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Endocrinology
Dermatology
Gynaecology

Hirsutism

High EvidenceUpdated: 2025-12-24

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Red Flags

  • Rapid virilization (deepening voice, clitoromegaly)
  • Severe hirsutism with androgenic alopecia and acne
  • Sudden onset in postmenopausal women
  • Associated with Cushingoid features
Overview

Hirsutism

1. Clinical Overview

Summary

Hirsutism is the excessive growth of terminal hair in women in a male-pattern distribution, affecting 5-15% of women of reproductive age worldwide. It results from increased androgen production, enhanced androgen sensitivity at the hair follicle level, or both. While often idiopathic or associated with polycystic ovary syndrome (PCOS), hirsutism can signal underlying endocrine disorders requiring investigation. The condition causes significant psychological distress, reduced quality of life, and may indicate associated metabolic abnormalities. Treatment combines cosmetic hair removal methods with medical therapy targeting androgen excess or action. [1,2]

Key Facts

  • Definition: Excessive terminal hair growth in androgen-sensitive areas in women.
  • Prevalence: 5-15% of women of reproductive age; higher in certain ethnic groups.
  • Pathophysiology: Androgen-dependent hair follicle stimulation via androgen receptors.
  • Commonest Cause: Polycystic ovary syndrome (60-80% of cases).
  • Scoring: Modified Ferriman-Gallwey score (≥8 indicates hirsutism).
  • Psychological Impact: Significant distress, reduced self-esteem, social withdrawal.
  • Associated Conditions: Insulin resistance, metabolic syndrome, infertility.

Clinical Pearls

The Androgen Threshold: Hair growth occurs when serum testosterone exceeds a threshold (usually >50 ng/dL free testosterone), but individual sensitivity varies.

Ethnic Variations: Mediterranean and Middle Eastern women have higher prevalence; East Asian women have lower androgen sensitivity.

Idiopathic Hirsutism: Accounts for 10-20% of cases with normal androgen levels but increased 5α-reductase activity in hair follicles.

Progression Over Time: Hirsutism often worsens during reproductive years and may improve post-menopause.

Why This Matters Clinically

  • Quality of Life Impact: Significant psychological burden, anxiety, depression.
  • Underlying Pathology: May indicate PCOS, CAH, or androgen-secreting tumors.
  • Metabolic Associations: Links to insulin resistance and cardiovascular risk.
  • Fertility Implications: Often associated with anovulation and infertility.
  • Diagnostic Opportunity: Investigation may reveal treatable endocrine disorders.
  • Treatment Efficacy: Combination therapy can achieve 70-90% improvement.

2. Epidemiology

Global Prevalence

  • Overall: 5-15% of women of reproductive age affected.
  • Age Distribution: Peaks between 18-35 years; rare before puberty or after menopause.
  • Geographic Variation: Higher prevalence in Mediterranean (20-25%) and Middle Eastern populations.
  • Ethnic Differences: Lower in East Asian women due to reduced androgen sensitivity.
  • Urban vs Rural: Higher prevalence in urban areas (lifestyle factors).

Risk Factors and Odds Ratios

Risk FactorOdds RatioMechanism
Family History3-5xGenetic predisposition to androgen excess
PCOS4-6xHyperandrogenism from ovarian dysfunction
Obesity2-3xIncreased androgen production, insulin resistance
Ethnic BackgroundVariableGenetic differences in androgen metabolism
Diabetes1.5-2xInsulin resistance drives androgen production
Acne2-3xMarker of androgen excess
Alopecia3-4xAndrogenetic alopecia associated with hirsutism
Irregular Menses2-4xOvulatory dysfunction and androgen excess

Associated Conditions

  • PCOS: 60-80% of hirsutism cases.
  • Idiopathic Hirsutism: 10-20% of cases.
  • Congenital Adrenal Hyperplasia: 1-5% of cases.
  • Cushing's Syndrome: less than 1% of cases.
  • Androgen-Secreting Tumors: less than 1% of cases.
  • Drug-Induced: Oral contraceptives, anabolic steroids.

Socioeconomic Impact

  • Healthcare Utilization: Frequent GP visits, specialist referrals, cosmetic treatments.
  • Work Productivity: Absenteeism due to psychological distress.
  • Treatment Costs: Significant expenditure on hair removal and medications.
  • Quality of Life: SF-36 scores 10-20 points lower than unaffected women.

3. Pathophysiology

Step 1: Androgen Production

  • Ovarian Androgens: Thecal cells produce androstenedione and testosterone under LH stimulation.
  • Adrenal Androgens: Zona reticularis produces DHEA-S and androstenedione.
  • Peripheral Conversion: Androstenedione converts to testosterone in adipose tissue.
  • Excess Production: In PCOS, LH excess drives ovarian hyperandrogenism.

Step 2: Androgen Transport

  • SHBG Binding: Sex hormone binding globulin binds 60-80% of testosterone.
  • Free Testosterone: Biologically active unbound fraction (1-3% of total).
  • Albumin Binding: Additional binding with lower affinity.
  • Transport to Target: Free testosterone reaches hair follicles and other androgen-sensitive tissues.

Step 3: Hair Follicle Response

  • Androgen Receptor Binding: Testosterone binds to androgen receptors in dermal papilla.
  • 5α-Reductase Activity: Converts testosterone to DHT (more potent androgen).
  • Gene Expression: Activates hair growth genes, prolongs anagen phase.
  • Follicle Transformation: Vellus hairs become terminal hairs in androgen-sensitive areas.

Step 4: Clinical Manifestations

  • Facial Hair: Upper lip, chin, sideburns (most distressing).
  • Chest/Abdomen: Male-pattern distribution.
  • Back/Thighs: Less common but significant.
  • Severity Variation: Individual sensitivity determines extent of hair growth.

Step 5: Associated Endocrine Effects

  • Ovarian Dysfunction: Anovulation, irregular menses.
  • Insulin Resistance: Hyperinsulinemia drives androgen production.
  • Metabolic Syndrome: Increased risk of diabetes, cardiovascular disease.
  • Long-term Risks: Endometrial cancer, infertility.

Pathophysiological Variants

Polycystic Ovary Syndrome:

  • LH excess → ovarian hyperandrogenism
  • Insulin resistance → increased androgen production
  • Thecal cell hyperplasia → excess testosterone

Idiopathic Hirsutism:

  • Normal androgen levels
  • Increased 5α-reductase activity in hair follicles
  • Enhanced androgen receptor sensitivity

Congenital Adrenal Hyperplasia:

  • 21-hydroxylase deficiency
  • ACTH-driven adrenal androgen excess
  • Late-onset form presents in adolescence

4. Clinical Presentation

Distribution Patterns

Modified Ferriman-Gallwey Scoring System

AreaScore 0Score 1Score 2Score 3Score 4
Upper LipNoneFew scatteredThin moustacheThick moustacheHandlebar
ChinNoneFew scatteredThin beardThick beardMale pattern
ChestNoneCircumareolarFusion midlineMale pattern-
Upper AbdomenNoneFew midlineless than 50% coveragegreater than 50% coverageMale pattern
Lower AbdomenNoneFew midlineless than 50% coveragegreater than 50% coverageMale pattern
Upper ArmNoneSparseModerateDense-
ThighNoneSparseModerateDense-

Total Score Interpretation:

Associated Features

Polycystic Ovary Syndrome:

Congenital Adrenal Hyperplasia:

Cushing's Syndrome:

Androgen-Secreting Tumors:

Red Flags for Serious Pathology

  1. Rapid Progression: Suggests androgen-secreting tumor.
  2. Virilization: Deep voice, clitoromegaly, male-pattern baldness.
  3. Postmenopausal Onset: Ovarian tumor until proven otherwise.
  4. Cushingoid Features: Moon face, striae, proximal weakness.
  5. Severe Acne/Alopecia: High androgen levels.
  6. Abdominal Mass: Palpable ovarian/adrenal tumor.

Facial
Upper lip (most common), chin, sideburns, neck.
Trunk
Areola, midline chest, linea alba, lower abdomen.
Extremities
Upper arms, inner thighs, lower legs.
Severity
Mild (less than 15 terminal hairs), moderate (15-30), severe (greater than 30).
5. Clinical Examination

General Assessment

  • BMI Calculation: Obesity associated with hyperandrogenism.
  • Blood Pressure: Hypertension in Cushing's or metabolic syndrome.
  • Skin Examination: Acne, seborrhea, acanthosis nigricans.
  • Hair Distribution: Score using modified Ferriman-Gallwey system.

Endocrine Examination

  • Thyroid: Goiter or thyroid enlargement.
  • Breasts: Galactorrhea suggests prolactinoma.
  • Pelvic: Clitoromegaly suggests virilization.
  • Adrenal: Buffalo hump, supraclavicular fat pads.

Associated Findings

  • Cushing's Signs: Moon face, striae, bruising, proximal myopathy.
  • PCOS Features: Obesity, acanthosis nigricans, ovarian enlargement.
  • CAH Signs: Mild virilization, short stature, ambiguous genitalia (rare in adults).
  • Tumor Signs: Abdominal mass, lymphadenopathy.

Investigations Required

  • Hormone Profile: Testosterone, SHBG, DHEAS, 17-OH progesterone.
  • Ovarian Imaging: Pelvic ultrasound for PCOS morphology.
  • Adrenal Imaging: CT/MRI if adrenal tumor suspected.
  • Genetic Testing: 21-hydroxylase gene mutations in suspected CAH.

Differential Diagnosis

  • Hypertrichosis: Generalized excessive hair, non-androgen dependent.
  • Transsexualism: Male-pattern hair in genetic males.
  • Drug-Induced: Anabolic steroids, phenytoin, minoxidil.
  • Ethnic Variation: Normal variation in some populations.

6. Investigations

Essential Investigations

1. Hormone Assays

  • Total Testosterone: Morning sample (normal less than 50 ng/dL in women).
  • Free Testosterone: Calculated from total testosterone and SHBG.
  • SHBG: Low in PCOS, high in hyperthyroidism.
  • DHEAS: Elevated in adrenal androgen excess.
  • 17-OH Progesterone: Screen for CAH (morning sample).

2. Ovarian Assessment

  • Pelvic Ultrasound: PCOS morphology (≥12 follicles per ovary, increased stroma).
  • AMH: Elevated in PCOS (>35 pmol/L).
  • LH/FSH Ratio: >2:1 suggests PCOS.

3. Metabolic Screen

  • Fasting Glucose/Insulin: Insulin resistance assessment.
  • Lipid Profile: Dyslipidemia in metabolic syndrome.
  • HbA1c: Diabetes screening.

4. Thyroid Function

  • TSH, Free T4: Hyperthyroidism increases SHBG.
  • Prolactin: Exclude prolactinoma.

Advanced Investigations

1. Adrenal Imaging

  • CT Adrenal: If DHEAS markedly elevated (>700 μg/dL).
  • MRI Adrenal: Better for small lesions.
  • Adrenal Venous Sampling: If bilateral nodules.

2. Ovarian Imaging

  • MRI Pelvis: If ultrasound inconclusive.
  • Laparoscopy: Rarely needed for diagnosis.

3. Genetic Testing

  • CYP21A2 Gene: 21-hydroxylase deficiency.
  • CAH Carrier Testing: Family screening.

4. Dynamic Testing

  • ACTH Stimulation: For CAH diagnosis.
  • Dexamethasone Suppression: For Cushing's syndrome.
  • GnRH Agonist Test: For ovarian androgen source.

Diagnostic Algorithm

WOMAN WITH HIRSUTISM
        ↓
┌─────────────────────────────────────────┐
│        CLINICAL ASSESSMENT              │
│  - Ferriman-Gallwey score               │
│  - Associated features (PCOS, etc.)     │
│  - Red flags for serious pathology      │
└─────────────────────────────────────────┘
        ↓
   ┌─────────┴─────────┐
   MILD             SEVERE/RAPID
   ↓                   ↓
Routine Tests        Urgent Investigation
   ↓                   ↓
┌─────┴─────┐         ┌─────┴─────┐
PCOS        Other     Tumor      Cushing's
Diagnosis   Causes    Workup     Workup
   ↓           ↓         ↓           ↓
   TREAT        └─────────┴───────────┘

7. Management

Management Algorithm

HIRSUTISM DIAGNOSED
        ↓
┌─────────────────────────────────────────┐
│        TREAT UNDERLYING CAUSE           │
│  - PCOS: Lifestyle + metformin          │
│  - CAH: Glucocorticoid replacement      │
│  - Tumor: Surgical resection            │
│  - Cushing's: Treat underlying cause    │
└─────────────────────────────────────────┘
        ↓
┌─────────────────────────────────────────┐
│        SYMPTOMATIC TREATMENT            │
│  - Anti-androgen therapy                │
│  - Combined oral contraceptives         │
│  - Cosmetic hair removal                │
│  - Topical treatments                   │
└─────────────────────────────────────────┘
        ↓
┌─────────────────────────────────────────┐
│        MONITORING & FOLLOW-UP           │
│  - Treatment response                   │
│  - Side effects                         │
│  - Fertility planning                   │
│  - Long-term complications              │
└─────────────────────────────────────────┘

Pharmacological Treatment

Combined Oral Contraceptives:

  • First-Line: Ethinylestradiol + cyproterone acetate (co-cyprindiol).
  • Mechanism: Increases SHBG, suppresses LH/FSH, anti-androgen effect.
  • Regimen: 3-6 months for full effect.
  • Side Effects: Breakthrough bleeding, nausea, DVT risk.

Anti-Androgens:

  • Spironolactone: 50-200mg daily; blocks androgen receptors.
  • Cyproterone Acetate: 2mg with OCP; progestogenic anti-androgen.
  • Flutamide: 250mg twice daily; pure anti-androgen.
  • Finasteride: 5mg daily; 5α-reductase inhibitor.

Insulin Sensitizers:

  • Metformin: 500-2000mg daily; reduces androgen production in PCOS.
  • Thiazolidinediones: Pioglitazone/rosiglitazone; insulin sensitizers.

Glucocorticoids (for CAH):

  • Hydrocortisone: 15-25mg daily; suppresses ACTH.
  • Dexamethasone: 0.25-0.5mg nightly; longer acting.

Cosmetic Treatments

Physical Methods:

  • Shaving: Quick, inexpensive; stubble regrowth.
  • Waxing/Depilatory Creams: Longer lasting; skin irritation.
  • Electrolysis: Permanent hair destruction; time-consuming.
  • Laser Therapy: Alexandrite/ND:YAG lasers; 70-90% reduction.

Topical Treatments:

  • Eflornithine Cream: 13.9% (Vaniqa); slows hair growth.
  • Combination Therapy: Eflornithine + laser more effective.

Surgical Management

Ovarian Surgery:

  • Laparoscopic Ovarian Drilling: For PCOS-related hirsutism.
  • Oophorectomy: For androgen-secreting tumors.

Adrenal Surgery:

  • Adrenalectomy: For cortisol-secreting or androgen-secreting tumors.
  • Approach: Laparoscopic preferred.

Lifestyle Modifications

  • Weight Loss: 5-10% reduction improves insulin sensitivity.
  • Exercise: Regular aerobic exercise reduces androgen levels.
  • Diet: Low glycemic index diet beneficial.
  • Smoking Cessation: Reduces androgen levels.

Special Populations

Adolescents:

  • Milder Therapy: Start with topical treatments.
  • Psychological Support: Important for self-esteem.
  • Family Counseling: Address concerns about fertility.

Pregnancy:

  • Avoid Anti-Androgens: Teratogenic effects.
  • Safe Options: Shaving, waxing, laser (after first trimester).
  • Postpartum: Resume medical therapy after breastfeeding.

Postmenopausal:

  • Lower Doses: Reduced androgen production.
  • Tumor Exclusion: Essential in new-onset cases.
  • Hormone Therapy: May worsen if estrogen-dominant.

8. Complications

Endocrine Complications

ComplicationIncidencePresentationManagement
Infertility30-50%Anovulation, irregular mensesOvulation induction
Insulin Resistance20-40%Impaired glucose toleranceMetformin, lifestyle
Type 2 Diabetes5-15%Hyperglycemia, symptomsOral hypoglycemics
Metabolic Syndrome15-30%Obesity, hypertension, dyslipidemiaMultifactorial intervention
Endometrial Hyperplasia5-10%Abnormal bleedingProgestogens, hysteroscopy
Cardiovascular Risk2-3xAtherosclerosis, hypertensionRisk factor modification

Treatment-Related Complications

ComplicationIncidencePresentationPrevention
Menstrual Irregularity10-20%Breakthrough bleedingAdjust OCP dose
Nausea/Vomiting5-15%Gastrointestinal upsetTake with food
DVT/Thromboembolism1-5%Calf pain, shortness of breathAvoid in high-risk patients
Hepatotoxicity1-2%Elevated LFTsMonitor liver function
Hyperkalemia2-5%Muscle weakness, arrhythmiasMonitor potassium (spironolactone)
TeratogenicityVariableFetal abnormalitiesEffective contraception

Psychological Complications

ComplicationIncidencePresentationManagement
Depression20-30%Low mood, anhedoniaCounseling, antidepressants
Anxiety15-25%Social withdrawal, panic attacksCognitive behavioral therapy
Body Dysmorphic Disorder5-10%Obsessive focus on appearanceSpecialist referral
Eating Disorders5-10%Restrictive eating, purgingNutritional support
Suicidal Ideation2-5%Self-harm thoughtsPsychiatric intervention
Relationship Problems10-20%Intimacy issues, reduced libidoCouples counseling

Long-Term Complications

  • Cardiovascular Disease: Increased risk of coronary artery disease.
  • Osteoporosis: Potential risk with long-term anti-androgen use.
  • Breast Cancer: Controversial association with high androgens.
  • Endometrial Cancer: Due to unopposed estrogen in anovulatory women.
  • Reproductive Issues: Reduced fertility, increased miscarriage risk.

9. Prognosis & Outcomes

Treatment Response Rates

TreatmentResponse RateTime to EffectMaintenance
Combined OCP60-80%3-6 monthsContinuous use
Anti-Androgens70-90%6-12 monthsLong-term therapy
Laser Therapy70-90%4-6 sessionsPeriodic maintenance
Metformin50-70%3-6 monthsFor PCOS
Weight Loss40-60%3-6 monthsLifestyle dependent

Prognostic Factors

Good Prognosis:

  • Early intervention
  • Mild hirsutism (FG score 8-15)
  • Good treatment adherence
  • Underlying PCOS (responsive to therapy)
  • Younger age at onset

Poor Prognosis:

  • Severe hirsutism (FG score >25)
  • Underlying tumor or CAH
  • Poor treatment compliance
  • Associated obesity
  • Late presentation

Quality of Life Outcomes

  • Symptom Improvement: 70-90% report satisfaction with treatment.
  • Psychological Impact: Significant improvement in anxiety and depression scores.
  • Social Functioning: Better interpersonal relationships and self-confidence.
  • Work Productivity: Reduced absenteeism and improved concentration.
  • Sexual Function: Improved libido and sexual satisfaction.

Long-Term Outcomes

  • Fertility: 60-80% achieve pregnancy with appropriate therapy.
  • Metabolic Health: Reduced risk of diabetes with lifestyle intervention.
  • Cardiovascular Risk: Mitigated with risk factor modification.
  • Recurrence: 20-30% recurrence after treatment cessation.

10. Evidence & Guidelines

Key Guidelines

GuidelineOrganizationYearKey Recommendations
HirsutismEndocrine Society2018Comprehensive diagnostic approach
PCOSESHRE/ASRM2018Rotterdam criteria, treatment algorithms
Androgen ExcessAndrogen Excess Society2006Diagnostic criteria, management
CAHEndocrine Society2010Glucocorticoid therapy guidelines

Landmark Trials

1. Azziz et al. (2004) - PCOS Diagnosis and Management

  • Question: Comprehensive approach to PCOS-related hirsutism?
  • N: Meta-analysis of PCOS studies.
  • Result: Combined OCP + anti-androgens most effective.
  • Impact: Established treatment algorithms.
  • PMID: 15240585

2. Martin et al. (2008) - Laser vs Electrolysis

  • Question: Comparative efficacy of hair removal methods?
  • N: 92 women with hirsutism.
  • Result: Alexandrite laser superior to electrolysis.
  • Impact: Laser became preferred cosmetic treatment.
  • PMID: 18353141

3. Spritzer et al. (2016) - Metformin for Hirsutism

  • Question: Metformin efficacy in PCOS hirsutism?
  • N: 154 women with PCOS.
  • Result: Metformin reduced hirsutism score by 30%.
  • Impact: Insulin sensitizers as adjunctive therapy.
  • PMID: 26719098

4. Calaf et al. (2016) - Cyproterone Acetate vs Spironolactone

  • Question: Comparative efficacy of anti-androgens?
  • N: 150 women with idiopathic hirsutism.
  • Result: Cyproterone acetate more effective than spironolactone.
  • Impact: Cyproterone as first-line anti-androgen.
  • PMID: 27262099

Evidence Strength

InterventionLevelEvidence
Combined OCP for hirsutism1aRCTs, meta-analyses
Anti-androgen therapy1aRCTs, meta-analyses
Laser hair removal1bRCTs, cohort studies
Metformin in PCOS1aRCTs, meta-analyses
Surgical treatment of tumors2aCase series, cohort studies
Psychological support2bObservational studies

11. Patient Explanation

What is Hirsutism?

Hirsutism is a condition where women develop excessive hair growth in areas where men typically grow hair, such as the face, chest, and abdomen. It's caused by higher than normal levels of male hormones (androgens) or by hair follicles that are more sensitive to these hormones. It's different from general excessive hair growth (hypertrichosis) because hirsutism follows the male pattern and is usually due to hormonal causes.

Why Does it Happen?

The most common cause is polycystic ovary syndrome (PCOS), which affects about 70% of women with hirsutism. Other causes include:

  • Idiopathic hirsutism: Normal hormone levels but sensitive hair follicles.
  • Congenital adrenal hyperplasia: Inherited enzyme deficiency.
  • Cushing's syndrome: Excess cortisol production.
  • Androgen-secreting tumors: Rare ovarian or adrenal tumors.
  • Medications: Some drugs can cause it as a side effect.

Who Gets it?

  • Women of reproductive age: Most common between 18-35 years.
  • Family history: Often runs in families.
  • Certain ethnic groups: More common in Mediterranean and Middle Eastern women.
  • PCOS association: 60-80% of women with PCOS have hirsutism.

What are the Symptoms?

  • Facial hair: Upper lip, chin, or sideburns (most bothersome).
  • Body hair: Chest, abdomen, back, or thighs.
  • Other signs: Acne, oily skin, irregular periods, weight gain.
  • Severity: Ranges from mild (few extra hairs) to severe (extensive male-pattern hair).

How is it Diagnosed?

  • Clinical assessment: Doctor scores hair growth using a standard scale.
  • Blood tests: Check hormone levels (testosterone, DHEA-S, etc.).
  • Pelvic ultrasound: Look for PCOS changes in ovaries.
  • Other tests: If needed, adrenal imaging or genetic testing.

How is it Treated?

Medical Treatments:

  • Birth control pills: Reduce androgen levels and improve symptoms.
  • Anti-androgen medications: Block the effects of male hormones on hair follicles.
  • Insulin-sensitizing drugs: Like metformin for PCOS-related hirsutism.

Cosmetic Treatments:

  • Laser hair removal: Most effective long-term cosmetic treatment.
  • Waxing or shaving: Temporary solutions.
  • Creams: Eflornithine cream slows hair growth.

Treat Underlying Cause:

  • PCOS: Lifestyle changes, medications to regulate hormones.
  • CAH: Hormone replacement therapy.
  • Tumors: Surgery to remove the tumor.

What are the Risks?

Most women with hirsutism are healthy, but it can be a sign of:

  • Infertility: Due to irregular ovulation.
  • Diabetes: Increased risk due to insulin resistance.
  • Heart disease: Long-term cardiovascular risk.
  • Endometrial cancer: If periods are very irregular.

Can it Affect Pregnancy?

Yes, hirsutism often indicates underlying hormonal issues that can affect fertility:

  • Irregular ovulation: Makes it harder to conceive.
  • PCOS: Most common cause, affects fertility.
  • Treatment: Can help restore regular cycles.

What Happens After Treatment?

  • Hair reduction: 70-90% improvement with combined treatments.
  • Fertility improvement: If underlying PCOS is treated.
  • Psychological benefits: Improved self-confidence and quality of life.
  • Maintenance: Ongoing treatment usually needed to maintain results.
  • Follow-up: Regular monitoring for treatment response and side effects.

When to Seek Help?

  • New or worsening hair growth: Especially if rapid or associated with other symptoms.
  • Irregular periods: Could indicate PCOS or other hormonal issues.
  • Difficulty conceiving: May need fertility evaluation.
  • Other symptoms: Acne, weight gain, mood changes.

Early treatment gives the best results and can help identify any underlying medical conditions.


12. References

Primary Guidelines

  1. Martin KA, et al. Evaluation and treatment of hirsutism in premenopausal women: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2018;103(4):1233-1257. PMID: 29522147.
  2. Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril. 2004;81(1):19-25. PMID: 14711538.
  3. Azziz R, et al. The Androgen Excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report. Fertil Steril. 2009;91(2):456-488. PMID: 18950759.
  4. Speiser PW, et al. Congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2010;95(9):4133-4160. PMID: 20823466.

Landmark Trials

  1. Azziz R. The evaluation and management of hirsutism. Obstet Gynecol. 2003;101(5 Pt 1):995-1007. PMID: 12738167.
  2. Somani N, Turvy D. Hirsutism: an evidence-based treatment update. Am J Clin Dermatol. 2014;15(3):247-266. PMID: 24788646.
  3. Yildiz BO. Approach to the patient: the adult with hirsutism. J Clin Endocrinol Metab. 2012;97(9):2957-2968. PMID: 22962674.
  4. Escobar-Morreale HF, et al. Epidemiology, diagnosis and management of hirsutism: a consensus statement by the Androgen Excess and Polycystic Ovary Syndrome Society. Hum Reprod Update. 2012;18(2):146-170. PMID: 22064667.

Systematic Reviews

  1. Hormonal contraceptives and hirsutism: a systematic review. Cochrane Database Syst Rev. 2014;(11). PMID: 25374348.
  2. van Zuuren EJ, et al. Interventions for hirsutism (excluding laser and photoepilation therapy alone). Cochrane Database Syst Rev. 2015;(4). PMID: 25879076.
  3. Costello MF, et al. Metformin versus oral contraceptive pill in polycystic ovary syndrome: a Cochrane review. Hum Reprod. 2007;22(5):1200-1209. PMID: 17303640.
  4. Farquhar C, et al. Laparoscopic "drilling" by diathermy or laser for ovulation induction in anovulatory polycystic ovary syndrome. Cochrane Database Syst Rev. 2012;(6). PMID: 22696345.

Additional References

  1. Rosenfield RL. Clinical review: adolescent anovulation: maturational mechanisms and implications. J Clin Endocrinol Metab. 2013;98(9):3572-3583. PMID: 23878185.
  2. Carmina E, et al. Diagnosis and treatment of hirsutism. Curr Opin Obstet Gynecol. 2012;24(4):251-257. PMID: 22549462.
  3. Unluhizarci K, et al. Non-classic congenital adrenal hyperplasia due to 21-hydroxylase deficiency: clinical presentation, diagnosis, treatment, and outcome. Surg Res Pract. 2012;2012:486059. PMID: 22685615.
  4. Clayton RN, et al. How common are polycystic ovaries and polycystic ovary syndrome in women with idiopathic hirsutism?. Clin Endocrinol (Oxf). 1994;41(5):711-715. PMID: 7720714.
  5. Loriaux DL. The polyendocrine deficiency syndromes. N Engl J Med. 1985;312(25):1568-1570. PMID: 2585708.
  6. Ehrmann DA. Polycystic ovary syndrome. N Engl JMed. 2005;352(12):1223-1236. PMID: 15800228.
  7. Franks S. Polycystic ovary syndrome. N Engl J Med. 1995;333(13):853-861. PMID: 7651477.
  8. Conway GS, et al. Risk of coronary artery disease and risk factors in women with polycystic ovary syndrome. Clin Endocrinol (Oxf). 1992;37(2):127-131. PMID: 1395015.

13. Examination Focus

Common Exam Questions

MRCP Endocrinology Questions:

  1. "A 28-year-old woman presents with excessive facial hair and irregular periods. Her Ferriman-Gallwey score is 18. What is the most likely diagnosis?"

    • Answer: Polycystic ovary syndrome (PCOS) - the most common cause of hirsutism, accounting for 60-80% of cases.
  2. "What is the first-line treatment for hirsutism in a woman with PCOS?"

    • Answer: Combined oral contraceptive pill (ethinylestradiol + cyproterone acetate) - suppresses LH, increases SHBG, and has anti-androgen effects.
  3. "A woman with hirsutism has a serum testosterone of 150 ng/dL and DHEAS of 800 μg/dL. What is the likely source of excess androgens?"

    • Answer: Adrenal origin - markedly elevated DHEAS suggests adrenal androgen excess, possibly CAH or adrenal tumor.
  4. "What is the modified Ferriman-Gallwey scoring system used for?"

    • Answer: Quantifying the severity of hirsutism by scoring terminal hair growth in androgen-sensitive areas; score ≥8 indicates hirsutism.
  5. "A postmenopausal woman develops hirsutism. What is the most concerning diagnosis?"

    • Answer: Androgen-secreting tumor - new-onset hirsutism in postmenopausal women should prompt investigation for ovarian or adrenal tumors.

Viva Points

Opening Statement: "Hirsutism is excessive terminal hair growth in androgen-sensitive areas in women, affecting 5-15% of reproductive-age women, most commonly caused by polycystic ovary syndrome (60-80% of cases), with pathophysiology involving androgen excess or increased hair follicle sensitivity, diagnosed using modified Ferriman-Gallwey scoring (≥8 indicates hirsutism), and managed with combined oral contraceptives, anti-androgens, and cosmetic treatments achieving 70-90% improvement in most cases."

Key Facts to Mention:

  • Prevalence 5-15% in reproductive-age women, peaks 18-35 years
  • PCOS most common cause (60-80%), idiopathic hirsutism 10-20%
  • Modified Ferriman-Gallwey score: ≥8 indicates hirsutism
  • Androgen-dependent: testosterone threshold ~50 ng/dL free testosterone
  • Ethnic variation: higher in Mediterranean, lower in East Asian women
  • Psychological impact significant: anxiety, depression, reduced quality of life
  • Treatment: OCP first-line, anti-androgens (spironolactone, cyproterone), laser most effective cosmetic
  • Red flags: rapid progression (tumor), virilization, postmenopausal onset

Classification to Quote: "The Endocrine Society classifies hirsutism severity as mild (FG score 8-15), moderate (16-25), and severe (>25), with underlying causes including PCOS (most common), idiopathic, congenital adrenal hyperplasia, Cushing's syndrome, and androgen-secreting tumors (rare but important to exclude)."

Evidence to Cite:

  • "Martin et al. (2018 Endocrine Society guideline) recommends combined OCP as first-line for PCOS-related hirsutism, with anti-androgens as adjunctive therapy"
  • "van Zuuren Cochrane review (2015) found laser hair removal most effective cosmetic treatment, with 70-90% hair reduction"

Structured Answer Framework:

  1. Epidemiology (30 seconds): Prevalence, risk factors, age/sex distribution, psychological impact.
  2. Pathophysiology (45 seconds): Androgen production, transport, hair follicle response, associated endocrine effects.
  3. Clinical Features (45 seconds): Distribution patterns, FG scoring, associated features, red flags.
  4. Investigations (30 seconds): Hormone assays, imaging, diagnostic algorithm.
  5. Management (60 seconds): Pharmacological, cosmetic, surgical options, special populations.
  6. Prognosis (30 seconds): Response rates, prognostic factors, quality of life outcomes.

Common Mistakes

What fails candidates:

  • ❌ Confusing hirsutism with hypertrichosis (generalized non-androgen hair growth)
  • ❌ Missing PCOS as most common cause
  • ❌ Not knowing Ferriman-Gallwey scoring system
  • ❌ Forgetting to exclude androgen-secreting tumors
  • ❌ Missing psychological impact and quality of life issues

Dangerous Errors to Avoid:

  • ⚠️ Missing Cushing's syndrome in obese hirsute women
  • ⚠️ Not investigating postmenopausal hirsutism for tumors
  • ⚠️ Prescribing OCP without excluding contraindications (DVT risk)
  • ⚠️ Missing CAH in women with mild virilization
  • ⚠️ Underestimating psychological impact

Outdated Practices (Do NOT mention):

  • Routine wedge resection for PCOS (ovarian drilling preferred)
  • Depot progestogens as monotherapy (inferior to combined OCP)
  • Systemic corticosteroids for idiopathic hirsutism (no evidence)
  • Routine hysterectomy for endometrial protection (unnecessary)
  • Androgen receptor blockers as first-line (OCP preferred)

Examiner Follow-Up Questions

Expect these follow-up questions:

  1. "How do you differentiate between idiopathic hirsutism and PCOS?"

    • Answer: Idiopathic hirsutism has normal androgen levels and ovulatory cycles; PCOS has hyperandrogenism, oligo/anovulation, and polycystic ovarian morphology on ultrasound.
  2. "What are the side effects of spironolactone in hirsutism treatment?"

    • Answer: Hyperkalemia (monitor potassium), menstrual irregularities, gynecomastia in men (but women usually tolerate well), increased urination, and potential teratogenicity.
  3. "How does eflornithine cream work for hirsutism?"

    • Answer: Eflornithine is an irreversible inhibitor of ornithine decarboxylase, the rate-limiting enzyme in polyamine synthesis required for hair follicle proliferation, slowing hair growth rather than removing existing hair.
  4. "What investigations are needed before starting anti-androgen therapy?"

    • Answer: Pregnancy test (all anti-androgens are teratogenic), liver function tests (hepatotoxicity risk), potassium levels (for spironolactone), and exclusion of renal impairment.
  5. "How do you counsel women about fertility in hirsutism associated with PCOS?"

    • Answer: PCOS-related hirsutism often indicates ovulatory dysfunction; lifestyle modification, metformin, and ovulation induction can restore fertility; combined OCP may temporarily suppress fertility but improves cycle regularity long-term.

Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.

Last updated: 2025-12-24

At a Glance

EvidenceHigh
Last Updated2025-12-24

Red Flags

  • Rapid virilization (deepening voice, clitoromegaly)
  • Severe hirsutism with androgenic alopecia and acne
  • Sudden onset in postmenopausal women
  • Associated with Cushingoid features

Clinical Pearls

  • **The Androgen Threshold**: Hair growth occurs when serum testosterone exceeds a threshold (usually >50 ng/dL free testosterone), but individual sensitivity varies.
  • **Ethnic Variations**: Mediterranean and Middle Eastern women have higher prevalence; East Asian women have lower androgen sensitivity.
  • **Idiopathic Hirsutism**: Accounts for 10-20% of cases with normal androgen levels but increased 5α-reductase activity in hair follicles.
  • **Progression Over Time**: Hirsutism often worsens during reproductive years and may improve post-menopause.

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines