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Hyperandrogenis
m and virilization
Assoc Prof Dr Hanifullah
         Khan
  Amira, Atiqah, Sufia
Objectives
1.   Androgen
2.   Virilization
3.   Causes and patophysiology
4.   Sign and symptoms
5.   Question
What are androgens?
 These are generally referred to as
  male hormones
 They stimulate or control the
  development and maintenance of
  male characteristics
 They are also the precursors of
  estrogens
Relationships between
hormones
Androgens
   Testosterone, dehydroepiandrosterone sulfate
    (DHEAS), dehydroepiandrosterone
    (DHEA), androstenedione, and androstenediol
   The ovaries produce 50% of circulating
    testosterone, 50% of the androstenedione and
    20% of DHEA.
   The adrenal glands produce all the DHEAS and
    80% of the DHEA. The adrenals also secrete 50%
    of androstenedione and 25% of circulating
    testosterone.
   Adrenal androgens increase in response to ACTH
    stimulation
   LH stimulates theca cells of the ovaries to secrete
    androgens
Figure 1 Schematic overview of the generation of androgen precursors and their conversion
                               towards active androgens in women.




                           Arlt W Eur J Endocrinol 2006;154:1-11



© 2006 Society of the European Journal of Endocrinology
Effect of androgens
   Fat deposition (small breast)
     Androgens inhibit the ability of some fat
      cells to store lipids
   Muscle mass (heavy mascular
    mass)
     Androgens promote the enlargement of
      skeletal muscle cells
   Brain
     Enhanced libido.
Effects of androgens on skin
   Pilosebaceous unit (PSU)
      Androgens cause excess sebum secretion.
      Lesions of the PSU are called acne.
   Hair
      androgens promote the conversion of vellus
       hairs to coarser terminal hair.
      excess growth of terminal hair in a male pattern
       is called hirsutism.
      Follicles shrink causing a receding hair line
Hirsutism
 Excessive male pattern hair growth
  (face, back, chest, abdomen and inner
  thighs)
 Graded with the Ferriman and Gallwey
  scoring system
 Hirsutism of rapid onset and growth
  (over a few months) should raise the
  concern of an androgen secreting
  tumour or intersex state
   Please note that the appearance of hair on the upper lip or
    mild hirsutism does not necessarily constitute
    hyperandrogenism, and ethnic origin should be taken into
    consideration.
Ferrimen-Gallwey
Facial hair
Overview of
androgenic effects
Male esutheon        Receding hair line




Acanthosis nigricans     Hirsutism
Why do women have
androgens?
   Androgens have important functions in
    women
    ◦ Essential in the production of E2 (in ovary &
      adipose tissue)
    ◦ Responsible for dev. & maint. of axillary &
      pubic hair
    ◦ Important for libido
Virilization
The development of exaggerated masculine
characteristics, usually in women, often as a result of
overproduction of androgens
So, if hyperandrogenism becomes
extreme, virilization occurs
Symptoms of virilization
   Symptoms of virilization include
    ◦   excess facial and body hair (hirsutism),
    ◦   baldness
    ◦   acne
    ◦   deepening of the voice
    ◦   increased muscularity
    ◦   an increased sex drive.
   In women,
    ◦   the uterus shrinks
    ◦   the clitoris enlarges (clitoromegaly)
    ◦   the breasts become smaller
    ◦   normal menstruation stops (amenorrhea)
CAUSES AND
PATHOPHYSIOLOGY
Hyperandrogenism
   Excess of androgens may be caused by:
    ◦ primary gonadal disorders
    ◦ primary adrenal disorders
    ◦ iatrogenic
    In practice though, the causes are
    restricted to a few conditions:
    PCOS
    Cushing’s syndrome
    CAH
    Tumours
PCOS
 ◦ A primary gonadal disorder
   Characterized by multiple small cysts within the
    ovary and by excess androgen production from
    the ovaries
 ◦ Increase in LH and androgen secretion
 ◦ Low aromatase levels (due to  FSH
   levels) therefore androgens can’t be
   converted to estrogens in peripheral
   tissue
   Excess androgens converted to testosterone in
    peripheral tissue
Developmental origin of PCOS (adapted from Abbott et al., 2002).




           Hum. Reprod. Update 2008;14:293-307


© The Author 2008. Published by Oxford University Press on behalf of the European Society of
 Human Reproduction and Embryology. All rights reserved. For Permissions, please email:
 journals.permissions@oxfordjournals.org
Features of PCOS
•   Symptoms-
    •   Oligomenorrhoea/ammenorhea
    •   Excessive hair
    •   Infertility
    •   May present with metabolic symptoms
•   Sign-
    • Hirsutism
    • Acne
    • Acanthosis nigricans (increased velvety skin pigmentation
      ex at the axilla)
    • Obesity
•   Ix –
    • Clinical/biochemical signs of hyperandrogenism (hirsutism)
    • Polyystic ovaires by ultrasound
Ovaries
Other features
Metabolic syndrome
Acanthosis nigricans
Rotterdam criteria 2003
   A meeting in Rotterdam crafted compromise
    criteria
    ◦ Any two features from
       Irregular cycles
       Hyperandrogenism
       Ultrasound demonstration of polycystic ovaries
    ◦ (Rotterdam ESHRE/ASRM Sponsored PCOS Consensus Workshop
      Group: Revised 2003 consensus on diagnostic criteria and long term
      health risks related to polycystic ovary syndrome. Fertil Steril 2004; 81:19)
   Importantly, the Rotterdam criteria allows for
    ◦ the previously excluded ovulatory women with
      features of PCOS
    ◦ as well as for women with irregular cycles and
      polycystic ovaries, but without any evidence of
      androgen excess
Primary adrenal disorders
 Cushing’s disease
 Congenital adrenal hyperplasia
 Adrenocortical neoplasms
Cushing’s disease
 ◦ Primary hypothalamic-pituitary disease
 ◦ Oversecretion of ACTH from pituitary
 ◦ Presence of adenoma or areas of
   corticotroph cell hyperplasia in the
   anterior pituitary
 ◦ Lead to cortical hyperplasia
 ◦ Causes
   hypercortisolism, hyperandrogenism
Signs of Cushing’s
   Hypercortisolism
    ◦ central obesity, hyperhidrosis
    ◦ buffalo hump, moon face, striae
   Hyperandrogenism
    ◦ hirsutism, male pattern
      baldness, acne, deepening of the
      voice,  muscularity, and an  sex drive
    ◦ uterus shrinks, (clitoromegaly), the
      breasts become smaller, and normal
      menstruation stops (amenorrhea)
Congenital adrenal
hyperplasia
Depends on the nature and severity of
the enzymytic defect. Onset of clinical
symptoms can occur in the
• Perinatal period
• Later childhood
• Adulthood (less common)
Congenital adrenal
   hyperplasia
◦ Autosomal recessive deficiency of an enzyme
  in the cortisol synthetic pathways.
◦ Cortisol secretion is reduced and feedback
  leads to increased ACTH secretion to maintain
  adequate cortisol leading to adrenal
  hyperplasia.
◦ Diversion of the steroid precursors into the
  androgenic steroid pathways occurs. Thus, 17-
  hydroxyprogesterone, androstenedione and
  testosterone levels are increased, leading to
  virilization.
Anterior pituitary              Congenital
                                   ACT
                                                               adrenal
                                   H
                             Adrenal cortex (bilateral
                                                            hyperplasia
                             hyperplasia)
                                 Cholesterol

                                 Pregnolon
                                 e
  Progesteron
  e                        17 - hydroxypregnenolone      Dehydroxypiandrosteron
           21
                                                         e
11 -
                           17 -                              Androstenedion
deoxycortisone
                           hydroxyprogesterone               e
                                            21
   Corticosterone
                              11 – deoxycortisol
      Aldosteron                                              Testosterone
      e
      Mineralocorticoids
                                   Cortisol                    Sex
                                                               steroids
                                Glucocorticoids
Adrenocortical neoplasms
 Adrenocortical neoplasms associated
  with symptoms of excess of androgen
  are more likely to be androgen
  secreting adrenal carcinomas than
  adenomas.
 It is also often assoc with
  hypercortisolism (mixed syndrome)
 The tumour secretes androgen thus
  increasing in circulation and converted
  to testosterone at the peripheral
Tumours
Androgen secreting tumours
 May occur at any age.
 relatively rare.
 should be suspected when the onset of
  androgenic symptoms is sudden
  (i.e., generally <2 yr) and the pace of
  symptoms is rapid, and when they lead
  to virilization and masculinization.
 may be associated with other systemic
  symptoms including weight
  loss, anorexia, a feeling of abdominal
  bloating, back pain.
The goals of lab testing

  1            2               3
           Other causes
           of androgen       Look for
Document      excess/        metabolic
androgen     irregular     abnormalities
 excess    periods to be   Eg Glucose/
             ruled out        Lipids
Lab
   Testosterone and Dehydroepiandrosterone
    sulphate (DHEAS)
    ◦ DHEAS hyperandrogenemia of adrenal origin
 Serum prolactin
 thyroid stimulating hormone (TSH)
 Serum 17 hydroxyprogesterone (17-OHP) test –if
  suspect CAH
 LH and FSH ( suggestive of PCOS if ratio >2)
 Lipid profile
 OGTT
    ◦ Relying on a fasting glucose level alone is inadequate
      as it is a poor predictor of impaired glucose tolerance
      or diabetes
TVS
Therapy
A 22 year old nulligravid women presents to her
gynaecologist because of irregular widely spread
menses

CASE SCENARIO
History



1.   What question would like to ask the
     patient?
Examination
1.   Firstly, what systems would you like
     to assess
2.   Secondly, what are the specific signs
     would you like to elicit?
Further clues
   Menarche was at the age of 14, but she
    has rarely had regular cycles. For the
    past year she has had only three
    complete menses. Once going 6 months
    between period. She is 165cm and
    weighs 83kg. She is over weight, with
    acne and a few dark hairs on her upper
    lip and chin. She is sexually active and
    uses condom for contraception.

3. What is the likely diagnosis
Summary of causes &
diagnosis
   PCOS.
    ◦ At least two of the following three abnormalities were present:
      chronic anovulation, clinical or biochemical hyperandrogenism,
      and polycystic ovaries on ultrasound
   NCAH.
    ◦ Clinical hyperandrogenism + increased serum 17OHP or mildly
      increased serum 17OHP with an increased response to ACTH (
   Androgen-secreting tumors.
    ◦ The finding of an androgen-secreting tumors (ovarian or adrenal)
      in women with very high serum androgen levels
   Idiopathic hirsutism.
    ◦ Normal serum androgen levels (T, free T, and DHEAS) in the
      presence of normal ovulatory cycles and normal ovaries on
      ultrasound.
   Idiopathic hyperandrogenism.
    ◦ Clinical hyperandrogenism, increased serum androgen levels in
      the presence of normal ovulatory cycles, and normal ovaries on
      ultrasound
References
   Zawadski JK, Dunaif A. Diagnostic criteria for polycystic ovary syndrome: toward a
    rational approach. In: Dunaif A,
   ESHRE/ASRM Revised 2003 consensus on diagnostic criteria and long-term
    health risks related to polycystic ovary syndrome. Fertil Steril 2004; 81:19-25.
   The Rotterdam ESHRE/ASRM-sponsored PCOS Consensus Workshop Group .
    Revised 2003 consensus on diagnostic criteria and long-term health risks related
    to polycystic ovary syndrome (PCOS). Hum Reprod 2004;19:41- 47.
   Azziz R, Carmina E, Dewailly D, et al. Androgen Excess Society. Position
    statement: criteria for defining polycystic ovary syndrome as a predominantly
    hyperandrogenic syndrome: an androgen excess society guideline. J Clin Endo &
    Metab 2006; 91(11): 4237-4245.
   Azziz R, Sanchez LA, Knochenhauer ES, Moran C, Lazenby J, Stephens
    KC, Taylor K, Boots LR 2004 Androgen excess in women: experience with over
    1000 consecutive patients. J Clin Endocrinol Metab 89:453–462
   E. Carmina, F. Rosato, A. Jannì, M. Rizzo, and R. A. Longo Relative Prevalence of
    Different Androgen Excess Disorders in 950 Women Referred because of Clinical
    Hyperandrogenism. JCEM 2006 91: 2-6; doi:10.1210/jc.2005-1457
Manage wisely

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Hyperandrogenism ppt 25.1.2011

  • 1. Hyperandrogenis m and virilization Assoc Prof Dr Hanifullah Khan Amira, Atiqah, Sufia
  • 2. Objectives 1. Androgen 2. Virilization 3. Causes and patophysiology 4. Sign and symptoms 5. Question
  • 3. What are androgens?  These are generally referred to as male hormones  They stimulate or control the development and maintenance of male characteristics  They are also the precursors of estrogens
  • 5. Androgens  Testosterone, dehydroepiandrosterone sulfate (DHEAS), dehydroepiandrosterone (DHEA), androstenedione, and androstenediol  The ovaries produce 50% of circulating testosterone, 50% of the androstenedione and 20% of DHEA.  The adrenal glands produce all the DHEAS and 80% of the DHEA. The adrenals also secrete 50% of androstenedione and 25% of circulating testosterone.  Adrenal androgens increase in response to ACTH stimulation  LH stimulates theca cells of the ovaries to secrete androgens
  • 6. Figure 1 Schematic overview of the generation of androgen precursors and their conversion towards active androgens in women. Arlt W Eur J Endocrinol 2006;154:1-11 © 2006 Society of the European Journal of Endocrinology
  • 7. Effect of androgens  Fat deposition (small breast)  Androgens inhibit the ability of some fat cells to store lipids  Muscle mass (heavy mascular mass)  Androgens promote the enlargement of skeletal muscle cells  Brain  Enhanced libido.
  • 8. Effects of androgens on skin  Pilosebaceous unit (PSU)  Androgens cause excess sebum secretion.  Lesions of the PSU are called acne.  Hair  androgens promote the conversion of vellus hairs to coarser terminal hair.  excess growth of terminal hair in a male pattern is called hirsutism.  Follicles shrink causing a receding hair line
  • 9. Hirsutism  Excessive male pattern hair growth (face, back, chest, abdomen and inner thighs)  Graded with the Ferriman and Gallwey scoring system  Hirsutism of rapid onset and growth (over a few months) should raise the concern of an androgen secreting tumour or intersex state  Please note that the appearance of hair on the upper lip or mild hirsutism does not necessarily constitute hyperandrogenism, and ethnic origin should be taken into consideration.
  • 13. Male esutheon Receding hair line Acanthosis nigricans Hirsutism
  • 14. Why do women have androgens?  Androgens have important functions in women ◦ Essential in the production of E2 (in ovary & adipose tissue) ◦ Responsible for dev. & maint. of axillary & pubic hair ◦ Important for libido
  • 15. Virilization The development of exaggerated masculine characteristics, usually in women, often as a result of overproduction of androgens So, if hyperandrogenism becomes extreme, virilization occurs
  • 16. Symptoms of virilization  Symptoms of virilization include ◦ excess facial and body hair (hirsutism), ◦ baldness ◦ acne ◦ deepening of the voice ◦ increased muscularity ◦ an increased sex drive.  In women, ◦ the uterus shrinks ◦ the clitoris enlarges (clitoromegaly) ◦ the breasts become smaller ◦ normal menstruation stops (amenorrhea)
  • 18. Hyperandrogenism  Excess of androgens may be caused by: ◦ primary gonadal disorders ◦ primary adrenal disorders ◦ iatrogenic  In practice though, the causes are restricted to a few conditions: PCOS Cushing’s syndrome CAH Tumours
  • 19. PCOS ◦ A primary gonadal disorder  Characterized by multiple small cysts within the ovary and by excess androgen production from the ovaries ◦ Increase in LH and androgen secretion ◦ Low aromatase levels (due to  FSH levels) therefore androgens can’t be converted to estrogens in peripheral tissue  Excess androgens converted to testosterone in peripheral tissue
  • 20. Developmental origin of PCOS (adapted from Abbott et al., 2002). Hum. Reprod. Update 2008;14:293-307 © The Author 2008. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
  • 21. Features of PCOS • Symptoms- • Oligomenorrhoea/ammenorhea • Excessive hair • Infertility • May present with metabolic symptoms • Sign- • Hirsutism • Acne • Acanthosis nigricans (increased velvety skin pigmentation ex at the axilla) • Obesity • Ix – • Clinical/biochemical signs of hyperandrogenism (hirsutism) • Polyystic ovaires by ultrasound
  • 26. Rotterdam criteria 2003  A meeting in Rotterdam crafted compromise criteria ◦ Any two features from  Irregular cycles  Hyperandrogenism  Ultrasound demonstration of polycystic ovaries ◦ (Rotterdam ESHRE/ASRM Sponsored PCOS Consensus Workshop Group: Revised 2003 consensus on diagnostic criteria and long term health risks related to polycystic ovary syndrome. Fertil Steril 2004; 81:19)  Importantly, the Rotterdam criteria allows for ◦ the previously excluded ovulatory women with features of PCOS ◦ as well as for women with irregular cycles and polycystic ovaries, but without any evidence of androgen excess
  • 27. Primary adrenal disorders  Cushing’s disease  Congenital adrenal hyperplasia  Adrenocortical neoplasms
  • 28. Cushing’s disease ◦ Primary hypothalamic-pituitary disease ◦ Oversecretion of ACTH from pituitary ◦ Presence of adenoma or areas of corticotroph cell hyperplasia in the anterior pituitary ◦ Lead to cortical hyperplasia ◦ Causes hypercortisolism, hyperandrogenism
  • 29. Signs of Cushing’s  Hypercortisolism ◦ central obesity, hyperhidrosis ◦ buffalo hump, moon face, striae  Hyperandrogenism ◦ hirsutism, male pattern baldness, acne, deepening of the voice,  muscularity, and an  sex drive ◦ uterus shrinks, (clitoromegaly), the breasts become smaller, and normal menstruation stops (amenorrhea)
  • 30. Congenital adrenal hyperplasia Depends on the nature and severity of the enzymytic defect. Onset of clinical symptoms can occur in the • Perinatal period • Later childhood • Adulthood (less common)
  • 31. Congenital adrenal hyperplasia ◦ Autosomal recessive deficiency of an enzyme in the cortisol synthetic pathways. ◦ Cortisol secretion is reduced and feedback leads to increased ACTH secretion to maintain adequate cortisol leading to adrenal hyperplasia. ◦ Diversion of the steroid precursors into the androgenic steroid pathways occurs. Thus, 17- hydroxyprogesterone, androstenedione and testosterone levels are increased, leading to virilization.
  • 32. Anterior pituitary Congenital ACT adrenal H Adrenal cortex (bilateral hyperplasia hyperplasia) Cholesterol Pregnolon e Progesteron e 17 - hydroxypregnenolone Dehydroxypiandrosteron 21 e 11 - 17 - Androstenedion deoxycortisone hydroxyprogesterone e 21 Corticosterone 11 – deoxycortisol Aldosteron Testosterone e Mineralocorticoids Cortisol Sex steroids Glucocorticoids
  • 33. Adrenocortical neoplasms  Adrenocortical neoplasms associated with symptoms of excess of androgen are more likely to be androgen secreting adrenal carcinomas than adenomas.  It is also often assoc with hypercortisolism (mixed syndrome)  The tumour secretes androgen thus increasing in circulation and converted to testosterone at the peripheral
  • 35. Androgen secreting tumours  May occur at any age.  relatively rare.  should be suspected when the onset of androgenic symptoms is sudden (i.e., generally <2 yr) and the pace of symptoms is rapid, and when they lead to virilization and masculinization.  may be associated with other systemic symptoms including weight loss, anorexia, a feeling of abdominal bloating, back pain.
  • 36.
  • 37. The goals of lab testing 1 2 3 Other causes of androgen Look for Document excess/ metabolic androgen irregular abnormalities excess periods to be Eg Glucose/ ruled out Lipids
  • 38. Lab  Testosterone and Dehydroepiandrosterone sulphate (DHEAS) ◦ DHEAS hyperandrogenemia of adrenal origin  Serum prolactin  thyroid stimulating hormone (TSH)  Serum 17 hydroxyprogesterone (17-OHP) test –if suspect CAH  LH and FSH ( suggestive of PCOS if ratio >2)  Lipid profile  OGTT ◦ Relying on a fasting glucose level alone is inadequate as it is a poor predictor of impaired glucose tolerance or diabetes
  • 39. TVS
  • 41. A 22 year old nulligravid women presents to her gynaecologist because of irregular widely spread menses CASE SCENARIO
  • 42. History 1. What question would like to ask the patient?
  • 43. Examination 1. Firstly, what systems would you like to assess 2. Secondly, what are the specific signs would you like to elicit?
  • 44. Further clues  Menarche was at the age of 14, but she has rarely had regular cycles. For the past year she has had only three complete menses. Once going 6 months between period. She is 165cm and weighs 83kg. She is over weight, with acne and a few dark hairs on her upper lip and chin. She is sexually active and uses condom for contraception. 3. What is the likely diagnosis
  • 45. Summary of causes & diagnosis  PCOS. ◦ At least two of the following three abnormalities were present: chronic anovulation, clinical or biochemical hyperandrogenism, and polycystic ovaries on ultrasound  NCAH. ◦ Clinical hyperandrogenism + increased serum 17OHP or mildly increased serum 17OHP with an increased response to ACTH (  Androgen-secreting tumors. ◦ The finding of an androgen-secreting tumors (ovarian or adrenal) in women with very high serum androgen levels  Idiopathic hirsutism. ◦ Normal serum androgen levels (T, free T, and DHEAS) in the presence of normal ovulatory cycles and normal ovaries on ultrasound.  Idiopathic hyperandrogenism. ◦ Clinical hyperandrogenism, increased serum androgen levels in the presence of normal ovulatory cycles, and normal ovaries on ultrasound
  • 46. References  Zawadski JK, Dunaif A. Diagnostic criteria for polycystic ovary syndrome: toward a rational approach. In: Dunaif A,  ESHRE/ASRM Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril 2004; 81:19-25.  The Rotterdam ESHRE/ASRM-sponsored PCOS Consensus Workshop Group . Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod 2004;19:41- 47.  Azziz R, Carmina E, Dewailly D, et al. Androgen Excess Society. Position statement: criteria for defining polycystic ovary syndrome as a predominantly hyperandrogenic syndrome: an androgen excess society guideline. J Clin Endo & Metab 2006; 91(11): 4237-4245.  Azziz R, Sanchez LA, Knochenhauer ES, Moran C, Lazenby J, Stephens KC, Taylor K, Boots LR 2004 Androgen excess in women: experience with over 1000 consecutive patients. J Clin Endocrinol Metab 89:453–462  E. Carmina, F. Rosato, A. Jannì, M. Rizzo, and R. A. Longo Relative Prevalence of Different Androgen Excess Disorders in 950 Women Referred because of Clinical Hyperandrogenism. JCEM 2006 91: 2-6; doi:10.1210/jc.2005-1457