1

HIRSUTISM

Prof, M.C.Bansal.

Founder Principal & Controller;

Jhalwar Medical college And hospital, Jhalawar.

Ex . Principal & controller;

Mahatmagandhi Medical College And Hospital,

Sitapura, Jaipur.

EXCESSIVE HAIR GROWTH

IT MAY BE EITHER

HYPERTRICHOSIS—Excess of hair growth all over the body.

HIRSUTISM—Male type sex hair growth in females.

VIRILIZATION—Excess sex hair growth and other hyper androgenic effects on female genitalia and body.

3

DEFINITIONHYPERTRICHOSIS : REFERS TO HAIR

DENSITY OR LENGTH BEYOND THE ACCEPTED LIMITS OF THE NORMAL FOR THE PARTICUALR AGE,RACE OR SEX.

• The excess hair may be generalised or localised and may consist of lanugo, vellus or terminal hair.

• It is frequently associated with the use of medication such as antiepileptics

Inherited typesCONGENITAL HYPERTRICHOSIS

LANUGINOSA – confluent generalised over growth of silvery blonde to grey lanugo hair at birth or early infancy, autosomal dominant, associated dental anomalies.

AMBRAS syndrome- longer thicker hair more over the face,ears and shoulders, facial dysmorphism and dental anomalies.

CONGENITAL GENERALISED HYPERTRCHOSIS – X linked dominant

4

Acquired typesACQUIRED HYPERTRICHOSIS

LANUGINOSA – seen in underlying malignancyDRUG INDUCED – following minoxidil therapy,

diazoxide, phenytoin sodium, cyclosporine, topical tacrolimus.

POEMS syndrome PORPHYRIA CUTANIA TARDA –

hexachlorobenzene, underlying hepatic tumour.

5

Localised hypertrichosisCongenital

Hairy elbowSpina bifidaTrichomegaly

Acquired InterferonRepeated traumaCongenital AV fistula

6

7

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 abdomen.

Hirsutism in an young girl with PCOD

Abdominal Hair Growth ___PCOD

HIRSUTISM

11

DEFINITIONVIRILIZATION : REFERS TO CONCURRENT

PRESENTATION OF HIRSUTISM WITH A BROAD RANGE OF SIGNS SUGGESTIVE OF ANDROGEN EXCESS,SUCH AS ACNE,FRONTOTEMPORAL BALDING,DEEPENING OF THE VOICE ,A DECREASE IN BREAT SIZECLITORAL HYPERTROPHY

12

INCREASED MUSCLE MASS AMENORREA / OLIGOMENORRHEAVirilization is seen less frequently than hirsutism and may reflect a severe underlying pathologic condition ,such as Male sex hormone producing Ovarian / adrenal tumorsHirsutism and virilization are closely interlinked and hirsutism may actually be the first manifestation of a condition that ultimately will lead to virilization if left untreated

Acne & Hirsutism

Clitoral Enlargement In female hrmophodyte secondary to cogenital adrenal hyperplasia

15

BASIC FACTS ABOUT HAIREach hair follicle develops at about 8-10wks of gestation as a derivative of epidermis.Number of hair follicles is set from birthHair grows from a individual hair follicle that are part of a pilosebaceous gland unitMain difference between sexes is the degree of differentiation of the hairHuman hair growth is continuousHair grows in a mosaic pattern(in a given area ,hair are in different stages of development)

16

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

17

BASIC FACTS ABOUT HAIR

Growth cycle of the Hair: ACTAnagen : Growth phase,85- 90 % of the life cycleCatagen : rapid involution PhaseTelogen : Quiescent phase

The growth phase or the anagen phase is primarily influenced by disorders that stimulate hair growth as well as therapeutic modalities.

18

BASIC FACTS ABOUT HAIR

Three types of Hair :Lanugo : Body hair seen in the fetus and newbornVellus : Fine adult hair covering the bodyTerminal 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

19

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

ANDROGEN INDUCED HAIR GROWTH

20

adrenal

pitutary

ovary

ACTH LH

TESTOSTERONE

HAIR FOLLICLE

Androgens are C-19 steroids produced in:• Adrenal gland• Ovary • Androgens are metabolised in: Skin Adipose tissue Liver Placenta

21

22

Testosterone Androstendione DHA DHAS

ADRENAL

CORTEX

OVARY

50

50

90

10

99

50

25

25

Origin of circulating androgens

The production rate of testosterone in the normal female is 0.2 to 0.3 mg/day

Normal total testosterone concentration in serum is below 0.8ng/ml

23

Hair & sebaceous Follicle Response to Hyperandrogenism

25

PRESENTATION OF HIRSUTISM

HIRSUTISM ALONEHIRSUTISM AND ASSOCIATED PILOSEBACEOUS UNIT OVERACTIVITY (ACNE)HIRSUTISM AND OVULATORY DISORDERSHIRSUTISM AND SIGNS OF VIRILIZATION

26

PRESENTATION OF HIRSUTISM

Hirsutism alone is the greatest challenge,patients usually go to dermatologist

Hirsutism wIth acne is frequently develop in teenage girls

Hirsutism with ovulatory disorders comes mostly to gynecologist

Hirsutism with virilization requires immediate work-up

27

CAUSES OF HIRSUTISM

Excess androgen production

Relative circulating androgen excess and low binding globulins

Excess end organ response

Patient perception

28

DISORDERS OF EXCESS ANDROGEN PRODUCTION

Source of androgen :

Exogenous

Endogenous (most common)

Two primary endogenous sources :

Adrenal glands

Ovaries

Mechanism of excessive hair growth

Main stimulus- Testosterone

Testosterone – binds – androgen receptors

29

Activation of 5 alpha reductase

DHT

TERMINAL HAIR

ANDROSTENEDION

ANDROGEN

Lengthen Anagen phase

Increase hair follicle size

Increase hair follicle diameter

Increase sebum secretion

30

31

Normal women Hirsute women

80% SHBG 79% SHBG

19% Albumin 19% Albumin

1% Free 2% Free

Causes of hirsutism

Androgenic ( 75-85% )

Non Androgenic

Idiopathic

32

ANDROGENICPCOD(70-80%)

Hyperandrogenism - 6.8%

The hyperandrogenic insulin-resistant acanthosis nigricans syndrome (HAIR-AN) - 3 %

21-hydroxylase non-classicaI adrenal hyperplasia (late-onset CAH) - 1.6%

Hypothyroidism - 0.7%

21-hydroxylase-deficient congenital adrenal hyperplasia - 0.7%

Hyperprolactinemia - 0.3%

Androgenic tumors - 0.2%

Cushing’s syndrome - 0-1%33

NON ANDROGENICAcromegalics.

chronic skin problems,

Non-androgenic anabolic drugs.

Danazol (Danocrine)

Norplant

Metoclopramide (Reglan)

Anabolic steroids

Methyldopa (Aldomet)

Phenothiazines

Progestins

Reserpine (Serpasil)

Testosterone

34

Tumor related causes of hirsutism

Tumors of the ovaries and the adrenal glands secrete excess hormones including androgen.

Ovarian tumors Adrenal tumors

Granulosa -theca cell tumors Adrenal adenoma

Arrhenoblastoma Adrenal carcinoma

Gonadoblastomas

Lipoid cell tumors ACTH secreting tumors

Dysgerminoma

Brenner's tumor

35

36

COMMON CAUSES OF ECTOPIC ACTH SECRETION

Small cell carcinoma of the lung 50%

Endocrine tumors of foregut origin35% Thymic carcinoid

Islet cell tumor

Medullary carcinoma thyroid

Bronchial carcinoid

Pheochromocytoma 5%

Ovarian tumors 2%

Miscellaneous causes of hirsutism

Functional adrenal hyperandrogenism

Hypereactio luteinalis of pregnancy - transient increase

in androgen levels during pregnancy

Thecoma of pregnancy - Transient androgen secreting

tumor during pregnancy

True hermaphroditism - condition where both male and

female internal sex organs are present

37

Genetics

There are very obvious family and racial differences in hirsutism patients. In some women, the skin is very sensitive to even low levels of androgens and their follicles produce primarily terminal (coarse and dark) hair.

38

39

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

40

DISORDERS OF EXCESS ANDROGEN PRODUCTION

ADRENAL ANDROGEN EXCESSThree recognised adrenal enzyme deficiencies :21 alpha Hydroxylase defieiency11-beta-Hydroxylase deficiency3-beta-ol-dehydrogenase deficiencyClassical forms are usually presented in

prenatal or neonatal period as ambiguous genitalia in female

Nonclassic forms are linked with hirsutism

The enzyme deficiency causes reduction in end-products, accumulation of hormone precursors & increased ACTH production.

The clinical picture reflects the effects of inadequate production of cortisol & aldosterone and the increased production of androgens & steroid metabolites.

41

42

43

ACTH ↑ Cortisol ↓ Aldosterone ↓ 17-OH-progesterone↑ Testosterone ↑ Urinary 17-ketosteroids↑

ESSENTIALS OF DIAGNOSIS

44

In less severe forms (late onset CAH) Genitalia is normal at birth. Precocious pubic hair & Clitoromegaly Excess facial or body hair appear later in childhood, often accompanied by tall stature

GIRLS WITH CAH

Varying virilizing symptoms ranging from oligomenorrhea to hirsutism and infertility

45

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

causes

46

ACTH-dependent States

ACTH-secreting pituitary tumor ( Cushing’ s disease ) 90-95% Pituitary CRH-secreting neoplasm ( ectopic CRP syndrome ) Nonpituitary ACTH-secreting neoplasm ( ectopic ACTH syndrome )

ACTH-independent States Adrenal adenoma/carcinoma

Micronodular /macronodular adrenal disease

Exogenous Sources Glucocorticoid intake

Psychiatric Conditions (Pseudo-Cushing Disorders)

Depression Alcoholism

47

CLINICAL FEATURES OF GLUCOCORTICOID EXCESS

Weight gain

90%“ Moon facies” 75 Hypertension 75

Violaceous striae 65 Hirsutism 65% Glucose intolerance 65 Proximal muscle weakness 60 Plethora 60Menstrual dysfunction 60Acne 40Easy bruising 40Osteopenia 40Dependent edema 40Hyperpigmentation 20Hypokalemic metabolic alkalosis

15

48

DISORDERS OF EXCESS ANDROGEN PRODUCTION

OVARIAN ORIGIN

Most common cause is

POLYCYSTIC OVARIAN SYNDROME

Other

Neoplastic ovarian disease

PCOS In 70-80 % cases of hirsutism

5-10% of women in reproductive age

Fulfills the Rotterdam criteria

Hyperandrogenism

Amenorrhoea /oligomenorrhoea

USG features of PCOD

Anovulation

Infertility

Obesity49

Pathogenesis

dpankar 50

Increased ovarian androgen biosynthesis in the polycystic ovary syndrome results from abnormalities at all levels of the hypothalamic–pituitary–ovarian axis. The increased frequency of luteinizing hormone (LH) pulses in the polycystic ovary syndrome appears to result from an increased frequency of hypothalamic gonadotropin-releasing hormone (GnRH) pulses.

The latter can result from an intrinsic abnormality in the hypothalamic GnRH pulse generator, favoring the production of luteinizing hormone over follicle-stimulating hormone (FSH) in patients with the polycystic ovary syndrome, in whom the administration of progesterone can restrain the rapid pulse frequency

51

. By whatever mechanism, the relative increase in pituitary secretion of luteinizing hormone leads to an increase in androgen production by ovarian theca cells.

Increased efficiency in the conversion of androgenic precursors in theca cells leads to enhanced production of androstenedione, which is then converted by 17 -hydroxysteroid dehydrogenase (17 ) to form testosterone or aromatized by the aromatase enzyme to form estrone. Within the granulosa cell, estrone is then converted into estradiol by 17.

52

. Numerous autocrine, paracrine, and endocrine factors modulate the effects of both luteinizing hormone and insulin on the androgen production of theca cells; insulin acts synergistically with luteinizing hormone to enhance androgen production. Insulin also inhibits hepatic synthesis of sex hormone–binding globulin, the key circulating protein that binds to testosterone and thus increases the proportion of testosterone that circulates in the unbound, biologically available, or "free," state. Testosterone inhibits and estrogen stimulates hepatic synthesis of sex hormone–binding globulin. The abbreviation scc denotes side-chain cleavage enzyme, StAR steroidogenic acute regulatory protein, and 3 -HSD 3 -hydroxysteroid dehydrogenase. Solid arrows denote a higher degree of stimulation than dashed arrows.

53

54

Lab.Evaluation of Hirsutism

Three basic hormonal evaluation

1. Total testosterone

2. DHEAS

3. 17-hydroxyprogesterone

Normal ranges

Total testosterone 20-80 ng/dl

Free testosterone 0.3-1.9 ng/dl

Bioavailable testosterone 0.8- 10 ng/dl

Free androgen index ( T/SHBG x 100)

Androgen producing tumor > 200 ng/dl

55

The Testosterone level

56

RELATIVE ANDROGEN EXCESS AND SHBG

<3 % TESTOSTERONE IS FREEMostly bound to Sex hormone binding globuline(SHBG)Dcrease in SHBG leads to Excess free TestosteroneCauses of Reduced SHBG : PCOS(Chronic anovulation) and Obesity

57

EXCESS REPONSIVITY TO ANDROGEN

TESTOSTERONE5-ALPHA –

REDUCTASE

DIHIDROTESTOSTERONE 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 )

TARGET CELLSRECEPTOR

58

Flowchart for investigation of hirsutism

59

BASIC APPROACH TO THE DIAGNOSIS OF HIRSUTISM

AND VIRILIZATION

SYMPTOMS AND HISTORYSIGNSPHYSICAL EXAMINATIONINVESTIGATION

60

APPROACH TO DIAGNOSIS

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

61

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

62

APPROACH TO DIAGNOSIS

Physical examinationEstablish presence of hirsutism and quantifying itPresence of acne and virilization and rule out hypertrichosisSkin hyperpigmentation,acanthosis nigricans suggests insulin resistance.Often associated with PCOD

63

APPROACH TO DIAGNOSIS

Measurement of weight and height and blood pressure: defects relates to adrenal enzyme defectsGalactorrhoeaTanner staging : Hirsutism before Tanner stage 3 to 4 is alarming and suggests a serious pathologyVisual genital examination for virilization

64

APPROACH TO DIAGNOSISDegree and extent

FERRIMAN GELLWAY SCORE score

Quantifies the extent of hair growth in 9 most androgenic sensitive sites

Hair growth is graded 0-4 at each site

Score of 8 or more (max 36) indicates hirsutism

 

65

66

APPROACH TO DIAGNOSIS

INVESTIGATION:FOR VIRILIZATION :Work-up focuses of the identification on the

source of androgen excessRule out exogenous androgenEvidence of endogenous androgen excess: Serum total testosteroneSerum dehydroepiandrosterone sulfate

(DHEAS)

67

APPROACH TO DIAGNOSIS

INVESTIGATION:

FOR VIRILIZATION

Imaging studies:Pelvic sonography

Adrenal imaging(USG,CT)

Specialized studies :

Selective venous catherization(adrenal or ovarian)

Radioisotope studies

68

Any ageRapid onsetHirsutes++Virilism+AmenorrhoeaDHEAS ↑↑(>700µg/100ml)T- normal or ↑Dexa suppression test- negativeIVPCT-scanMRI

Any ageRapid onsetHirsutes++Virilism+AmenorrhoeaT- ↑( >200 ng/100ml)DHEAS- normal SonographyLaparoscopybiopsy

ADRENAL TUMOR OVARIAN TUMOR

69

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 preferredDHEASIn selected cases : 17-OHP(fasting morning sample)

70

APPROACH TO DIAGNOSIS

Evaluation of accompanying medical disorderOvulation disorder :FSH,LHThyroid dysfunction:TSHHyperprolactinemia :PRL

Other investigations ( inselected cases)Androgen production :Androstenedione,

3-alpha Androstenediol glucuronideProvocative tests : Corticotropin stimulation tests,Insulin resistance determination

Differentation of hyperandrogenism

71

Diagnosis Menstrual Total DHAS LH 17OHP Sourse of

Pattern Testoste- Androgens ronePCOS Irregular Elevated mildly Elevated Normal OVARY elevated

CAH Irregular Elevated Often Usually Markedly Adrenals Normal Normal elevated

Idiopatic Regular Normal Normal Normal Normal Skinhirsutism

72

THERAPEUTIC OPTIONS

VIRILIZATION

GOAL: Identify the underlying cause and correcting it

Usually related to malignant process and requires surgical approach

73

THERAPEUTIC OPTIONS

HIRSUTISM

GOAL:

The prevention of further stimulation of hair growth

Cosmetic correction of the

problem

74

THERAPEUTIC OPTIONS

BASIC STEPS OF MANAGEMENT OF HIRSUTISM ARE:DEFINE THE PROBLEMQUANTIFY THE DEGREE OF HIRSUTISMINDENTIFY THE PATHOPHYSIOLOGYCORRECT THE PROBLEM,WHETHER ACUTE OR CHRONICDEFINE SUCESSWITH THE PATIENTFOLLOW UP

75

THERAPEUTIC OPTIONS

Regular follow up is indicated at appropriate intervals,usually every 3- 6 months

76

THERAPEUTIC OPTIONS

GENERAL MEASURES :

Eliminating causative factors

Optimizing weight Weight Reduction

Associated with reduction of hyperinsulinemia and androgen excess.BMI should not be > 25

Manage hair

Bleaching Cutting or shaving

Electrolysis Laser epilation

77

Removal of the source

78

Adrenal or ovarian tumour – surgically treated

Cushing disease –

Adrenalectomy

Radiation to pituitary Removal of ACTH producing tumor

Iatrogenic cases – Offending drug to be stopped

79

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

80

THERAPEUTIC OPTIONSChoice of OC

EE + Norgestimate approved in USACyproteroneacetate used as progesterone component in Ocs

Cyproterone acetate:

A progestin that also has strong antiandrogenic action.

Inhibits gonadotrophin secretion and interferes with androgen action on target organs by competing for androgen receptors

Dosage- 100mg from D5-D14 with ethinyloestradiol

30µg, from D 5 to D25

Side effects: Nausea, fatique, weight gain, loss of libido, mastalgia

OVARIAN SUPPRESSION BY LONG ACTING GnRH ANALOGUECan be used for functional ovarian androgen overproduction and even for malignant conditionBut to be used for long with back-up

Treatment is expensive and results are inconsistent

Use is reserved for patients resisting to initial therapy.

81

82

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

83

Drosperinone in PCOSCLINICAL BENEFITS

Helpful in treatment of Hirsutism Excellent cycle controlDecreases acne No weight gain.

METABOLIC BENEFITSNo effect on carbohydrate metabolismNo deterioration in the glycemic and insulinemic response to glucose load.No effect on serum lipid concentration.Safe for long term use

84

THERAPEUTIC OPTIONS

MANAGEMENT OF EXCESS ADRENAL ANDROGEN PRODUCTION

Metabolic correction of the disorder,usually with exogenous steroids

Dexamethasone,mostly used,But LIMITED ROLE

Glucocorticoids

85

Mode of action Suppress pituitary adrenal axis -

suppression of endogenous ACTH secretion

Use –

In adrenal or mixed adrenal and ovarian hyperandrogenism

Glucocorticoid Dosage Frequency

Hydrocortisone 10-20 mg Twice daily

Prednisone 2.5-5 mg Nightly or a alternate days

Dexamethasone 0.25-0.50 mg Nightly

86

Glucocorticoid preparations used in monotherapy & combined with antiandrogens

87

THERAPEUTIC OPTIONS

Management directed to the target organ and cells

Competition with Androgen receptors:Spironolactone,Flutamide, Ketoconazole,Cyproterone acetate

5-alpha reductase Inhibitors :Finasteride

88

CPA

50-100 mg/day on menstrual cycle days5-15 with ethinyl estradiol 20-35 mg on days 5-25

Spironolactone

100-200 mg/day (given in divided doses twice daily)

Finasteride

2.5-5 mg/day

Flutamide

250-500 mg/day (high dose)

62.5 to - <250 mg (low dose)

DOSES

89

THERAPEUTIC OPTIONSandrogen receptors

competitorsSPIRONOLACTONE:

Best studied and as Gold standardMechanism :Androgen receptors blockadeSuppression of Androgen biosynthesisIncreased metabolic clearance of teststerone ( Testosterone Estrogen )50-200 mg/day in two divided dosesSpironolactone + OC is well established regimen

90

THERAPEUTIC OPTIONSandrogen receptors

competitorsFLUTAMIDE :

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

Last resort of treatment.

CIMETIDINE= 300mg BD

LEAST POTENT ANDROGEN RECEPTOR BLOCKER

Clinical reports disappointing.

CLINICALLY NOT EFFECTIVE.

91

Recent

Eflornithien: vaniqua (13.9% cream)

US FDA approved

It irreversibly inhibits ornithine decarboxylase (ODC), an enzyme that catalyzes the rate-limiting step for follicular polyamine synthesis, which is necessary for hair growth.

Improvement occurs gradually over a period of 4-8 weeks or longer.

Most reported adverse reactions consisted of minor skin irritation.

92

93

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

Cosmetic treatments for Hirsutism

94

Bleaching - can cause irritation, purities, skin discolorationShaving - Shaving does not lead to worsening of

hirsutism and is a good short-term solution for

facial hair. - Does not affect the rate or duration of

anagen phase, or diameter of hair - But yields a blunt tip – illusion of thicker hair

Plucking, Waxing - scarring, folliculitis, hyperpigmentation

Depilatory creams - Irritant dermatitisElectrolysis - painful, erythema, inflammation, scarringLaser

95

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

96

Hirsutism is a symptom of underlying cause

Commonest cause is PCO

Progression may hint to diagnosing tumor

Treatment – Medicines/ Cosmetic

To summarise