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7/28/2019 HIRSUT
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dpankar 1
EXCESSIVE HAIRGROWTH IN
ADOLESCENTDr. DPankar BanerjiConsulting Gynecologist
Infertility SpecialistIdeal Fertility :IVF and Genetic
Center
Jabalpur, India
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EXCESSIVE HAIR
GROWTHIT MAY BE EITHER
HIRSUTISM
VIRILIZATION
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DEFINITION
HIRSUTISM : APPEARANCE OF
EXCESSIVE COARSE
(TERMINAL)HAIR IN A PATTERN NOTNORMAL IN THE FEMALE
Definition highlights the abnormal
distribution of excess hair growth ,suchas facial ,chest,or upper abdominal hair
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DEFINITION
HYPERTRICHOSIS : GROWTH OF HAIR
IN EXCESS OF THE NORMAL WHILE
LIMITED TO A NORMAL PATTERN OFDISTRIBUTION
It is frequently associated with the use
of medication such as antiepileptics
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DEFINITION
VIRILIZATION : REFERS TO CONCURRENTPRESENTATION OF HIRSUTISMWITH ABROAD RANGE OF SIGNS SUGGESTIVEOFANDROGEN EXCESS,SUCH AS
ACNE,
FRONTOTEMPORAL BALDING,
DEPPENING OF THE VOICE ,A DECREASE IN BREAT SIZE
CLITORAL HYPERTROPHY
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DEFINITION
INCREASED MUSCLE MASS
AMENORREA / OLIGOMENORRHEA
Virilization is seen less frequently thanhirsutism and may reflect a severe underlyingpathologic condition ,such as malignancy
Hirsutism and virilization are closely linked
and hirsutism may actually be the firstmanifestation of a condition that ultimately willlead to virilization in left untreated
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BASIC FACTS ABOUT
HAIRHair grows from a individual hair follicle thatare part of a pilosebaceous gland unit
Number of hair follicles is set from birthMain difference between sexes is the degreeof differentiation of the hair
Human hair growth is continuous
Hair grows in a mosaic pattern(in a givenarea ,hair are in different stages ofdevelopment)
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BASIC FACTS ABOUT
HAIRSome condition may cause a high level
of synchrony between the growth cycles
of hair ,leading to the appearance ofeither massive hair loss (alopecia)or
excess hair for a limited period of time
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BASIC FACTS ABOUT
HAIRGrowth cycle of the Hair: ACT
Anagen : Growth phase,85- 90 % of the life
cycleCatagen : rapid involution Phase
Telogen : Quiescent phase
The growth phase or the anagen phase is
primarily influenced by disorders thatstimulate hair growth as well as therapeuticmidalities.
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BASIC FACTS ABOUT
HAIRThree types of Hair :
Lanugo : Body hair seen in the fetus and
newbornVellus : Fine adult hair covering the body
Terminal hair : Thick pigmented hair of scalpand pubic area
Thickness of the terminal hair varies form oneindividual to other depending upon genetic,and possibly nutritional
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BASIC FACTS ABOUT
HAIRAndrogen sensitive hair : depend upon
androgen input for hair growth.
Face,neck,chest,abdomen,axillary,upperarms ,inner thighs and pubic hair,+ part
of the scalp hair.
Less Androgen independent :
Forearms ,hands .lower legs
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BASIC FACTS ABOUT
HAIRPITUITARY
ADRENALOVARY
PITUITARY
ADRENAL
OVARY
DHEAS
DHEA
AND,STEN,ONE
PERIPHERAL
CONVERSION
TESTOSTERONE
HAIR FOLLICLE
DIHYDROTESTERONE
DHEASACTH
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PRESENTATION
Most of the cases of virilization seen
clinically are acute and striking in nature
and seldom go unrecognized andusually prompt immediate medical
intervention
Hirsutism may present in variety ofways
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PRESENTATION OF
HIRSUTISMHIRSUTISM ALONE
HIRSUTISM AND ASSOCIATED
PILOSEBACEOUS UNITOVERACTIVITY (ACNE)
HIRSUTISM AND OVULATORY
DISORDERSHIRSUTISM AND SIGNS OFVIRILIZATION
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PRESENTATION OF
HIRSUTISMHirsutism alone is the greatest
challenge,patients usually go to dermatologist
Hirsutism wIth acne is frequently in teenagegirls
Hirsutism with ovulatory disorders comes
mostly to gynecologist
Hirsutism with virilization requires immediate
work-up
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CAUSES OF HIRSUTISM
Excess androgen production
Relative circulating androgen excess
and low binding globulins
Excess end organ response
Patient perception
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DISORDERS OF EXCESS
ANDROGEN PRODUCTION
Source of androgen :
Exogenous
Endogenous (most common)
Two primary endogenous sources :
Adrenal glandsOvaries
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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 Cushings syndrome
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DISORDERS OF EXCESS
ANDROGEN PRODUCTIONADRENAL ANDROGEN EXCESS
Three recognised adrenal enzyme deficiencies :
21 alpha Hydroxylase defieiency11-beta-Hydroxylase deficiency
3-beta-ol-dehydrogenase deficiency
Classical forms are usually presented in
prenatal or neonatal period as ambiguousgenitalia in female
Nonclassic forms are linked with hirsutism
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DISORDERS OF EXCESS
ANDROGEN PRODUCTION21-alpha-Hydroxylase deficiency:
Most common ,10%
Prevalence depends on ethnicorigin(common in slavs,1/50 Hispanics 1/40,ashkenazi jews 1/27
Cushings syndrome :Hirsutism with weight gain
and growth retardation as the primarymanifestation,with acne and other cutaneousproblems
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DISORDERS OF EXCESS
ANDROGEN PRODUCTION
OVARIAN ORIGIN
Most common cause is
POLYCYSTIC OVARIAN SYMDROME
Other
Neoplastic ovarian disease
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Lab.Evaluation of
HirsutismThree basic hormonal evaluation
1. Total testosterone
2. DHEAS
3. AM 17-hydroxyprogesterone
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Total Testosterone
Normal Value (0.2
0.9 ng/ml)
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DHEAS (600 2800 ng/ml)
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AM 17
hydroxyprogesterone(0.1 0.8ng/ml )
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RELATIVE ANDROGEN
EXCESS AND SHBG
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EXCESS REPONSIVITY
TO ANDROGENTESTOSTERONE 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 ChromosomeOver activity of the 5-alpha-reductase (Type1 and
Type 2,type1 is involved in hirsutism )
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BASIC APPROACH TOTHE DIAGNOSIS OF
HIRSUTISM AND
VIRILIZATION
SYMPTOMS AND HISTORY
SIGNSPHYSICAL EXAMINATION
INVESTIGATION
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APPROACH TO
DIAGNOSISIt should be methodical.
First step : True nature of presentation
Patient may present with ovulatory problemsand 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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APPROACH TO
DIAGNOSISCareful history regarding the timing of
onset and chronological progression
Precocious puberty with androgenexcess suggests adrenal enzyme defect
Family history : androgen excess
disorders
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APPROACH TO
DIAGNOSISPhysical examination
Establish presence of hirsutism and
quantifying itPresence of acne and virilization andrule out hypertrichosis
Skin hyperpigmentation,acanthosisnigricans suggests insulinresistance.Often associated with PCO
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APPROACH TO
DIAGNOSISMeasurement of weight and height andblood pressure: defects relates to
adrenal enzyme defectsGalactorrhoea
Tanner staging : Hirsutism beforeTanner stage 3 to 4 is alarming andsuggests a serious pathology
Visual genital examination for virilization
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APPROACH TO
DIAGNOSISSemiobjective scoring system :
Ferriman and Gallwey system ,between
6-12 is the lower limit.
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APPROACH TO
DIAGNOSISINVESTIGATION:
FOR VIRILIZATION :
Work-up focuses of the identification on thesource of androgen excess
Rule out exogenous androgen
Evidence of endogenous androgen excess:
Serum total testosteroneSerum dehydroepiandrosterone sulfate
(DHEAS)
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APPROACH TO
DIAGNOSISINVESTIGATION:
FOR VIRILIZATION
Imaging studies:Pelvic sonographyAdrenal imaging(USG,CT)
Specialized studies :
Selective venous catherization(adrenal orovarian)
Radioisotope studies
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APPROACH TO
DIAGNOSISINVESTIGATION :
HIRSUTISM: Goal is to rule out seriouspotential life threatening conditions and gaininformation that helps in treatment
Evaluation of Androgen excess:
Testosterone ,total preferred
DHEASIn selected cases : 17-OHP(fasting morningsample)
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APPROACH TO
DIAGNOSISEvaluation of accompanying medical disorder
Ovulation disorder :FSH,LH
Thyroid dysfunction:TSHHyperprolactinemia :PRL
Other investigations ( inselected cases)
Androgen production :Androstenedione,
3-alpha Androstenediol glucuronide
Provocative tests : Corticotropin stimulationtests,Insulin resistance determination
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THERAPEUTIC OPTIONS
VIRILIZATION
GOAL: Identify the underlying cause
and correcting it
Usually related to malignant process
and requires surgical approach
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THERAPEUTIC OPTIONS
HIRSUTISM
GOAL:
The prevention of further stimulation of
hair growth
Cosmetic correction of the problem
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THERAPEUTIC OPTIONS
BASIC STEPS OF MANAGEMENT OFHIRSUTISM ARE:
DEFINE THE PROBLEM
QUANTIFY THE DEGREE OF HIRSUTISM
INDENTIFY THE PATHOPHYSIOLOGY
CORRECT THE PROBLEM,WHETHER
ACUTE OR CHRONICDEFINE SUCESSWITH THE PATIENT
FOLLOW UP
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THERAPEUTIC OPTIONS
A key element of any therapeutic plan is
to define what will ultimately be viewed
and successful therapyRegular follow up is indicated at
appropriate intervals,usually every 3- 6
months
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THERAPEUTIC OPTIONS
GENERAL MEASURES :
Eliminating causative factors
Optimizing weightManage hair
Bleaching
Cutting or shavingElectrolysis
Laser epilation
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THERAPEUTIC OPTIONS
Management of excess ovarian androgen
production :
Standard therapy is :combined E+P,mostcommonly 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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THERAPEUTIC OPTIONS
Choice of OC
EE + Norgestimarte approved in USA
Cyproterone acetate used as progesteronecomponent in Ocs
OVARIAN SUPPRESSION BY LONG ACTINGGnRH ANALOGUE
Can be used for functional ovarian androgenoverproduction and even for malignantcondition
But to be used for long with back-up
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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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THERAPEUTIC OPTIONS
MANAGEMENT OF EXCESS
ADRENAL ANDROGEN PRODUCTION
Metabolic correction of thedisorder,usually with exogenous
steroids
Dexamethasone,mostly used,ButLIMITED ROLE
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THERAPEUTIC OPTIONS
Management directed to the target organ
and cells
Competition with Androgenreceptors:Spironolactone,Flutamide,
Ketoconazole,Cyproterone acetate
5-alpha reductase Inhibitors :Finasteride
THERAPEUTIC OPTIONS
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THERAPEUTIC OPTIONS
androgen receptors
competitorsSIPRONOLACTONE:
Best studied and as Gold standard
Mechanism :Androgen receptors blockade
Suppression of Androgen biosynthesis
Increased metabolic clearance of teststerone
( Testosterone
Estrogen )50-200 mg/day in two divided doses
Spironolactone + OC is well establishedregimen
THERAPEUTIC OPTIONS
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THERAPEUTIC OPTIONS
androgen receptors
competitorsFLUTAMIDE :
Blocks the androgen receptors
Decreases androgen production
May have therapeutic value in cases of
PCOS
Usually used with OcsKETOCONAZOLE:
Equally effective but danger of liver toxicity
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THERAPEUTIC OPTIONS
SELECTING BEST THERAPY:
Correct underlying medical problem
Correct thyroid/hyperprolactinemiaPCO :oral contraceptives
Ocs + spironolactone is usually the choice
7580% patients shows responseAtleast 6 months is needed for evidence of
response
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THERAPEUTIC OPTIONS
If response is seen in 6 months then
treatment should be continued for
further 6 months and in most cases fornumber of years