hirsutism - كلية الطب
TRANSCRIPT
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