Hirsutism Done by : Rina Karborani

Definition

Excess hair growth in male pattern

Includes : Chin, upper lip, chest, upper and lower back, upper and lower

abdomen, upper arm, thigh and buttocks

May signal the presence of hormonal imbalance or a hormone producing

tumor

The Ferriman Gallwey scoring system is used to evaluate the degree of

hirsutism before and after treatment

Stages of hair cycle

The length of each phase is different in various parts of

the body affecting hair length : for example scalp has long

anagen and short telogen resulting in long hair

Anagen: Active growing phase: 2-7 years

Catagen: shedding phase: 2-3 week

Telogen: resting phase: 3 months

Types of hair

Adults have two types of hair :Vellus and Terminal

Vellus ::Soft , fine, colorless ,and usually short.

Grow on the face, chest, and back and give the

impression of "hairless“ skin.

Terminal : longer , darker hair that grows on the

scalp , pubic and armpit areas in both adult men

and women

Androgens in women

Androgens are steroids produced from:

1- ovaries 2- adrenal gland

metabolized in :

1-skin

2-liver

3- adipose tissue

4- placenta

Androgens in (free active form ) causes hair growth

# Androgens:

Testosterone

Dihydrotestosterone

Androstenodione

Dehydroepiandrosterone(DHEA)

Dehydroepiandrosterone sulphate(DHEAS)

Strongest androgen is DHT

It is 10 times stronger than T

The enzyme responsible for conversion of T to DHT is 5-alpha reductase

Other androgens are weaker

Function of androgen in females ?

Estradiol production (E2)

Libido

Muscle mass

*Ovaries and adrenals contribute

equally

*Half T is from peripheral

androstenedione conversion and

half from glandular secretion of

ovaries and adrenals

Nearly 70-80% of testosterone is bound to SHBG

and is biologically inactive. most of the remaining is

bound to albumin and 1% is free testosterone. 19 %

SHBG is increased in : Pregnancy, OCP use,

hyperthyroidism, cirrhosis, anorexia nervosa.

SHBG is decreased in response to androgens like

androgenic disorders, androgenic medications,

hyperinsulinemia and obesity, hypothyroidism and

hyperprolactenemia … all resulting in increased

free testosterone levels.

Important points

Hirsutism is not an increase in the number of hair follicles BUT an alteration in

their character (which is an increase in the transformation from vellus to

terminal hair)

Hirsutism is a consequence of an increase in :

1)androgen level

2)sensitivity of androgen receptors at the level of hair follicle

3)The activity of 5- alpha reductase

Other manifestations of hyperandrognism

Causes

1) idiopathic

2) ovarian causes

3) adrenal

4) drugs

5) obesity

6) pituitary causes

Idiopathic(constitutional)

More in African race

Positive family history

No menstrual abnormalities / no hormonal abnormaloties

Increased sensitivity of hair follicles to androgens

Ovarian causes

1) PCOS 90% { hyperandrogenism, PCO, anovulation)

2) ovarian hyperthecosis

Describes the presence of luteinised theca cell nests in the ovarian stroma.

Accounts for most of the cases of hyperandrogenaemia in postmenopausal women.

When compared with PCOS, hyperthecosis is typically associated with more severe hyperandrogenism and virilisation.

Testosterone concentrations are much higher than in PCOS

Ovarian tumors

*Sertoli Leydig cell tumours: most common virilising ovarian tumours account

for 0.5% of all ovarian neoplasms.

*Hilar cell tumour

*Brenner tumour.

*These tumours are characterised by striking elevations in serum testosterone

but normal DHEA‐S

Computerised tomography, magnetic resonance imaging and ultrasound are

used to make the diagnosis

Adrenal causes

1) CAH

2) cushing’s syndrome

3) Adrenal tumors ( DHEA-S high)

Congenital adrenal hyperplasia

Due to 21-hydroxylase deficiency

Autosomal recessive

21 hydroxylase deficiency in 95% of cases results in low cortisol, then ACTH

increased and drives androgen production

Accounts for 5% of women with hirsutism

Strong family history

T level above 5 nmol/l

Short Synacthen test:

Synthetic ACTH is injected IV or IM , and adrenal hormones are measured after 30

mins & 1 hour.

Low level of hormones indicate enzyme deficiency despite ACTH stimulation

17 hydroxyprogesterone will be high (precursor)

Cushing’s syndrome

Hirsutism is present in 80% of patients.

Cushing's syndrome results from increased circulating concentrations of cortisol

and can present gradually with central weight gain, facial plethora,

supraclavicular fat pads, abdominal striae and

signs of hyperandrogenism, such as hirsutism, acne and male pattern baldness

Causes of cushing syndrome

1-Secondary to an ACTH secreting pituitary tumour (Cushing's disease)

2-Autonomous cortisol secretion by the adrenal glands due to adrenocortical

neoplasms or hyperplasia

3-Exogenous administration of glucocorticoids

4-Ectopic ACTH secretion in neoplasia including small cell lung carcinomas and

carcinoid tumours.

Pituitary

pituitary adenoma (prolactinoma)

Hyperprolactinemia may induce hirsutism via several mechanisms.

Prolactin inhibits the hepatic synthesis of SHBG, thereby raising the concentration

of plasma-free (unbound) testosterone. An elevation in the plasma-free

testosterone level is the most consistent finding in hirsutism.

Drugs

Many drugs can cause hirsutism: androgens, glucocorticosteroids, progestins,

estrogen antagonists (clomiphene, tamoxifen), minoxidil, cyclosporine, danazol,

phenytoin.

obesity

The chronology of symptom and its progression is important and can be

indicative of specific disease processes. For example :

Rapid excessive hair growth, deepened voice and breast atrophy would

be more indicative of an adrenal/ovarian tumour .

Slow development of hirsutism and menstrual irregularities occurring

soon after puberty, classically due to PCOS.

A family history is also important as both PCOS and CAH can occur in

other family members

The Ferriman Gallwey scoring system

Scoring scale of androgen sensitive hair in 9 body areas rated 1-4

Score above 8 is defined as hirsutism

Evaluation of hirsutism

History

1) drugs history

2) medical disorders

3) course of symptoms ( rapid may indicate tumor)

4) menstrual disorders

Physical examination

Thyroid exam

Signs of cushing syndrome

Signs of virilization ((hirsutism), baldness, acne, deepening of the voice,

increased muscularity)

Signs of insulin resistance ( acanthosis nigricans )

Investigations

Lab tests :

Testosterone / Dihydroepiandrosterone

suphate ( DHEAS) level

TSH

* DHEAS is formed from the adrenal cortex

Management of Hyperandrogenism

Find out the underlying cause & treat:

1)Stop offending drugs

2)Treat tumors by surgical removal

3)Treat medical disorders

Encourage Weight loss

Antiandrogens :

1)Cyproterone actetate )a progestin),25-50 mg

2)Spironolactone , weak diuretic 25 mg-200 mg daily

3)Flutamide:

blocks androgen receptors {S/E hepatotoxicity }

Finasteride : of 5 alpha reductase inhibitor given 5 mg daily less S/E’s

( mechanism : reduce LH,increase SHBG, and decrease free T)

Ovarian suppression : COC pills { suppress FSH&LH and suppresses

androgen production}.

Treatments

Cosmetic treatments: Waxing, Laser, & depilatory creams: effective while

waiting for medical TX to work

Thank you