📋 Key Information Summary
- Hair disorders affect approximately 49% of women and 76% of men over their lifetime; androgenetic alopecia (AGA) is the most prevalent cause in both sexes.
- Classify hair loss as non-scarring vs scarring and diffuse vs focal before considering aetiology — this diagnostic model guides all subsequent investigation and management.
- The hair pull test is a simple bedside tool: ≥6 hairs extracted with gentle traction from multiple scalp sites indicates active shedding (positive test).
- Androgenetic alopecia presents with progressive miniaturisation of hair follicles — vertex and frontal recession in men (Hamilton–Norwood scale), diffuse central thinning in women (Ludwig scale).
- First-line pharmacotherapy for AGA: topical minoxidil 5% (men) or 2% (women) applied BD, and finasteride 1 mg daily (men only, not PBS-listed for alopecia).
- Alopecia areata is a T-cell–mediated autoimmune condition presenting with well-circumscribed patches of non-scarring alopecia; may progress to totalis (scalp) or universalis (body-wide).
- For patchy alopecia areata, intralesional triamcinolone acetonide 5–10 mg/mL every 4–6 weeks is first-line; extensive disease requires systemic therapy.
- Baricitinib 2 mg daily (Olumiant®) is TGA-approved and PBS-listed (Authority Required) for severe alopecia areata in adults — a landmark JAK inhibitor option.
- Telogen effluvium presents as diffuse hair shedding 2–3 months after a physiological or psychological trigger; usually self-limiting within 6 months.
- All scarring (cicatricial) alopecias require urgent dermatology referral — irreversible follicular destruction demands early aggressive treatment to prevent permanent hair loss.
- Always check serum ferritin, TFTs, zinc, vitamin D, and FBC in diffuse hair loss; target ferritin ≥30 µg/L for optimal hair regrowth.
- ATSI populations face barriers including remote access to dermatology, cultural factors affecting health-seeking behaviour, and higher rates of nutritional deficiency contributing to hair loss.
Introduction & Australian Epidemiology
Hair disorders encompass a broad spectrum of conditions ranging from benign, self-limiting shedding to progressive scarring alopecia resulting in permanent hair loss. Hair loss carries significant psychosocial morbidity — studies consistently demonstrate reduced quality of life, impaired self-esteem, increased anxiety and depression, and social withdrawal in affected individuals.
In Australia, hair loss is a common presenting complaint in general practice. Androgenetic alopecia accounts for the majority of consultations, affecting approximately 50% of men by age 50 and up to 30% of Caucasian women by age 70. Alopecia areata has a lifetime prevalence of approximately 2% in the Australian population, while telogen effluvium is among the most frequent causes of acute diffuse hair loss in women of reproductive age.
| Condition | Prevalence (Australia) | Peak Demographic | Key Feature |
|---|---|---|---|
| Androgenetic alopecia | ~50% men by age 50; ~30% women by age 70 | Men 20–50; Women post-menopausal | Progressive miniaturisation |
| Alopecia areata | ~2% lifetime prevalence | Bimodal: 20–40 and <10 years | Well-circumscribed patches |
| Telogen effluvium | Common; exact prevalence unknown | Women 30–60 | Diffuse shedding post-trigger |
| Scarring alopecia | ~3–7% of alopecia referrals | Middle-aged women (LPP/FFA) | Permanent follicular loss |
| Anagen effluvium | Variable (treatment-related) | Cancer patients on chemotherapy | Rapid onset during anagen phase |
The psychosocial burden of hair loss is frequently underestimated. General practitioners play a central role in early recognition, classification, initial investigation, and referral when indicated. A systematic approach — classifying hair loss by pattern (diffuse vs focal), presence or absence of scarring, and associated features — is essential before initiating management.
Hair Loss Diagnostic Model & Hair Pull Test
Diagnostic Framework
A structured approach to hair loss begins with distinguishing four key features: pattern (diffuse vs focal/patchy), scalp changes (scarring vs non-scarring), onset and course (acute vs chronic), and hair shaft abnormalities (if present). This classification narrows the differential diagnosis and guides investigation.
Hair Pull Test — Technique & Interpretation
Technique: The patient should not wash their hair for 24–48 hours before testing. Grasp a lock of 40–60 hairs firmly at the base between the thumb and index finger. Apply steady traction while sliding the fingers along the hair shaft. Perform at 3–4 different sites across the scalp (frontal, vertex, occipital, temporal).
Interpretation: Extracting ≥6 hairs per pull at one or more sites = positive (active shedding phase). Anagen hairs have dark, bulbous roots; telogen hairs have small, depigmented, club-shaped roots. Examine the roots under magnification or send for pathology.
| Hair Pull Result | Root Appearance | Suggests | Next Step |
|---|---|---|---|
| Positive — telogen roots | Small, white club-shaped | Telogen effluvium, early AGA, drug-induced | Bloods: FBC, ferritin, TFTs, zinc, vitamin D |
| Positive — anagen roots | Dark, elongated, may be tapered/dystrophic | Anagen effluvium (chemotherapy), alopecia areata | Correlate medication/chemotherapy history |
| Negative | No significant extraction | Stable AGA, scarring alopecia, resolved effluvium | Dermoscopy; consider biopsy if scarring suspected |
| Positive — broken shafts | Fractured mid-shaft, no root | Tinea capitis, trichorrhexis nodosa, hair abuse | Fungal culture, shaft examination |
When to Refer to Dermatology
Urgent referral indications: Suspected scarring alopecia (loss of follicular ostia), rapidly progressive alopecia areata involving >50% of the scalp, alopecia totalis/universalis, hair loss with systemic features (rash, joint pain, oral ulcers suggesting lupus/lichen planus), and any diagnostic uncertainty requiring scalp biopsy.
Androgenetic Alopecia & Anagen Effluvium
Androgenetic Alopecia (AGA)
Androgenetic alopecia is the most common form of hair loss, driven by the effects of dihydrotestosterone (DHT) on genetically predisposed hair follicles. DHT binds to androgen receptors in dermal papilla cells, leading to progressive follicular miniaturisation — terminal hairs are replaced by vellus hairs over successive hair cycles. The condition has a strong polygenic inheritance pattern with variable expressivity.
Clinical Classification
- Type I–II: Minimal frontal recession
- Type III: Deep frontal-temporal recession
- Type III vertex: Vertex thinning begins
- Type IV–V: Significant frontal and vertex loss, bridge of hair separating the two areas thins
- Type VI–VII: Extensive loss, only a band of hair remains laterally and occipitally
- Grade I: Mild central thinning, frontal hairline preserved
- Grade II: Moderate widening of the central part, visible scalp through hair
- Grade III: Extensive diffuse thinning over the crown with frontal hairline preservation
- Occipital and temporal hair typically spared
- Savin scale also used in some Australian dermatology practices
Pharmacological Management
Combination therapy: Combining topical minoxidil with oral finasteride (men) or spironolactone (women) provides superior outcomes compared with monotherapy. Low-level laser therapy (LLLT) devices (e.g., HairMax®) have TGA clearance and may provide modest additive benefit as adjunctive therapy.
Anagen Effluvium
Anagen effluvium results from abrupt cessation of mitotic activity in the hair matrix during the anagen (growth) phase, most commonly due to chemotherapy agents. The hallmark is rapid, diffuse hair loss occurring within days to 2–3 weeks of initiating cytotoxic therapy. Hair loss is often severe and may involve the entire scalp, eyebrows, eyelashes, and body hair.
| Chemotherapy Agent | Hair Loss Risk | Typical Onset | Reversibility |
|---|---|---|---|
| Doxorubicin | Near 100% | 2–4 weeks | Regrowth 3–6 months post-cessation |
| Cyclophosphamide | High (dose-dependent) | 2–4 weeks | Usually complete regrowth |
| Docetaxel / Paclitaxel | Near 100% | 2–3 weeks | Regrowth 3–6 months |
| Vincristine | Moderate–High | 4–8 weeks | Usually complete |
| 5-Fluorouracil | Low–Moderate | Variable | Complete |
| Targeted therapy (e.g., erlotinib) | Low–Moderate | Weeks to months | Reversible |
Management of Anagen Effluvium
- Scalp cooling (cryotherapy): Reduces chemotherapy delivery to hair follicles. Available at many Australian cancer centres (e.g., DigniCap®, Paxman®). Reduces hair loss severity by 50% with taxane-based regimens. Funded by some private health insurers and available at select public hospitals.
- Wigs and head coverings: State-based programs (e.g., Wig Library services through Cancer Council Australia) provide free or subsidised wigs. A prescription from a GP or oncologist may be required for insurance rebates.
- Topical minoxidil 5%: May accelerate regrowth after chemotherapy cessation (limited evidence); typically started 2–4 weeks after completing chemotherapy.
- Psychosocial support: Refer to Cancer Council 13 11 20 or oncology social work for counselling and support regarding body image changes.
Differential — alopecia areata post-immunotherapy: Immune checkpoint inhibitors (nivolumab, pembrolizumab, ipilimumab) can trigger alopecia areata rather than anagen effluvium. This presents with patchy, non-scarring hair loss with positive pull test (anagen roots). Dermatology referral is recommended for appropriate management (often requires immunosuppression rather than supportive care alone).
Alopecia Areata, Totalis & Universalis
Pathophysiology
Alopecia areata (AA) is a T-cell–mediated autoimmune condition targeting hair follicles in the anagen phase. CD8+ cytotoxic T lymphocytes surround the hair bulb in a characteristic "swarm of bees" pattern on histopathology. There is collapse of the immune privilege of the hair follicle bulb, with upregulation of MHC class I and II antigens and interferon-γ signalling. Genetic susceptibility is strongly associated with HLA class II alleles (particularly HLA-DRB1), and there is an association with other autoimmune conditions including thyroid disease, vitiligo, and atopic dermatitis.
Classification & Severity
Investigations
Pharmacological Management
JAK inhibitor safety monitoring (baricitinib): Baseline FBC, LFTs, lipid profile, renal function, hepatitis B/C serology, and TB screening (IGRA or Mantoux) are mandatory before initiation. Repeat FBC, LFTs, and lipids at 4 weeks, 12 weeks, then every 3 months. Counsel patients regarding thromboembolic risk (DVT/PE) and increased infection susceptibility. Baricitinib carries a TGA boxed warning regarding thromboembolic events and major adverse cardiovascular events observed in the RA safety population — discuss risk-benefit with patients.
Non-Pharmacological Management
- Cosmetic camouflage: Scalp micropigmentation, hair fibres (e.g., Toppik®), and strategic hairstyling can reduce psychosocial impact.
- Wigs: The Australian Alopecia Areata Foundation (AAAF) provides a wig subsidy program and peer support networks nationally.
- Psychological support: Cognitive-behavioural therapy (CBT) has demonstrated benefit in improving quality of life in AA patients. Refer to clinical psychologist as needed. Beyond Blue (1300 22 4636) and AAAF (alopecia.org.au) are valuable Australian resources.
- Contact immunotherapy (DPCP/diphencyprone): Available at some specialist dermatology centres in Australia. Topical sensitiser applied weekly to induce allergic contact dermatitis, redirecting the immune response. Requires specialist supervision.
Telogen Effluvium & Scarring Alopecia
Telogen Effluvium (TE)
Telogen effluvium is a reactive, non-scarring diffuse hair loss triggered by an event that shifts a large proportion of anagen hairs prematurely into the telogen phase. The latent period between the inciting event and onset of shedding is typically 2–3 months, corresponding to the time for telogen club hairs to be released. TE may be acute (<6 months duration) or chronic (>6 months).
Common Triggers
| Category | Examples | Mechanism |
|---|---|---|
| Physiological | Postpartum (3–6 months post-delivery), cessation of OCP, menopause | Oestrogen withdrawal shifts anagen to telogen |
| Nutritional | Iron deficiency (ferritin <30 µg/L), crash dieting, zinc deficiency, vitamin D deficiency, protein malnutrition | Impaired hair matrix cell proliferation |
| Psychological stress | Major life events, bereavement, surgery, illness, COVID-19 infection | Cortisol-mediated follicular signalling disruption |
| Medications | β-blockers, anticoagulants (heparin, warfarin), anticonvulsants (valproate, carbamazepine), lithium, retinoids, ACE inhibitors | Direct follicular toxicity or metabolic disruption |
| Systemic illness | Thyroid dysfunction (hypo- and hyperthyroidism), systemic lupus erythematosus, chronic renal failure, malignancy | Multifactorial |
| Post-infectious | COVID-19 (reported 2–3 months post-infection), influenza, high febrile illness | Systemic inflammatory stress response |
Diagnosis
- History: Diffuse hair shedding (increased hair on pillow, in shower drain, on clothing), with identifiable trigger 2–3 months prior.
- Examination: Diffuse thinning more apparent at the vertex and frontal scalp. Positive hair pull test (telogen club roots). No scalp inflammation, erythema, or scarring. Frontal hairline typically preserved.
- Dermoscopy: Predominantly empty follicular ostia, short regrowing vellus hairs (indicating recovery), no specific disease pattern.
- "Christmas tree" pattern: On parting, widening of the central part in a characteristic triangular pattern is typical of chronic TE in women.
Management
Acute telogen effluvium is self-limiting. Reassurance is the cornerstone of management — patients must understand that shedding will cease and full regrowth is expected within 6–12 months. The psychosocial impact should not be underestimated; validate the patient's distress and provide written information and support resources.
- Treat underlying cause: Iron supplementation (ferrous sulfate 325 mg PO daily if ferritin <30 µg/L, taken with vitamin C to enhance absorption), thyroid replacement, medication review.
- Optimise nutrition: Balanced diet with adequate protein (1.0–1.2 g/kg/day), iron-rich foods, and zinc. Consider supplementation: zinc 30 mg daily, vitamin D if deficient (<50 nmol/L).
- Minoxidil 2–5% topical: May be considered in chronic TE (>6 months) to support regrowth and mask thinning. Not typically required in acute TE.
- Chronic TE (>6 months): Investigate for overlapping AGA, nutritional deficiency, and thyroid disease. Dermatology referral recommended. May require scalp biopsy to distinguish from early AGA.
Scarring (Cicatricial) Alopecia
Scarring alopecias are a group of disorders characterised by irreversible destruction of hair follicles and replacement with fibrous tissue. They account for approximately 3–7% of hair loss referrals in Australia. Early recognition and aggressive treatment are critical — once follicles are destroyed, regrowth is impossible. All suspected scarring alopecias require urgent dermatology referral.
Critical red flags for scarring alopecia: Loss of visible follicular ostia (smooth, shiny scalp patches), perifollicular erythema and scale, permanent hair loss in focal areas, symptoms of burning, tenderness or pruritus on the scalp. If any of these features are present, refer to dermatology urgently — do not delay for empirical treatment.
Classification
| Type | Key Features | Demographics | First-Line Treatment |
|---|---|---|---|
| Lichen Planopilaris (LPP) | Perifollicular erythema and scale, particularly at the frontal hairline. Follicular hyperkeratosis. May be itchy/tender. | Women 40–60 years | Topical/intralesional corticosteroids + hydroxychloroquine |
| Frontal Fibrosing Alopecia (FFA) | Band-like recession of the frontotemporal hairline (1–5 cm). Loss of eyebrows. Perifollicular erythema at the leading edge. Variant of LPP. | Post-menopausal women (increasing incidence in Australia) | Topical corticosteroids + 5α-reductase inhibitors (finasteride/dutasteride) + hydroxychloroquine |
| Discoid Lupus Erythematosus (DLE) | Disc-shaped plaques with follicular plugging, dyspigmentation, atrophy, and scale. DLE may co-exist with systemic lupus (1–5%). | Women 20–40; higher prevalence in ATSI and darker-skinned populations | Photoprotection + potent topical corticosteroids + hydroxychloroquine |
| Central Centrifugal Cicatricial Alopecia (CCCA) | Progressive scarring from the vertex outward. Associated with hair grooming practices (heat, chemicals). | Women of African descent | Cessation of chemical/heat treatments + topical corticosteroids + doxycycline |
Investigations
Investigation is guided by the clinical pattern of hair loss. The following provides a framework for first-line and specialist investigations available in Australian general practice and pathology services.
Monitoring & Follow-Up
Special Populations
Pregnancy
Paediatrics
Elderly
Renal Impairment
Hepatic Impairment
Immunocompromised
Hair and scalp conditions are a significant but under-recognised health concern in Aboriginal and Torres Strait Islander communities. Culturally safe, trauma-informed care is essential when addressing hair disorders in this population.
📚 References
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