Hirsutism and virilism /. pdf

Presentation about hirsutsim

1. University of Mosul
College of Medicine
Lecture: 2 5
th
year
Subject/year: Hirsutism and virilism
Lecturer: Ass.Prof. Dr. Ahmed Jasim
Department: Obstetric & Gynecology
Date:-2023 -2024

2. Hirsutism & virilization
Ass.Prof.
Dr.AhmedJasim
MBChB.DOG.FICMS

3. The AIMof this lecture is
Revise the androgen production and
understand the pathology of
hirsutism and virilism.

4. ❖Intended learning outcomes:
By the end of this lecture the student will be able to:
Revise the normal physiology of androgen production in female.
1.Differentiate between hirsutism and hypertrichosis.
2.Examine for other signs of virilism.
3.Know the warning symptoms and signs that alert to significant pathology.
4.Assess the severity of hirsutism using the Ferriman–Gallwey score.
5.Request appropriate investigations for hirsutism/virilismand have a knowledge
about treatment.

9. Definition
Hirsutismis increased terminal hair growth usually in areas where it
does not normally occur but which contain androgen receptors with a
tendency to male distribution. These areas include the face, chest,
areola, lower abdomen, inner thighs, and back.
Virilizationis the masculinization of a woman. In addition to
hirsutism, these women present with temporal hair recession, acne,
deepening of the voice, malodorous sweat, clitoral enlargement,
atrophy of the breasts, increased muscle mass, loss of female body
contours, and amenorrhea. Signs of virilizationusually appear over a
relatively short period of time and are indicative of serious endocrine
disease. Virilizationis associated with a marked increase in circulating
androgen levels.

12. Aetiology
1.Rise in secretion of free anderogen.
2.reduction in sex hormone binding globulin( SHBG)
SHBG level falls when testosterone production increase &drug induce
Hirsutism.
The amount of hair is related to the potency of the circulating
androgens,quantityof ciculatingfree androgens, duration of
exposure, sensitivity of the hair follicle, and density of the
hair follicle.

13. Androgen activity can be studied in three
stages:
•Androgen production by the adrenal gland
and ovaries.
•Transport in the blood stream by sex
hormone-binding globulin (SHBG) to the cell.
•Binding to the receptor and intracellular
modification.

14. CAUSES OF HIRSUTIM
1.Idiopathic
2.Ovarian
PCOS
hyperthecosis
Neoplasms
3.Adrenal
CAH
neoplasms
Cushing’s syndrome
4.Drugs
anabolic (testosterone/adrenal) steroids,phynitoin,diazoxideminoxidil,danazol,19-norsteroid derivative progestogens
5.Other endocrine disorders
acromegaly
menopause
thyroid disease

17. Clinical evaluation
The primary objective include:
•Grading the severity of the hirsutism using the modified
Ferriman-Gallway scale.
•Determining the source of the androgen excess.
•Ruling out the rare but potentially life -threatening causes.

19. Physical examination will reveal the severity of the hirsutism, signs of
virilization, and other associated endocrine disorders. The Ferriman–
Gallwey scoring system assesses the severity of hirsutism and is used to
analyse response to treatment. A modified Ferriman–Gallwey, scores
the degree of hirsutism from nine androgen-sensitive body sites
including chin, upper lip, mid-line hair between the breasts, upper and
lower abdomen. A score of 8 or more is considered abnormal. It is
important to consider racial and ethnic differences when determining
what is truly excessive hair growth.

20. TheFerriman–Gallwey scoreis a method of evaluating and quantifyinghirsutismin
women. The method was originally published in 1961 by D. Ferriman
The original method used 11 body areas to assess hair growth, but was decreased to 9
body areas in the modified method: UpperlipChinChestUpperbackLower back
UpperabdomenLower abdomen UpperarmsForearms(deleted in the modified method)
ThighsLegs(deleted in the modified method)
In the modified method, hair growth is rated from 0 (no growth ofterminal hair) to 4
(extensive hair growth) in each of the nine locations. A patient's score may therefore range
from a minimum score of 0 to a maximum score of 36. With each ethnic group, the amount
of hair expected for that ethnicity should be considered. For example,
inCaucasianwomen, a score of 8 or higher is regarded as indicative ofandrogenexcess.
The method was further modified in 2001 to include a total of 19 locations, with the 10
extra locations
being:sideburns,neck,buttocks,inguinalarea,perianalarea,forearm,leg,foot,toesandfi
ngers. Each area has its own specified definition of the four-point scale.
[

21. The modifiedFerriman–Gallwey score

22. Investigations
Initial laboratory investigation
1.Total testosterone:
measures the ovarian & adrenal activity.
2.17 OHP:
an intermediate metabolite in steroidogensisin the adrenals.
DHEAS:
Good marker of Adrenal androgen production
Not essential

24. Evaluation of accompanying
medical disorders:
Ovulation disorder :FSH,LH
Thyroid dysfunction:TSH
Hyperprolactinemia :PRL

25. Treatment
I. General
II. Specific
III. Local
IV. Surgery

27. I. General
•Weight reduction: the greater the weight and longer the time of
excess fat tissue, then greater the hyperandrogenismand hirsutism.
The hyperinsulinemia associated with obesity is associated with
stimulation of ovarian and adrenal androgen production.Obesity
also lowers SHBG levels and thereby increases the levels of
unbound, bio-active testosterone. Additionally,obesityis associated
with increased production rates of testosterone,
dihydrotestosterone, and the peripheral marker of androgen
activity,
•Stop smoking

28. II. Specific
I. Ovarian suppression:
1. OCPs 2. Progestagen 3. GnRha
II. Adrenal suppression: Corticosteroids
III. Antiandrogens:
1. Spironolactone 2. Cyproteroneacetate
3. Flutamide 4. Ketoconazole
IV. 5 alpha reductaseinhibitors: Finasteride
V.Insulin sensitizer: Metformin

29. 1. Oral contraceptive pills
Popular treatments for hirsutism:
Mechanism of action: Oral contraceptives (OCs) are the first line of
treatment for hirsutism and other hyperandrogenicconditions,
regardless of whether or not androgens are elevated.
OCs suppress ovarian production of testosterone (50%)
and adrenal DHEAS production (30%), increase SHBG
(thus decreasing free, bio-active testosterone), and
inhibit 5α-reductase activity (which decreases target tissue
androgen activity).

32. 2.Antiandrogen
A.Cyproteroneacetate (androcure)
Mechanism:
Dianetteis a special combined oral
contraceptive pill that contains 2mg
cyproteroneacetate.

33. B.Spironolactone:
Is an oral aldosterone antagonist with anti-androgenic properties.
a peripheral blocker of androgen activity, such as spironolactone,
improves the clinical response. Spironolactone may inhibit
steroidogenesis; its primary effectiveness lies in its peripheral
androgen-blocking ability. Spironolactone is an excellent inhibitor of
the androgen receptor in the peripheral compartment. Reports suggest
that spironolactone couples with the receptor to create a biologically
inactive complex. Additionally, spironolactone also inhibits 5α-
reductase activity and increases the clearance of testosterone. Some
patients complain of irregular bleeding or spotting after treatment.

34. C.Flutamideis a potent nonsteroidal compound that inhibits the androgen
receptor. At high doses, it may decrease androgen synthesis or increase its
metabolism.Itis necessary to monitor liver enzymes while using this product.
Therapeutically, it has an effect similar to that seen with spironolactone
treatment.
5ALFA REDUCTASE INHIBITOR
.Finasteride inhibits 5α-reductase activity and is approved for use in men for
prostatic hypertrophy or male-pattern baldness. It is effective in treating hirsute
women and results are often evident by 6 months. Side effects in women are
minimal.
.Ketoconazole, technically an antifungal agent, blocks the synthesis of androgens
through the suppression of P450-dependent ovarian and adrenal enzymes.
Treatment results in a reduction of serum testosterone levels and,increasesin
hydroxyprogesteronelevels

35. cream is the first topical prescription treatment to be approved by the US FDA for the reduction of unwanted facial hair in women. It irreversibly inhibits ornithine decarboxylase (ODC), an enzyme that catalyzes the rate-limiting step for follicular polyamine synthesis, which is necessary for hair growth. In clinical trials eflornithine cream slowed the growth of unwanted facial hair in up to
EflornithineHydochloride(Vaniqa)
EflornithineHCl13.9% cream is the first topicalprescription
treatment to be approved by the US FDA for the reduction of
unwanted facial hair in women.


38. 1. The most desirable & effective treatment is combination of OCP &
antiandrogen.
2. Response is relatively slow, & at least 6 months are required to
demonstrate an improvement.
3.Treatment should be continued for at least 1-2 yr.
Guidelines for management

39. To summarize:
●Polycystic ovarian syndrome is one of the most common causes of
hirsutism.
●Weight loss in obese patients may improve hirsutism.
●Virilismusually indicates significant pathology.
●The oral contraceptive pill is the most commonly used single
therapy for hirsutism.

40. References and recommended further readings:
•GYNAECOLOGY 20th EDITION by Ten Teachers
•Hacker & Moore’s Essentials of Obstetrics and Gynecology6
th
2016
•Dewhurst's Textbook of Obstetrics & Gynaecology, 9th Edition
November 2018