📋 Key Information Summary
- Hirsutism is defined as excessive terminal hair growth in androgen-sensitive areas in women, following a male-pattern distribution, affecting approximately 5–10% of Australian women of reproductive age.
- Polycystic ovary syndrome (PCOS) accounts for 70–80% of hirsutism cases and must be evaluated in every patient presenting with excess androgenic hair growth.
- The modified Ferriman–Gallwey (mFG) score ≥8 is the standard threshold for clinical hirsutism; scores ≥8 warrant full endocrine investigation.
- Initial investigations include total testosterone, sex hormone-binding globulin (SHBG), free androgen index (FAI), 17-hydroxyprogesterone, thyroid function, and prolactin.
- Total testosterone >5 nmol/L or DHEA-S >twice the upper limit of normal should prompt urgent investigation for androgen-secreting tumours.
- First-line pharmacotherapy for hirsutism in PCOS is a combined oral contraceptive pill (COCP) — ethinyloestradiol/cyproterone acetate or ethinyloestradiol/drospirenone are preferred in Australia.
- Spironolactone 100–200 mg daily is the most effective anti-androgen adjunct; it is PBS-listed for this indication and should be used with reliable contraception.
- Topical eflornithine 13.9% (Vaniqa®) is PBS Authority Required and provides adjunctive facial hair reduction when combined with hormonal therapy.
- Pharmacotherapy requires a minimum 6-month trial before efficacy can be assessed; hair growth cycles dictate that visible improvement takes 4–6 months.
- Mechanical and cosmetic therapies (laser hair removal, electrolysis, waxing) complement pharmacotherapy but do not address the underlying cause.
- Non-classic congenital adrenal hyperplasia (NCCAH) due to 21-hydroxylase deficiency must be excluded with a morning 17-hydroxyprogesterone level; prevalence is 1–2% of the general population and 5–10% among women with hirsutism.
- Aboriginal and Torres Strait Islander women have a higher prevalence of PCOS and metabolic syndrome, requiring earlier metabolic screening and culturally safe management approaches.
🎧 Audio Brief
Introduction & Australian Epidemiology
Hirsutism is the excessive growth of terminal hair in androgen-sensitive areas in women, following a male-pattern distribution. It results from the interaction of circulating androgens with hair follicle 5α-reductase activity, converting testosterone to the more potent dihydrotestosterone (DHT). Hirsutism must be distinguished from hypertrichosis, which is generalised excess vellus hair growth not androgen-dependent.
In Australia, hirsutism affects approximately 5–10% of women of reproductive age, with the prevalence varying by ethnicity. Women of Mediterranean, Middle Eastern, and South Asian descent are more likely to present due to both a higher biological predisposition and greater psychosocial impact. Aboriginal and Torres Strait Islander women have a higher prevalence of PCOS and associated metabolic risk factors.
The condition carries significant psychosocial burden, with studies demonstrating increased rates of anxiety, depression, and impaired quality of life comparable to those seen in chronic dermatological conditions. Many patients delay seeking medical advice for years, having normalised the condition or been reassured inappropriately.
Clinical alert: Sudden-onset rapidly progressive hirsutism with virilisation (deepening voice, clitoromegaly, male-pattern baldness) should prompt urgent investigation for an androgen-secreting tumour, even in younger women. Urgent endocrine referral is required.
Aetiology & Pathophysiology
Mechanism of Androgen-Mediated Hair Growth
Hair follicles in androgen-sensitive areas (face, chest, abdomen, back, upper arms, thighs) respond to circulating androgens — principally testosterone and DHT. In the hair follicle, testosterone is converted to DHT by type 2 5α-reductase. DHT binds to the androgen receptor, stimulating vellus-to-terminal hair conversion and increasing the duration of the anagen (growth) phase. The clinical expression of hirsutism depends on the balance between circulating androgen levels, local 5α-reductase activity, and individual genetic sensitivity.
Causes of Hirsutism
| Category | Conditions | Approximate Frequency |
|---|---|---|
| Ovarian | PCOS (most common), ovarian hyperthecosis, androgen-secreting ovarian tumours (thecoma, Sertoli–Leydig cell tumour) | 70–80% |
| Adrenal | Non-classic congenital adrenal hyperplasia (21-hydroxylase deficiency), Cushing syndrome, adrenal carcinoma, adrenal adenoma | 5–10% |
| Iatrogenic / Exogenous | Anabolic steroids, danazol, valproate, testosterone, ciclosporin, phenytoin, minoxidil | 5–10% |
| Idiopathic | Normal androgen levels, increased peripheral sensitivity; often familial | 5–15% |
PCOS — The Predominant Cause
PCOS accounts for 70–80% of hirsutism presentations. The pathophysiology involves a self-perpetuating cycle of:
- LH hypersecretion and increased LH:FSH ratio driving ovarian androgen production
- Insulin resistance and compensatory hyperinsulinaemia — insulin acts as a co-gonadotrophin on ovarian theca cells and suppresses hepatic SHBG production, increasing free testosterone
- Reduced SHBG leading to a higher free androgen index (FAI)
- Adrenal androgen excess (DHEA-S) in approximately 20–30% of PCOS patients
- Central adiposity amplifying insulin resistance through adipokine-mediated pathways
The Rotterdam criteria (2003) define PCOS as two of three: oligo-anovulation, clinical and/or biochemical hyperandrogenism, and polycystic ovarian morphology on ultrasound — after exclusion of other causes.
Non-Classic Congenital Adrenal Hyperplasia (NCCAH)
NCCAH due to partial 21-hydroxylase deficiency (CYP21A2 mutations) is present in 1–2% of the general population and 5–10% of women presenting with hirsutism. It is inherited in an autosomal recessive manner. Impaired cortisol synthesis leads to ACTH-driven adrenal androgen overproduction. A morning 17-hydroxyprogesterone level >30 nmol/L (or >45 nmol/L post-Synacthen stimulation) is diagnostic.
Idiopathic Hirsutism
Defined as hirsutism with normal ovulatory function and normal circulating androgen levels. This likely reflects increased peripheral 5α-reductase activity or enhanced androgen receptor sensitivity. It tends to be familial and is a diagnosis of exclusion.
Clinical Assessment & Investigations
History
A thorough history should include:
- Onset and progression: Gradual onset since puberty suggests PCOS or idiopathic hirsutism; rapid onset or progression over months raises concern for neoplasm
- Menstrual history: Oligomenorrhoea, amenorrhoea, or irregular cycles suggest anovulation (PCOS)
- Virilisation features: Deepening of voice, clitoromegaly, temporal recession, increased muscle bulk — any feature warrants urgent investigation
- Medication review: Anabolic steroids (including concealed use), valproate, danazol, testosterone therapy
- Family history: PCOS, type 2 diabetes, premature adrenarche, NCCAH
- Weight history and metabolic symptoms: Central obesity, acanthosis nigricans (insulin resistance marker), gestational diabetes
- Fertility goals: Influences management approach and urgency
- Psychosocial impact: Assess using validated tools where available; many patients minimise distress
Modified Ferriman–Gallwey Score
The modified Ferriman–Gallwey (mFG) scoring system is the gold standard for objectively grading hirsutism. Nine androgen-sensitive body areas are scored from 0 (no terminal hair) to 4 (frankly virile), yielding a total score of 0–36.
mFG scoring areas: Upper lip, chin, chest, upper back, lower back, upper abdomen, lower abdomen, upper arm, thigh. A score ≥8 is the accepted threshold for clinical hirsutism in most populations; some clinicians use ≥6 for women of East Asian descent.
Examination
- Calculate the mFG score systematically
- Assess for acanthosis nigricans (neck, axillae, groin) — a marker of insulin resistance
- Check for signs of Cushing syndrome: moon face, buffalo hump, striae, central obesity, proximal myopathy
- Palpate thyroid — goitre may indicate thyroid dysfunction
- Assess body habitus, BMI, waist circumference (metabolic risk)
- Examine for clitoromegaly (clitoral index >35 mm²) and temporal hair recession
- Assess galactorrhoea (hyperprolactinaemia)
Investigations
Essential
Total testosterone
Collect AM fasting sample. >5 nmol/L warrants urgent investigation for androgen-secreting tumour. MBS item 66720.
Essential
Sex hormone-binding globulin (SHBG)
Low in PCOS (suppressed by hyperinsulinaemia). Used to calculate FAI. MBS item 66720.
Essential
Free androgen index (FAI)
FAI = (total testosterone ÷ SHBG) × 100. FAI >5% indicates biochemical hyperandrogenism. Derived calculation.
Essential
17-hydroxyprogesterone (17-OHP)
Morning sample (follicular phase preferred). >30 nmol/L diagnostic of NCCAH; 5–30 nmol/L requires Synacthen stimulation test. MBS item 66720.
Available
DHEA-S
Elevated in adrenal androgen excess. >twice ULN raises concern for adrenal carcinoma. MBS item 66720.
Available
Thyroid function (TSH, free T4)
Hypothyroidism increases SHBG reduction and may exacerbate hirsutism. MBS item 66710.
Available
Prolactin
Hyperprolactinaemia may cause menstrual irregularity mimicking PCOS. MBS item 66720.
Available
Fasting glucose, insulin, HbA1c, lipid panel
Metabolic screening essential if PCOS suspected. OGTT preferred for PCOS. MBS items 66490, 66500, 66555.
Referral
Pelvic ultrasound
Transvaginal preferred (transabdominal if not sexually active). Polycystic morphology = ≥20 follicles per ovary or ovarian volume >10 mL (using updated 2018 IOTA criteria). MBS item 55034.
Specialist
ACTH stimulation test (Synacthen test)
250 µg IV Synacthen; 17-OHP at 60 minutes. Stimulated 17-OHP >45 nmol/L confirms NCCAH. Endocrine referral required.
Specialist
Adrenal and/or ovarian imaging
CT adrenals and/or pelvic MRI when total testosterone >5 nmol/L or DHEA-S >twice ULN. Urgent endocrine or gynaecological oncology referral.
Red flags for androgen-secreting tumour — urgent endocrine referral:
• Total testosterone >5 nmol/L
• DHEA-S >twice the upper limit of normal
• Rapid onset or rapidly progressive hirsutism (<1 year)
• Any virilisation (clitoromegaly, voice deepening, temporal recession)
• Postmenopausal new-onset hirsutism
• Total testosterone >5 nmol/L
• DHEA-S >twice the upper limit of normal
• Rapid onset or rapidly progressive hirsutism (<1 year)
• Any virilisation (clitoromegaly, voice deepening, temporal recession)
• Postmenopausal new-onset hirsutism
Differential Diagnosis
It is essential to distinguish hirsutism from hypertrichosis (generalised non-androgen-dependent hair growth) and to identify the underlying cause of true hirsutism.
Hirsutism vs Hypertrichosis
| Feature | Hirsutism | Hypertrichosis |
|---|---|---|
| Hair type | Terminal (dark, coarse) | Vellus or lanugo (fine, may be pigmented) |
| Distribution | Androgen-dependent (male pattern) | Non-androgen-dependent areas (forearms, legs, back) |
| Cause | Androgen excess or increased sensitivity | Drugs (phenytoin, ciclosporin, minoxidil), thyroid, anorexia, porphyria, familial |
| Androgens | Often elevated | class="guideline-td">Normal
Differential Diagnosis by Androgen Level
| Pattern | Differential | Key Distinguishing Features |
|---|---|---|
| Normal androgens | Idiopathic hirsutism | Normal menses, normal androgens, diagnosis of exclusion; familial |
| Hypertrichosis | Non-androgen distribution; consider drug causes | |
| Mild androgen elevation | PCOS | Oligomenorrhoea, polycystic ovaries, insulin resistance, acanthosis nigricans |
| NCCAH | Elevated 17-OHP, similar phenotype to PCOS, family history of consanguinity | |
| Moderate elevation | Cushing syndrome | Central obesity, striae, proximal myopathy, moon face, easy bruising |
| Classic CAH (late-onset) | Very high 17-OHP, ambiguous genitalia in neonates (if severe) | |
| Marked elevation | Ovarian tumour (thecoma, Sertoli–Leydig) | Rapid onset, virilisation, pelvic mass on examination or imaging |
| Adrenal carcinoma | Very high DHEA-S, abdominal mass, rapid onset virilisation, Cushingoid features | |
| Ovarian hyperthecosis | Postmenopausal, marked hyperandrogenism, insulin resistance |
Investigations to Exclude Differential Diagnoses
- Cushing syndrome: 24-hour urinary free cortisol, late-night salivary cortisol, or 1 mg overnight dexamethasone suppression test. If positive, proceed to low-dose dexamethasone suppression and ACTH level.
- Prolactinoma: Serum prolactin; if elevated, MRI pituitary with contrast.
- Acromegaly: IGF-1 level if clinical features present (coarse features, prognathism, carpal tunnel).
- Thyroid dysfunction: TSH and free T4.
- Drug-induced: Comprehensive medication review including supplements and over-the-counter products.
Treatment
Treatment of hirsutism involves a dual approach: (1) pharmacological suppression of androgen production/action, and (2) mechanical/cosmetic hair removal. Optimal outcomes require both modalities. Patients must understand that pharmacotherapy takes a minimum of 6 months to demonstrate effect due to the hair growth cycle.
Contraception requirement: All anti-androgen therapies (spironolactone, cyproterone, finasteride) are teratogenic. Reliable contraception must be confirmed before initiating therapy. Spironolactone can cause feminisation of a male foetus.
Pharmacological Therapy — First-Line
Ethinylestradiol / Cyproterone acetate
Estelle-35® · Diane-35® · Anti-androgen COCP
Adult dose
Ethinylestradiol 35 µg / Cyproterone acetate 2 mg daily for 21 days per cycle. Can be used as 35 µg/2 mg standard or higher-dose CPA regimen under specialist guidance.
Mechanism
Suppresses LH-driven ovarian androgen production; increases SHBG; CPA directly blocks androgen receptor.
Key side effects
VTE risk (relative risk ~1.5–2× baseline), mood changes, headache. Avoid with migraine with aura, age >35 + smoking, high BMI.
Duration
Minimum 6 months; typically 12–24 months or ongoing.
PBS status
✔ PBS General Benefit
Ethinylestradiol / Drospirenone
Yaz® · Yasmin® · Anti-mineralocorticoid COCP
Adult dose
EE 20 µg (Yaz) or 30 µg (Yasmin) / Drospirenone 3 mg daily for 21 days.
Mechanism
Drospirenone has anti-androgenic and anti-mineralocorticoid activity; reduces free testosterone via SHBG increase.
Advantages
Lower VTE risk than CPA-containing COCPs; anti-oedema effect; favourable metabolic profile in PCOS.
PBS status
✔ PBS General Benefit
Pharmacological Therapy — Second-Line / Adjunctive
Spironolactone
Aldactone® · Spiractin® · Aldactone® · Anti-androgen
Adult dose
Start 50 mg PO daily; titrate to 100–200 mg daily in divided doses. Maximum 200 mg/day.
Mechanism
Competitive androgen receptor antagonist; reduces ovarian androgen production; inhibits 5α-reductase.
Key side effects
Menstrual irregularity (combine with COCP), hyperkalaemia (monitor at 1 month, 3 months, then annually), dizziness, breast tenderness.
Renal adjustment
Avoid if eGFR <30 mL/min. Monitor potassium if eGFR 30–60.
Contraception
MANDATORY — teratogenic (anti-androgen effect on male foetus).
PBS status
✔ PBS General Benefit
Finasteride
Proscar® · Generic · 5α-reductase inhibitor
Adult dose
5 mg PO daily. Off-label for hirsutism; used when spironolactone contraindicated.
Mechanism
Type 2 5α-reductase inhibitor; reduces conversion of testosterone to DHT.
Contraception
MANDATORY — teratogenic (inhibits male foetal genital development).
PBS status
⚠ PBS — Authority (for BPH only; off-label use not PBS-subsidised for hirsutism)
Metformin
Diabex® · Glucophage® · Insulin sensitiser
Adult dose
Start 500 mg PO daily with meals; titrate over 2–4 weeks to 1000 mg BD (max 2000–2500 mg/day).
Role
Modest effect on hirsutism alone; primarily for metabolic management in PCOS (improves insulin sensitivity, ovulation). Consider as adjunct if BMI >25 or glucose intolerance.
Key side effects
GI disturbance (minimised by slow titration and taking with food), B12 deficiency with long-term use.
PBS status
✔ PBS General Benefit
Eflornithine hydrochloride 13.9%
Vaniqa® · Topical anti-androgen
Adult dose
Apply thin layer to affected facial areas BD. Wait at least 4 hours between applications. Not for use near eyes or mucous membranes.
Mechanism
Inhibits ornithine decarboxylase in hair follicle, slowing hair growth. Does not remove existing hair.
Efficacy
Reduces facial hair growth by ~30% at 24 weeks; most effective combined with hormonal therapy. Hair growth returns upon cessation.
PBS status
🔴 PBS Authority Required — for facial hirsutism where hormonal therapy is contraindicated or as adjunct
Treatment Algorithm
1
Identify & Treat Underlying Cause
Exclude NCCAH, Cushing, tumours. Treat PCOS metabolic features. Discontinue causative medications.
2
First-Line Hormonal Therapy
COCP (EE/CPA or EE/drospirenone). If COCP contraindicated, consider spironolactone alone (with contraception).
3
Add Anti-Androgen at 6 Months
If inadequate response to COCP alone, add spironolactone 100–200 mg/day (most evidence-based combination).
4
Adjunctive Topical & Cosmetic
Eflornithine 13.9% for facial hair. Refer for laser hair removal or electrolysis. Combine mechanical + pharmacological.
5
Review at 6-Month Intervals
Reassess mFG score, metabolic parameters, side effects, and quality of life. Adjust regimen as needed.
Mechanical & Cosmetic Therapies
Cosmetic measures should be offered to all patients alongside pharmacotherapy, as they provide immediate improvement while drug therapy takes effect.
| Method | Mechanism | Suitable Areas | Notes |
|---|---|---|---|
| Laser hair removal | Selective photothermolysis of melanin in hair follicle | All areas; most effective on dark hair / lighter skin (Fitzpatrick I–III) | Multiple sessions (6–10) required. Nd:YAG laser preferred for darker skin types. Not PBS-funded. Reduces hair by 50–80%. |
| Electrolysis | Thermolysis or galvanic current destroys individual follicles | Small areas (face, chin) | Only truly permanent method. Slow (individual follicles). Operator-dependent. Not PBS-funded. |
| Waxing / Threading | Mechanical epilation | Face, body | Temporary; regrowth in 2–6 weeks. May cause folliculitis or irritation. |
| Shaving | Cuts hair at skin surface | All areas | Does not worsen hair growth (myth). Convenient but requires daily maintenance. |
| Depilatory creams | class="guideline-td">Chemical dissolution of hair shaft (thioglycolate)Body (avoid face if sensitive) | Temporary; may cause irritation. Trial on small area first. | |
| Bleaching | Lightens hair colour | Face, arms | Does not reduce growth; reduces visibility. Simple and inexpensive. |
Special Populations
Pregnancy
All anti-androgens CONTRAINDICATED
COCP, spironolactone, finasteride, eflornithine — all contraindicated in pregnancy. Spironolactone causes feminisation of male foetus. Finasteride inhibits DHT essential for male genital development.
Safe options
Mechanical hair removal only (shaving, waxing, threading). Hair growth may worsen physiologically due to pregnancy-related androgen changes — this often resolves postpartum.
Pre-conception counselling
Stop anti-androgens ≥1 month before planned conception. Ensure metabolic optimisation (weight, glucose) pre-conception if PCOS.
Paediatrics & Adolescents
Premature adrenarche
Pubic/axillary hair before age 8 in girls. Usually benign; monitor for progression to PCOS (20–30% risk). Investigate if virilisation, rapid progression, or bone age advance >2 SD.
Adolescent hirsutism
Use mFG adjusted for age and pubertal stage. COCP may be considered post-menarche for menstrual regulation + anti-androgen effect. Avoid spironolactone in <18 unless specialist-directed.
Congenital adrenal hyperplasia
Classic CAH presents neonatally (ambiguous genitalia in 46,XX). Managed with hydrocortisone ± fludrocortisone under paediatric endocrinology.
Postmenopausal Women
New-onset hirsutism
Higher index of suspicion for androgen-secreting tumour (ovarian or adrenal). Urgent investigation with total testosterone, DHEA-S, and imaging.
Ovarian hyperthecosis
Benign condition causing gradually increasing hyperandrogenism postmenopause. Markedly elevated testosterone (5–15 nmol/L). Diagnosed by exclusion of tumour. Treated with spironolactone.
COCP contraindicated
Use spironolactone or finasteride as primary anti-androgen therapy (no contraception required postmenopause).
Renal Impairment
Spironolactone
Avoid if eGFR <30 mL/min. If eGFR 30–60: use lower doses (25–50 mg/day), monitor potassium closely (1 week, 1 month, then quarterly).
Metformin
Reduce dose if eGFR 30–45 (max 1000 mg/day). Discontinue if eGFR <30.
Finasteride
No dose adjustment required. Excreted hepatically.
Hepatic Impairment
COCP contraindicated
In significant hepatic impairment (Child–Pugh B or C). Mild hepatic steatosis common in PCOS does not contraindicate COCP.
Spironolactone
Hepatically metabolised; use with caution. Monitor for gynaecomastia. No specific dose adjustment guidelines.
Immunocompromised
Drug-induced hirsutism
Ciclosporin, tacrolimus, androgen-containing immunotherapies may cause hirsutism. Consider switching immunosuppressant if hirsutism is severe and alternative agent available.
Laser therapy
May be less effective or contraindicated if on photosensitising medications. Specialist dermatology advice recommended.
Aboriginal and Torres Strait Islander Health
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander women have a higher prevalence of PCOS, metabolic syndrome, type 2 diabetes, and cardiovascular disease compared to non-Indigenous Australians. Hirsutism in this population may be more common and more severe, with earlier onset and greater metabolic comorbidity. Culturally safe, patient-centred care is essential.
Monitoring & Follow-Up
Monitoring Schedule
Baseline
Full hormonal panel, metabolic screen (FBG, lipids, HbA1c or OGTT), BMI, waist circumference, mFG score. Document photography for comparison.
1 month
If spironolactone commenced: check serum potassium and creatinine. Assess tolerability and side effects.
3 months
Repeat potassium if spironolactone dose changed. Assess adherence and early response. Address cosmetic concerns.
6 months
Reassess mFG score. Assess treatment efficacy: if <25% improvement, consider dose optimisation or adding second agent. Repeat metabolic screen.
12 months
Comprehensive review: mFG score, metabolic parameters, quality of life, contraception adequacy. Consider step-down if well controlled.
Ongoing
6–12 monthly review. Annual metabolic screening in PCOS. Annual potassium monitoring if on spironolactone long-term.
When to Refer
- Urgent endocrine referral: Total testosterone >5 nmol/L, DHEA-S >twice ULN, virilisation features, rapid-onset hirsutism
- Routine endocrine referral: Suspected NCCAH (equivocal 17-OHP), suspected Cushing syndrome, failed first-line therapy at 12 months
- Gynaecology referral: Fertility concerns in PCOS, ultrasound findings suggesting ovarian pathology
- Dermatology referral: Specialist laser or electrolysis, complex skin-type considerations, refractory hirsutism
- Psychology referral: Significant psychological distress, body dysmorphic features, depression/anxiety related to hirsutism
Quick Reference — Investigation Interpretation
Normal testosterone, normal menses
Idiopathic hirsutism
COCP + cosmetic ± spironolactone
Diagnosis of exclusion
Elevated FAI, oligomenorrhoea
PCOS (most likely)
COCP ± spironolactone ± metformin
OGTT, lipids, USS pelvis
Elevated 17-OHP >30 nmol/L
Non-classic CAH
COCP ± low-dose prednisolone if refractory
Genetic counselling re: family planning
Testosterone >5 nmol/L or DHEA-S >2× ULN
? Androgen-secreting tumour
URGENT imaging + endocrine referral
CT adrenals, pelvic MRI, urgent surgery if confirmed
Clinical Cushing features
? Cushing syndrome
UFC, LNSC, 1 mg DST → endocrine referral
Source: pituitary, adrenal, ectopic
📚 References
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- 3. Teede HJ, Misso ML, Costello MF, et al. Recommendations from the international evidence-based guideline for the assessment and management of polycystic ovary syndrome. Human Reproduction. 2018;33(9):1602–1618.
- 4. Royal Australian College of General Practitioners (RACGP). General practice management of type 2 diabetes: 2016–2018. East Melbourne: RACGP; 2016.
- 5. Australian Institute of Health and Welfare (AIHW). Polycystic ovary syndrome (PCOS) in Australia. Cat. no. PHE 277. Canberra: AIHW; 2020.
- 6. Escobar-Morreale HF. Polycystic ovary syndrome: definition, aetiology, diagnosis and treatment. Nature Reviews Endocrinology. 2018;14(5):270–284.
- 7. Somani N, Turvy D. Hirsutism: an evidence-based treatment update. American Journal of Clinical Dermatology. 2014;15(3):229–239.
- 8. Yildiz BO, Bolour S, Woods K, et al. Visually scoring hirsutism. Human Reproduction Update. 2010;16(1):51–64.
- 9. Australasian College of Dermatologists. Position statement: laser and light-based therapies. Sydney: ACD; 2022.
- 10. National Aboriginal Community Controlled Health Organisation (NACCHO). Framework for the delivery of Aboriginal and Torres Strait Islander primary health care. Canberra: NACCHO; 2023.
- 11. Pharmaceuticals Benefits Scheme (PBS). PBS Schedule: spironolactone, eflornithine, combined oral contraceptives. Australian Government Department of Health. Accessed 2024. Available at: pbs.gov.au.
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