1. EXCESSIVE HAIR GROWTH IN ADOLESCENT
Dr. D’Pankar Banerji
Consulting Gynecologist
Infertility Specialist
Ideal Fertility :IVF and Genetic Center
Jabalpur, India
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2. EXCESSIVE HAIR GROWTH
IT MAY BE EITHER
HIRSUTISM
VIRILIZATION
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3. DEFINITION
HIRSUTISM : APPEARANCE OF EXCESSIVE COARSE (TERMINAL)HAIR IN A PATTERN NOT NORMAL IN THE FEMALE
Definition highlights the abnormal distribution of excess hair growth ,such as facial ,chest,or upper abdominal hair
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4. DEFINITION
HYPERTRICHOSIS : GROWTH OF HAIR IN EXCESS OF THE NORMAL WHILE LIMITED TO A NORMAL PATTERN OF DISTRIBUTION
It is frequently associated with the use of medication such as antiepileptics
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5. DEFINITION
VIRILIZATION : REFERS TO CONCURRENT PRESENTATION OF HIRSUTISM WITH A BROAD RANGE OF SIGNS SUGGESTIVE OF ANDROGEN EXCESS,SUCH AS
ACNE,
FRONTOTEMPORAL BALDING,
DEPPENING OF THE VOICE ,
A DECREASE IN BREAT SIZE
CLITORAL HYPERTROPHY
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6. DEFINITION INCREASED MUSCLE MASS AMENORREA / OLIGOMENORRHEA
Virilization is seen less frequently than hirsutism and may reflect a severe underlying pathologic condition ,such as malignancy
Hirsutism and virilization are closely linked and hirsutism may actually be the first manifestation of a condition that ultimately will lead to virilization in left untreated
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7. BASIC FACTS ABOUT HAIR
Hair grows from a individual hair follicle that are part of a pilosebaceous gland unit
Number of hair follicles is set from birth
Main difference between sexes is the degree of differentiation of the hair
Human hair growth is continuous
Hair grows in a mosaic pattern(in a given area ,hair are in different stages of development)
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8. BASIC FACTS ABOUT HAIR
Some condition may cause a high level of synchrony between the growth cycles of hair ,leading to the appearance of either massive hair loss (alopecia)or excess hair for a limited period of time
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9. BASIC FACTS ABOUT HAIR Growth cycle of the Hair: ACT
Anagen : Growth phase, % of the life cycle
Catagen : rapid involution Phase
Telogen : Quiescent phase
The growth phase or the anagen phase is primarily influenced by disorders that stimulate hair growth as well as therapeutic midalities.
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10. BASIC FACTS ABOUT HAIR Three types of Hair :
Lanugo : Body hair seen in the fetus and newborn
Vellus : Fine adult hair covering the body
Terminal hair : Thick pigmented hair of scalp and pubic area
Thickness of the terminal hair varies form one individual to other depending upon genetic, and possibly nutritional
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11. BASIC FACTS ABOUT HAIR
Androgen sensitive hair : depend upon androgen input for hair growth.
Face,neck,chest,abdomen,axillary,upper arms ,inner thighs and pubic hair,+ part of the scalp hair.
Less Androgen independent :
Forearms ,hands .lower legs
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12. BASIC FACTS ABOUT HAIR ACTH OVARY PITUITARY DHEAS PITUITARY OVARY
ADRENAL
OVARY
ADRENAL
AND,STEN,ONE
PERIPHERAL
CONVERSION
TESTOSTERONE
HAIR FOLLICLE
DIHYDROTESTERONE
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13. PRESENTATION
Most of the cases of virilization seen clinically are acute and striking in nature and seldom go unrecognized and usually prompt immediate medical intervention
Hirsutism may present in variety of ways
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14. PRESENTATION OF HIRSUTISM
HIRSUTISM ALONE
HIRSUTISM AND ASSOCIATED PILOSEBACEOUS UNIT OVERACTIVITY (ACNE)
HIRSUTISM AND OVULATORY DISORDERS
HIRSUTISM AND SIGNS OF VIRILIZATION
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15. PRESENTATION OF HIRSUTISM
Hirsutism alone is the greatest challenge,patients usually go to dermatologist
Hirsutism wIth acne is frequently in teenage girls
Hirsutism with ovulatory disorders comes mostly to gynecologist
Hirsutism with virilization requires immediate work-up
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16. CAUSES OF HIRSUTISM Excess androgen production
Relative circulating androgen excess and low binding globulins
Excess end organ response
Patient perception
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17. DISORDERS OF EXCESS ANDROGEN PRODUCTION
Source of androgen :
Exogenous
Endogenous (most common)
Two primary endogenous sources :
Adrenal glands
Ovaries
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18. DISORDERS OF EXCESS ANDROGEN PRODUCTION
ADRENAL ANDROGEN EXCESS
May be linked to genetically determined steroid synthesis enzyme deficiency
Malignant adrenal neoplastic process
Other conditions like Cushing’s syndrome
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19. DISORDERS OF EXCESS ANDROGEN PRODUCTION
ADRENAL ANDROGEN EXCESS
Three recognised adrenal enzyme deficiencies :
21 alpha Hydroxylase defieiency
11-beta-Hydroxylase deficiency
3-beta-ol-dehydrogenase deficiency
Classical forms are usually presented in prenatal or neonatal period as ambiguous genitalia in female
Nonclassic forms are linked with hirsutism
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20. DISORDERS OF EXCESS ANDROGEN PRODUCTION
21-alpha-Hydroxylase deficiency:
Most common ,<1% to >10%
Prevalence depends on ethnic origin(common in slavs,1/50 Hispanics 1/40, ashkenazi jews 1/27
Cushing’s syndrome :Hirsutism with weight gain and growth retardation as the primary manifestation,with acne and other cutaneous problems
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21. DISORDERS OF EXCESS ANDROGEN PRODUCTION
OVARIAN ORIGIN
Most common cause is
POLYCYSTIC OVARIAN SYMDROME
Other
Neoplastic ovarian disease
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22. Lab.Evaluation of Hirsutism
Three basic hormonal evaluation
1. Total testosterone
2. DHEAS
3. AM 17-hydroxyprogesterone
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23. Total Testosterone Normal Value (0.2 –0.9 ng/ml)
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24. DHEAS (600 –2800 ng/ml)
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25. AM 17 –hydroxyprogesterone(0.1 –0.8 ng/ml )
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26. RELATIVE ANDROGEN EXCESS AND SHBG
<3 % TESTOSTERONE IS FREE
Mostly bound to Sex hormone binding globuline(SHBG)
Dcrease in SHBG leads to Excess free Testosterone
Causes of Reduced SHBG : PCOS(Chronic anovulation) and Obesity
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27. EXCESS REPONSIVITY TO ANDROGEN
TESTOSTERONE TARGET CELLS
5-ALPHA -REDUCTASE
DIHIDROTESTOSTERONE RECEPTOR
Excessive response of the receptor to DHT(may be due to mutation of the highly polymorphic region in gene of the receptor located on X Chromosome
Over activity of the 5-alpha-reductase (Type –1 and Type 2,type –1 is involved in hirsutism )
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28. BASIC APPROACH TO THE DIAGNOSIS OF HIRSUTISM AND VIRILIZATION
SYMPTOMS AND HISTORY
SIGNS
PHYSICAL EXAMINATION
INVESTIGATION
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29. APPROACH TO DIAGNOSIS It should be methodical.
First step : True nature of presentation
Patient may present with ovulatory problems and hirsutism may not be reported
There may be normal hair pattern but patient complains about hirsutism
Evident virilization should investigated at once
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30. APPROACH TO DIAGNOSIS
Careful history regarding the timing of onset and chronological progression
Precocious puberty with androgen excess suggests adrenal enzyme defect
Family history : androgen excess disorders
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31. APPROACH TO DIAGNOSIS Physical examination
Establish presence of hirsutism and quantifying it
Presence of acne and virilization and rule out hypertrichosis
Skin hyperpigmentation,acanthosis nigricans suggests insulin resistance.Often associated with PCO
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32. APPROACH TO DIAGNOSIS
Measurement of weight and height and blood pressure: defects relates to adrenal enzyme defects
Galactorrhoea
Tanner staging : Hirsutism before Tanner stage 3 to 4 is alarming and suggests a serious pathology
Visual genital examination for virilization
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33. APPROACH TO DIAGNOSIS
Semiobjective scoring system : Ferriman and Gallwey system ,between 6-12 is the lower limit.
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34. APPROACH TO DIAGNOSIS INVESTIGATION: FOR VIRILIZATION :
Work-up focuses of the identification on the source of androgen excess
Rule out exogenous androgen
Evidence of endogenous androgen excess:
Serum total testosterone
Serum dehydroepiandrosterone sulfate (DHEAS)
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35. APPROACH TO DIAGNOSIS INVESTIGATION: FOR VIRILIZATION
Imaging studies:Pelvic sonography
Adrenal imaging(USG,CT)
Specialized studies :
Selective venous catherization(adrenal or ovarian)
Radioisotope studies
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36. APPROACH TO DIAGNOSIS INVESTIGATION :
HIRSUTISM: Goal is to rule out serious potential life threatening conditions and gain information that helps in treatment
Evaluation of Androgen excess:
Testosterone ,total preferred
DHEAS
In selected cases : 17-OHP(fasting morning sample)
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37. APPROACH TO DIAGNOSIS Evaluation of accompanying medical disorder
Ovulation disorder :FSH,LH
Thyroid dysfunction:TSH
Hyperprolactinemia :PRL
Other investigations ( inselected cases)
Androgen production :Androstenedione,
3-alpha Androstenediol glucuronide
Provocative tests : Corticotropin stimulation tests,Insulin resistance determination
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38. THERAPEUTIC OPTIONS VIRILIZATION
GOAL: Identify the underlying cause and correcting it
Usually related to malignant process and requires surgical approach
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39. THERAPEUTIC OPTIONS HIRSUTISM GOAL:
The prevention of further stimulation of hair growth
Cosmetic correction of the problem
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40. THERAPEUTIC OPTIONS BASIC STEPS OF MANAGEMENT OF HIRSUTISM ARE:
DEFINE THE PROBLEM
QUANTIFY THE DEGREE OF HIRSUTISM
INDENTIFY THE PATHOPHYSIOLOGY
CORRECT THE PROBLEM,WHETHER ACUTE OR CHRONIC
DEFINE SUCESSWITH THE PATIENT
FOLLOW UP
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41. THERAPEUTIC OPTIONS
A key element of any therapeutic plan is to define what will ultimately be viewed and successful therapy
Regular follow up is indicated at appropriate intervals,usually every 3- 6 months
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42. THERAPEUTIC OPTIONS GENERAL MEASURES : Eliminating causative factors
Optimizing weight
Manage hair
Bleaching
Cutting or shaving
Electrolysis
Laser epilation
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43. THERAPEUTIC OPTIONS Management of excess ovarian androgen production :
Standard therapy is :combined E+P,most commonly OCs
It reduces ovarian androgen production
It increases SHBG
It induces competition at the cellular level for binding to the androgen receptor
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44. THERAPEUTIC OPTIONS Choice of OC EE + Norgestimarte approved in USA
Cyproterone acetate used as progesterone component in Ocs
OVARIAN SUPPRESSION BY LONG ACTING GnRH ANALOGUE
Can be used for functional ovarian androgen overproduction and even for malignant condition
But to be used for long with back-up
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45. THERAPEUTIC OPTIONS Long acting GnRH analogues used
But there is doubt that this therapy will be beneficial over Ocs
INSULIN SENSITIZING AGENTS:
For PCO with acanthosis nigicans
Commonly used agent is : Metformin and Troglitazone,Pioglitazone,Rosiglitazone
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46. THERAPEUTIC OPTIONS MANAGEMENT OF EXCESS ADRENAL ANDROGEN PRODUCTION
Metabolic correction of the disorder,usually with exogenous steroids
Dexamethasone,mostly used,But LIMITED ROLE
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47. THERAPEUTIC OPTIONS Management directed to the target organ and cells
Competition with Androgen receptors:Spironolactone,Flutamide, Ketoconazole,Cyproterone acetate
5-alpha reductase Inhibitors :Finasteride
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48. THERAPEUTIC OPTIONS androgen receptors competitors
SIPRONOLACTONE:
Best studied and as Gold standard
Mechanism :Androgen receptors blockade
Suppression of Androgen biosynthesis
Increased metabolic clearance of teststerone ( Testosterone  Estrogen )
mg/day in two divided doses
Spironolactone + OC is well established regimen
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49. THERAPEUTIC OPTIONS androgen receptors competitors
FLUTAMIDE :
Blocks the androgen receptors
Decreases androgen production
May have therapeutic value in cases of PCOS
Usually used with Ocs
KETOCONAZOLE:
Equally effective but danger of liver toxicity
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50. THERAPEUTIC OPTIONS SELECTING BEST THERAPY:
Correct underlying medical problem
Correct thyroid/hyperprolactinemia
PCO :oral contraceptives
Ocs + spironolactone is usually the choice
75 –80% patients shows response
Atleast 6 months is needed for evidence of response
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51. THERAPEUTIC OPTIONS
If response is seen in 6 months then treatment should be continued for further 6 months and in most cases for number of years
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