Approach to Hirsutism and

Oligomenorrhea

Alice Y.Y. Cheng, MD, FRCPC

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Learning Objectives

By the end of this presentation, you will

be able to:

1. List the red flags of oligomenorrhea

and hirsutism

2. Discuss appropriate treatment options

for oligomenorrhea and hirsutism

Hirsutism

Martin KA et al. JCEM 2008;93:1105-1120.

Hirsutism

• Excessive hair growth in women in typically

androgenic areas (terminal hairs)

• 5-10% of women

• Increased androgens or increased sensitivity to

androgens

• Ferriman-Gallway score (FGS)

• FGS > 8 in Caucasion women = abnormal

• May be higher/lower in other ethnicities (Thai

>3)

Ferriman-Galway score

Non-midline hair less androgen-dependent. Best discriminator is

combination of upper lip, moustache, lower abdomen and thighs

Causes of Hirsutism

• Polycystic ovarian syndrome (60%)

• Idiopathic (38%)

• Other (2-3%)

– Drugs (androgens)

– Congenital adrenal hyperplasia (non-classical)

– Ovarian tumours

– Hyperthecosis of ovaries

– Adrenal tumours

– Severe insulin resistance syndromes

PCOS

• National Institutes of Health

– Oligo-ovulation

– Androgen excess (clinical or biochem)

– Exclude other diseases

Clinical Evaluation:

RED FLAGS

• Rule out the BAD THINGS = ovarian / adrenal tumor

• Early onset

• Rapid progression

• Virilization

– Voice change

– Change in body build

– Clitoromegaly

– Frontal balding

Clinical Evaluation: HISTORY

• Hirsutism details:

– Onset, progression, location, severity

• Associated features:

– alopecia, acne, virilization, Cushingoid

• Menstrual history

• Weight history

• Medication history

• Family history

– diabetes, PCOS, hirsutism

• Ethnicity

Clinical Evaluation: PHYSICAL

Vellous

Terminal

Acanthosis nigricans

Ferriman-Galway score

Non-midline hair less androgen-dependent. Best discriminator is

combination of upper lip, moustache, lower abdomen and thighs

Clinical Evaluation: PHYSICAL

• Weight

• Insulin resistance

– acanthosis nigricans, skin tags

• Virilization

– acne, oily skin, alopecia, voice, hair, muscle bulk,

clitoromegaly

• True hirsutism?

– Vellous vs Terminal

Clinical Evaluation: LABS

• Not ALL women require lab testing

• Total testosterone (normal < 2.8 nmol/L) (M > 11)

– Very high androgen-secreting tumour or ovarian

hyperthecosis?

– Normal to mild elevation PCOS or idiopathic?

• DHEA-S

– If very high … consider adrenal tumour

• Select cases:

– FSH (estrogen deficiency states)

– LH (may be high in PCOS)

– Prolactin

– 17-OH progesterone

Clinical Evaluation: IMAGING

• Only if you suspect an ovarian or

adrenal tumour

Martin KA et al. JCEM 2008;93:1105-1120.

Hirsutism - Treatment

• Discussion of “patient-imporant hirsutism”, goals, realistic expectations

• Local strategies may be perfectly adequate

– Waxing, threading, bleaching

– Laser and electrolysis +/- eflornithine cream (Vaniqa)

• Systemic treatment- only effective while taking

• Combining anti-androgens with local methods gives most effective control

Systemic Therapy

Oral Contraceptive Lowest to highest Androgen action (American Hair Loss Association):

• eliminates ovarian

androgen production

• raises SHBG which

reduces free testosterone

• androgenic progestin

• Yasmin (Drospirenone)

• Yaz (Drospirenone)

• Desogen (desogestrol)

• Ortho-Cept (desigestrol)

• Ortho-Cyclen (norgestimate)

• Ortho Tri-Cyclen

• Micronor (norethisterone)

• Nor-Q D

• Ovcon-35 (Norethisterone)

• Brevicon/Modicon

• Ortho Norvum 7/7/7

• Ortho Novum 10-11

• Tri-Norinyl

• Norinyl and Ortho 1/35

• Demulen 1/35 (ethynodiol diacetate)

• Triphasil/Tri-Levien (levonorgestrel)

• Nordette

• Lo/Ovral

• Ovrette

• Ovral

• Loestrin 1/20 (Norethidrone)

• Loestrin 1.5/30

Systemic Therapy

• ANTI-ANDROGEN

– Spironolactone 100-200 mg/d (divided BID)

– Cyproterone acetate 50-100 mg/d on menstrual cycle day 5-15, dose reduction after effect seen

– Finasteride (5a reductase inhibitor) 2.5-5 mg/day

• Only as ADD-ON to OCP

• Give at least SIX MONTHS before re-evaluating

Martin KA et al. JCEM 2008;93:1105-1120.

Summary

• Hirsutism vs Hypertrichosis

• Look for red flags

• May not require labs

• Androgens can be helpful

• Local, systemic, combination therapy

• Takes time to take effect

• Manage expectations

Oligomenorrhea /

Secondary amenorrhea

Learning Objectives

By the end of this presentation, you will

be able to:

1. Recite the common causes

2. Describe appropriate investigations

3. Utilize common treatments

Oligomenorrhea /

Secondary Amenorrhea

• OLIGOMENORRHEA:

– >35 day cycles

• SECONDARY AMENORRHEA

– Absence of menses for >3 cycles or 6 months

in women who previously had menses

Causes (categories)

• Pregnancy most common cause (20

amenorrhea)

• Ovarian — 40 %

• Hypothalamic — 35 %

• Pituitary — 19 %

• Uterine — 5 %

• PCOS (Polycystic ovarian syndrome) • Ovulatory dysfunction

• Clinical (acne, hirsutism, alopecia) or biochemical evidence of hyperandrogenism

• Exclusion of other diagnoses

• Premature ovarian failure (< 40y)

• Turner syndrome, Fragile X

• Autoimmune

• Radiation / chemo

• Infection

Differential Diagnosis – Ovary

Differential Diagnosis –

Hypothalamus

• Functional

– Stress, exercise, anorexia, chronic illness

• Tumours

• Infiltrative diseases

– Histiocytosis, sarcoid, hemochromatosis

• Brain injuries

• Genetic syndromes

– Usually primary amenorrhea

Differential Diagnosis –

Pituitary

• Prolactinoma – 90%

• Hypopituitarism• Adenoma, tumour

• Infiltrative, inflammation

• Radiation

• Postop

• Apoplexy/Infarction

• Sheehan’s syndrome

• Empty sella

Differential Diagnosis –Uterine

• Usually primary amenorrhea

• Asherman’s syndrome is the only uterine

cause of secondary amenorrhea

– Endometrial scarring – D&C, post-partum

hemorrhage, infection

– No uterine stripe on pelvic ultrasound

– No withdrawal bleed post estrogen and

progestin

General Approach

• Rule out pregnancy

• Rule out Asherman’s syndrome: • Previous instrumentation, D&C, uterine hemorrhage,

infection etc

• Once above excluded then consider • Hypothalamus

• Pituitary

• Ovary

History

• Hypothalamic – Functional, space-

occupying lesion (SOL)

• Pituitary – Galactorrhea, SOL, hormone

excess, hypopituitarism

• Ovarian

– PCOS – androgen excess

– POF – low estrogen, hot flashes,dryness

• Meds, PMH, etc

Physical Examination

• General

• BMI (high – PCOS, low – Functional, illness)

• Cushingoid, acromegalic, cachectic

• Visual fields

• Thyroid

• Galactorrhea

• Skin

• hirsutism, acne, striae, acanthosis nigricans, vitiligo, bruising, etc.

• Routine exam

Investigations

• Beta-HCG

• Pituitary –> LH, FSH, Prolactin

• Ovary –> Estradiol, DHEAS, Testosterone

• Thyroid –> TSH

Investigations

• Progestin withdrawal test

• Provera 10 mg/d x 10 days

• Withdrawal should induce a bleed IF there

is a lining

• Withdrawal bleed = adequate estrogen

• Pelvic imaging as needed

Narrowing it down…

Case A• 18 year old female

• Menarche at 13 yrs. Menses stopped 2y ago

• No hyperandrogenism symptoms

• No diet restriction but heavy exercise

• Low/normal LH & FSH, FSH>LH, low E2

• No withdrawal bleed post progestin

• Dx: Functional Hypothalamic Amenorrhea

(hypogonadotropic hypogonadism)

• Rx: increase calories, decrease exercise, Ca /

Vit D, +/- MRI head

Case B• 36F G2P2

• Menarche at 12.5y

• Regular menses monthly until 6 months ago

when suddenly stopped

• Some breast tenderness, no galactorrhea

• Low LH, FSH, E2

• High Prolactin, normal TSH

• Confirm, r/o secondary causes

• Imaging – MRI, BMD, visual field testing

• Tx: Dopamine agonist

Case C

• 38y F G0P0

• PMH: SLE on Imuran

• Secondary amenorrhea x 9 months

• Hot flashes

• High FSH, low E2

• No withdrawal bleed with progestin

• Hypergonadotropic hypogonadism

• Investigations – karyotype, adrenal

antibodies, BMD

• Tx – HRT / OCP, Ca/Vit D

Case D• 20F, G0P0

• Severe hirsutism over last 6 months

• Voice deepening, body build change

• Very high testosterone DHEAS

• Very high DHEAS and androstenedione

• Suspect virilizing tumour

• Imaging

• Refer for surgery

Take Home Points

• Pregnancy is most common cause

– Beta-hCG in all

• History/Physical usually diagnostic

• Organize approach anatomically

• Think of feedback loops when analyzing

lab results

• Refer appropriately