disease, T1DM, IBD) Ovarian dysfunction Gonadal dysgenesis (ie Turner-syndrome) Primary ovarian failure (autoimmune oophoritis, radiation, chemotherapy) Anatomical malformations Polycystic ovarian syndrome Imperforate hymen Intrauterine adhesions (Asherman-syndrome) Other Complete androgen insensivity syndrome (female phenotype - 46,XY) Hypothyroidism CAH Adrenal tumors

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