Hair Loss Algorithm

Done

Safety

Red Flags — Identify Scarring Alopecia & Systemic Disease

Scarring (cicatricial) alopecia causes irreversible follicle destruction — do not miss these. Also screen for underlying systemic causes.

Scarring alopecia (cicatricial) Loss of follicular openings, shiny/atrophic scalp, perifollicular erythema or scale, pustules, tufting, pain, burning, progression — irreversible. Early scarring can be subtle; a normal-looking scalp does not exclude it. Differentials: lichen planopilaris, frontal fibrosing alopecia, discoid lupus, folliculitis decalvans, dissecting cellulitis, central centrifugal cicatricial alopecia, traction alopecia with chronic follicular destruction. Document the features → Urgent dermatology via local pathway — escalate if rapid progression, significant inflammation, pustulation, ulceration or diagnostic uncertainty

Scalp malignancy Ulcerated scalp lesion, rapidly growing nodule, firm attached scalp lump, bleeding ulcer, known lymphoma → Suspected cancer · skin pathway according to morphology, duration and clinical suspicion — ulceration or bleeding alone is not a diagnosis of skin cancer

Tinea capitis with kerion Boggy painful scalp swelling, pustules, cervical lymphadenopathy, systemic illness (especially child) → Urgent same-day paediatric/dermatology assessment — delayed treatment may cause scarring alopecia. Take scalp scrapings and plucked hairs for mycology where feasible, but do not delay systemic treatment when suspicion is high

Secondary syphilis "Moth-eaten" patchy scalp and beard hair loss + systemic symptoms (rash, lymphadenopathy, oral ulcers) → Same-day STI clinic / GUM referral

Systemic lupus erythematosus Hair loss + clinical features of connective-tissue disease — malar/photosensitive rash, oral ulcers, inflammatory arthritis, serositis, Raynaud phenomenon, cytopenia, proteinuria or neurological features → Targeted serology; discuss/refer rheumatology

Malignancy-associated (telogen effluvium) Rapid diffuse hair loss + weight loss, fatigue, night sweats, lymphadenopathy, known cancer history → Urgent investigation for underlying malignancy

Severe nutritional deficiency Brittle hair + very low BMI, amenorrhoea, lanugo hair, marked muscle wasting → Suspected eating disorder — refer immediately to the eating-disorder service (NICE NG69); same-day medical assessment, admit if unstable

Trichotillomania in children Irregular areas of hair loss, short broken hairs of different lengths, scalp normal, behavioural distress → Safeguarding consideration + CAMHS referral

Scarring alopecia represents a dermatological emergency — once follicles are destroyed, hair loss is permanent and irreversible. Early treatment of lichen planopilaris, discoid lupus, or folliculitis decalvans can arrest progression. Delayed referral can result in extensive irreversible hair loss. Tinea capitis with kerion requires systemic antifungal therapy (terbinafine or griseofulvin) — topical antifungals do not penetrate the hair shaft and are ineffective. Secondary syphilis is a readily treatable STI that is frequently missed when presenting as hair loss.

Done

Diagnose

History — Pattern, Timeline & Triggers

The pattern and timeline of hair loss — combined with age, sex, and systemic symptoms — will usually point to the diagnosis.

Pattern of loss

Diffuse (all over scalp) → telogen effluvium, FPHL, hypothyroid. Patchy → alopecia areata, tinea capitis. Frontotemporal recession + vertex → MPHL. Frontal + crown parting → FPHL. Ask: shedding or gradual thinning? scarring or preserved follicular openings? scalp inflammation, scale, pustules, pain or itch? eyebrow, eyelash, beard or body-hair involvement? nail changes? Diffuse + receding hairline → FPHL.

Onset & timeline

Acute (<6 months) → telogen effluvium (trigger 2–3 months prior), alopecia areata. Chronic gradual → MPHL, FPHL. Chronic scarring pattern → LPP, discoid lupus (ask about progression).

Trigger history

3 months prior: major illness, surgery, high fever, COVID-19, childbirth, major psychological stress, extreme weight loss → telogen effluvium (hair sheds 8–12 weeks post-trigger).

Systemic symptoms

Fatigue, weight change, cold intolerance, constipation → hypothyroid. Irregular or absent periods, acne, hirsutism, virilisation, rapid progression, infertility, weight gain → hyperandrogenism/PCOS. Dietary restriction, malabsorption, bariatric surgery or eating-disorder features → nutritional deficiency. Fatigue, pallor, brittle nails → iron deficiency anaemia.

Medication history

Chemotherapy, anticoagulants (warfarin, heparin), retinoids, antithyroid drugs, lithium, beta-blockers, anticonvulsants, oral contraceptive pills (especially progesterone-dominant) — all cause hair loss.

Family history

AGA/FPHL: strong familial component (polygenic). Alopecia areata: may have a family history of AA or autoimmune disease. Autoimmune thyroid disease.

Hair care practices

Chemical relaxers, bleaching, permanent waving → traction alopecia. Heat styling, tight ponytails/braids → traction alopecia (frontal recession). Trichodynia (scalp pain) → inflammatory alopecia.

Psychological impact

Ask routinely about distress, social avoidance, body-image concerns, anxiety, depression and suicidal thoughts where clinically indicated. PHQ-9 should not be the only assessment — use formal tools only if clinically indicated. Refer for psychological support when distress is moderate or severe, and assess suicide risk where appropriate.

The 8–12 week lag between telogen effluvium trigger and shedding is the single most important piece of history in alopecia assessment — patients presenting with diffuse hair loss should always be asked about events 2–3 months prior. Failure to elicit this history leads to unnecessary investigation and incorrect diagnoses. Pattern hair loss is very common in men (MPHL) and significantly under-recognised in women (FPHL).

Done

Diagnose

Classification — Scarring vs Non-Scarring, Diffuse vs Patchy

The scarring vs non-scarring distinction is the critical first branch — it determines urgency and treatability.

Pattern hair loss (MPHL/FPHL)

Male pattern hair loss: Hamilton-Norwood pattern (frontotemporal recession, vertex). Female pattern hair loss: Ludwig pattern (diffuse vertex, preserved frontal hairline). Commonest alopecia. Follicle miniaturisation — androgen sensitivity is important in MPHL; the role of circulating androgens in FPHL is less straightforward. Non-scarring

Telogen effluvium (TE)

Diffuse shedding commonly beginning 2–3 months after a trigger. Hair-pull test may be positive (supportive only). Shedding often settles over several months, but visible density recovery may take 6–12 months or longer. Chronic TE (>6 months) may fluctuate for years. Non-scarring

Alopecia areata (AA)

Discrete round/oval patches, exclamation mark hairs at margins, normal scalp skin, nail pitting. Prognosis varies with age at onset, extent, totalis/universalis, nail disease, duration and rate of progression. AA totalis (all scalp), AA universalis (all body hair). Autoimmune (Th1-mediated). Non-scarring, autoimmune

Tinea capitis

Scale + hair loss + pruritus, fluorescence with Wood's lamp (Microsporum), kerion (boggy mass). Mainly children. Highly infectious. Non-scarring if treated promptly

Traction alopecia

Frontal/temporal hairline recession due to tension (braids, ponytails, extensions). Marginal alopecia pattern. Can become scarring if chronic. Non-scarring if caught early

Lichen planopilaris (LPP)

Scarring alopecia — follicular erythema, peripilar scale, atrophic patches, no follicular openings. Pruritic, painful. Dermoscopy: loss of follicular ostia. Scarring → urgent dermatology

Frontal fibrosing alopecia (FFA)

Scarring alopecia — progressive frontal hairline recession, loss of eyebrows, follicular red halo, perifollicular scale. Mainly postmenopausal women. Scarring → urgent dermatology

Discoid lupus

Scarring — erythematous scaly plaques, follicular plugging, central atrophy, pigmentary changes. Sun-exposed areas. Usually dermatology-led; serology and rheumatology only if systemic features. Scarring → urgent dermatology

Other scarring alopecias

Folliculitis decalvans (pustules, tufting), dissecting cellulitis (boggy, painful scalp), central centrifugal cicatricial alopecia (crown/vertex), traction alopecia with chronic follicular destruction. Scarring → urgent dermatology

The scarring vs non-scarring distinction dictates urgency. Non-scarring alopecia (MPHL/FPHL, TE, AA) is treatable and follicles remain viable. Scarring alopecia (LPP, FFA, discoid lupus, folliculitis decalvans) destroys follicles permanently — early dermatology referral arrests but does not reverse established scarring. Frontal fibrosing alopecia has become increasingly common and is now a frequent form of scarring alopecia seen in dermatology — GPs must be familiar with its presentation.

Done

Diagnose

Targeted Examination — Scalp, Pattern & Systemic

Examine in good light; use a magnifying glass or dermatoscope if available.

Scalp skin assessment

Normal-looking skin usually = non-scarring, but early scarring can be subtle. Atrophic, shiny, loss of follicular openings = scarring. Scaly/inflamed = tinea/psoriasis/seborrhoeic dermatitis. Boggy/pustular = kerion/folliculitis decalvans.

Hair pull test

A gentle hair-pull test may support active shedding (TE, early AA, active inflammatory alopecia), but results are technique-dependent and should not be used in isolation. Record the pattern of loss, hair breakage, scalp inflammation and follicular openings.

Pattern assessment

Hamilton-Norwood scale (MPHL Grades I–VII). Alopecia areata: document severity (SALT or comparable measure) and eyebrow, eyelash, beard and nail involvement. Baseline medical photography is useful for follow-up (alopecia areata, pattern hair loss). Ludwig scale (female: I–III). Describe exact distribution — vertex-dominant (MPHL/FPHL), frontal margin (FFA/traction), patchy (AA), diffuse (TE).

Exclamation mark hairs

Short hairs tapering at base (like "!") at periphery of bald patches → alopecia areata. Pathognomonic sign. Black dots = fractured hairs at surface (AA totalis).

Nails

Pitting, onycholysis, trachyonychia ("sandpaper nails") → alopecia areata. Also check for leukonychia (nutritional deficiency).

Systemic exam

Thyroid palpation, signs of hypothyroid (bradycardia, dry skin, puffiness). Hyperandrogenism/PCOS: hirsutism (Ferriman-Gallwey), acne, virilisation, obesity. Anaemia: pallor, koilonychia. Connective-tissue disease: malar rash, photosensitivity, oral ulcers, synovitis.

Lymph nodes

Cervical/occipital lymphadenopathy → tinea capitis (especially children). Generalised lymphadenopathy + hair loss → secondary syphilis, lymphoma.

Skin/body hair

Eyebrow thinning (outer third) → hypothyroid, FFA. Body hair loss → AA universalis. Eyelash loss → AA, trichotillomania.

Trichoscopy

Can assist diagnosis and distinguish preserved follicular openings from scarring, but suspected scarring alopecia should not be reassured away by a non-specialist dermoscopic assessment.

The hair-pull test may support active shedding but is technique-dependent and not diagnostic in isolation — a negative test in diffuse hair loss may mean the shedding phase has ended or the patient has pattern hair loss without active shedding. Exclamation mark hairs are pathognomonic for alopecia areata and their presence should prevent unnecessary investigation for systemic causes. Outer-third eyebrow loss is a classic, often missed, sign of hypothyroidism — always check eyebrows when examining the scalp.

Done

Diagnose

Investigations — Targeted Bloods & Scalp Tests

Investigate selectively, guided by history and examination (PCDS). Routine blood tests are not usually required for classic MPHL when the diagnosis is clear and there are no systemic features.

First-line bloods

FBC, ferritin/iron studies, TSH ± free T4 — for unexplained diffuse shedding. Consider U&E, LFTs, B12, folate, zinc or vitamin D only if suggested by dietary restriction or malabsorption, GI disease, bariatric surgery, systemic symptoms, anaemia or macrocytosis, restrictive eating disorder, relevant medication or persistent unexplained disease.

Ferritin interpretation

Interpret ferritin with the FBC, transferrin saturation, inflammation and clinical context — thresholds are laboratory- and context-dependent, and ferritin may be falsely normal or raised with inflammation. Treat confirmed iron deficiency according to standard iron-deficiency guidance. Do not promise hair regrowth from iron replacement, and do not use ferritin >70 mcg/L as a universal treatment target.

Hormone panel

Total testosterone, SHBG/free androgen index ± DHEAS — only in women with hirsutism, acne, irregular or absent periods, virilisation, rapid progression, infertility or suspected PCOS; DHEAS if an adrenal source is suspected; further tests per the local endocrine pathway. Do not request a broad hormone panel routinely in all women with hair loss.

Thyroid

TSH ± fT4 — hypothyroid and hyperthyroid both cause diffuse hair loss. TSH most sensitive. If abnormal: check TPO antibodies (autoimmune thyroiditis). Titrate levothyroxine to keep TSH within the reference range (NICE NG145).

Autoimmune screen

ANA ± further serology — only where clinical features of connective-tissue disease justify it, with urine protein assessment and other systemic tests according to presentation. Syphilis serology only if syphilis is clinically possible. Routine ANA, dsDNA, complement, ENA and VDRL are not appropriate for undifferentiated hair loss.

Scalp biopsy

4mm punch biopsy — via dermatology for suspected scarring alopecia (LPP, discoid lupus, FFA). Horizontal sections preferred for alopecia diagnosis. Not a primary care test.

Scalp swab / Wood's lamp

Scalp scrapings and plucked hairs (or brushings) for mycology — if tinea capitis suspected; bacterial swab if pustular or purulent; do not delay kerion treatment while awaiting culture. Wood's lamp: Microsporum fluoresces blue-green (Trichophyton does not). Confirm with scalp brushings sent for mycology.

Do NOT routinely order

Routine B12/folate, autoimmune or hormone panels in all hair loss; hormone panel in MPHL (not indicated), MRI head for alopecia (specialist only), scalp biopsy without dermatology involvement, zinc/copper levels (not evidence-based in routine alopecia)

The association between low or borderline ferritin and chronic diffuse hair loss is controversial (PCDS) — interpret ferritin in context, treat confirmed iron deficiency, and do not promise regrowth from iron replacement. Hypothyroidism is a recognised reversible cause of diffuse hair loss — missing it is a significant diagnostic error. Hormone panel in classic MPHL has no clinical utility — the diagnosis is clinical and treatment is empirical.

Done

Refer

Referral Criteria — Dermatology, Endocrinology, Mental Health

Suspected skin cancer

Suspected cancer Ulcerated/bleeding scalp lesion, rapidly growing nodule, suspicious pigmented lesion, scalp patch with features of squamous cell carcinoma — assess via the suspected skin-cancer pathway according to morphology, duration and clinical suspicion; ulceration or bleeding alone is not a diagnosis of skin cancer

Urgent dermatology

Urgent — local pathway Suspected scarring alopecia (LPP, FFA, discoid lupus, folliculitis decalvans) — delay causes irreversible follicle loss. Rapidly progressive inflammatory alopecia; pustules, tufting, boggy scalp or significant pain; diagnostic uncertainty; severe or rapidly progressive alopecia areata (incl. totalis/universalis); alopecia areata with major psychological distress; extensive eyebrow/eyelash involvement; treatment-resistant alopecia areata.

Routine dermatology

Within 18 weeks Non-severe alopecia areata not responding to primary care treatment, diagnostic uncertainty without scarring or inflammatory features (suspected FFA or traction alopecia with scarring features → urgent, above)

Paediatric dermatology / ED

Same-day (kerion) Suspected kerion → urgent same-day paediatric/dermatology assessment; mycology where feasible, but do not delay systemic treatment. Tinea capitis → systemic antifungal (topical alone is inadequate), organism-directed where possible, per the current paediatric formulary, SPC and local pathway. Screen household contacts; school exclusion is not routinely needed once treatment has started, subject to local public-health advice (BAD 2014).

Endocrinology

Local pathway Routine endocrinology referral is not required for PCOS-associated hair loss — manage suspected PCOS or hyperandrogenism according to local endocrine/gynaecology pathways. Urgent referral for rapid virilisation or markedly abnormal androgens (e.g. raised DHEAS suggesting an adrenal source). Resistant hypothyroidism.

Rheumatology

Discuss / refer When hair loss is accompanied by clinical features of connective-tissue disease — malar/photosensitive rash, oral ulcers, inflammatory arthritis, serositis, Raynaud phenomenon, cytopenia, proteinuria or neurological features. Do not refer solely because ANA is positive (limited specificity). Discoid lupus is usually dermatology-led; rheumatology involvement depends on systemic features.

CAMHS / safeguarding

Urgent Trichotillomania in children with significant distress or safeguarding concerns. Adult trichotillomania — NHS Talking Therapies OCD pathway (HAbit Reversal Training).

Primary care manage

Clear pattern hair loss — MPHL/FPHL (topical minoxidil, counselling, refer to trichologist/hair transplant if desired). Uncomplicated TE post-trigger (reassurance + address cause). TE with confirmed iron deficiency or thyroid disease (treat per standard guidance and review at 3–6 months).

Frontal fibrosing alopecia (FFA) is now the most common scarring alopecia in dermatology departments in the UK — it is frequently missed in primary care as a "receding hairline" in postmenopausal women. Diagnosis of FFA is often delayed by years — during which time irreversible scarring progresses. Tinea capitis is highly infectious within households and schools — household contacts should be screened (BAD tinea capitis guideline, 2014); it is not a notifiable disease, and children on treatment can usually attend school, subject to local public-health advice. Drug choice, dose and duration depend on age, weight, formulation, likely organism, liver disease, drug interactions and local availability — use the current paediatric formulary, SPC and local dermatology pathway (terbinafine is unlicensed in children in the UK).

Done

Treat

Pharmacological Treatment — Condition-Specific Pathway

Address reversible causes first. Condition-specific pharmacological treatments below.

Male pattern hair loss (MPHL)

Minoxidil 5% topical OTC

Men: twice daily (5% solution 1 ml, maximum 2 ml/day; 5% foam per the product directions) — check the product SPC for formulation, age restrictions, application and contraindications. Response takes at least 4–6 months and may be modest; early increased shedding may occur; scalp irritation, contact dermatitis and hypertrichosis are recognised. Long-term treatment — benefit is lost after stopping. Oral minoxidil is not a routine primary-care treatment — specialist initiation only (hypertrichosis, tachycardia, hypotension, dizziness, fluid retention, headache, rarely serious cardiovascular effects). Finasteride 1 mg OD (adult men only; not prescribable on an FP10 — Drug Tariff Part XVIIIA, so usually a private prescription): before prescribing ask about current or previous depression, suicidal thoughts and sexual dysfunction; discuss reduced libido, erectile dysfunction, ejaculation disorders and possible persistence after stopping; women who are or may become pregnant must not handle crushed or broken tablets; provide MHRA patient alert-card information; stop if depression or suicidal thoughts develop and contact a healthcare professional — the same day for suicidal thoughts; 999 or A&E if at immediate risk of self-harm (MHRA 2026). No routine PSA monitoring — finasteride lowers PSA, so adjust interpretation if PSA is clinically indicated.

Female pattern hair loss (FPHL)

Minoxidil topical (2% or 5%) OTC

Women: 2% solution 1 ml twice daily (maximum 2 ml/day) or 5% foam half a capful (about 1 g) once daily — different licensed regimens; check the product SPC. Discuss facial hypertrichosis and scalp irritation. Avoid in pregnancy; generally stop during pregnancy/breastfeeding unless specialist advice supports use. Spironolactone (off-label): consider only after diagnostic assessment, particularly where hyperandrogenism or PCOS is present, preferably with dermatology/endocrine advice. Confirm pregnancy status and contraception; check renal function, potassium, BP and interacting medicines (ACE inhibitors, ARBs, potassium supplements, potassium-retaining drugs) before and during treatment per local protocol.

Alopecia areata (limited)

Potent topical corticosteroid

Assess extent and activity (SALT or comparable), eyebrows, eyelashes, beard, nails, functional effect, distress and rate of progression — do not treat solely by % scalp involved. Potent or very potent topical corticosteroid for scalp disease (e.g. betamethasone valerate 0.1% solution or clobetasol propionate 0.05% scalp application); caution re atrophy and hypopigmentation, particularly in darker skin. Intralesional triamcinolone is specialist-led (scalp, eyebrows, face), not a routine primary-care procedure. Prognosis varies — avoid a single remission statistic. Severe disease (generally 50–100% scalp loss, or less with rapid progression, eyebrow/eyelash involvement, functional impact or major distress), rapidly progressive, uncertain or distressing → specialist assessment for systemic options including licensed JAK inhibitors (e.g. ritlecitinib) where eligible (BAD 2024).

Tinea capitis

Griseofulvin or Terbinafine

Systemic antifungal required — topical treatment alone is inadequate. Send scalp scrapings and plucked hairs for mycology before treatment where feasible (do not delay for kerion). Choose drug, dose and duration by likely organism/mycology, age, weight, formulation, liver disease, drug interactions and local resistance/availability — use the current paediatric formulary (BNFc), SPC and local dermatology pathway. Plus selenium sulfide/ketoconazole shampoo to reduce spore shedding. Household contact advice; no routine school exclusion once treatment has started, subject to local public-health advice.

Telogen effluvium

Treat underlying cause

Iron: ferrous sulfate 200 mg once daily or on alternate days (BSG 2021) if iron deficient. Thyroid: levothyroxine titrated to keep TSH within the reference range (NICE NG145). B12: treat confirmed deficiency by cause (NICE NG239) — oral cyanocobalamin if diet-related; IM hydroxocobalamin for autoimmune gastritis, malabsorption or neurological features. Do not promise regrowth from iron replacement. Explain that shedding commonly begins 2–3 months after the trigger and often settles over several months, but visible density recovery may take 6–12 months or longer; reassess if the pattern becomes focal, scarring, progressive or atypical. Minoxidil has no clear routine role in acute TE (specialist use may occasionally be considered).

Scarring alopecia

Dermatology-led Rx

Specialist-led only — LPP/FFA: e.g. hydroxychloroquine, topical steroids or other off-label agents per dermatology. Discoid lupus: dermatology-led treatment + photoprotection. Arrest not reversal is the goal.

Next steps: see Male pattern hair loss · Female pattern hair loss · Fungal skin infection · Hypothyroidism · Iron deficiency anaemia · PCOS

Minoxidil's mechanism involves prolonging the anagen (growth) phase and increasing follicle size — it does not treat the androgenetic cause. Benefit is lost after stopping, making it a long-term commitment. Finasteride 1 mg is licensed for MPHL in adult men only (not women) — it reduces DHT and can slow progression. Sexual dysfunction may persist after stopping finasteride, and depression and suicidal ideation are recognised (MHRA Drug Safety Update, May 2026) — counsel patients explicitly, ask about any history of depression/suicidal ideation before prescribing, advise them to stop and seek advice if mood changes (the same day for suicidal thoughts; 999 or A&E if at immediate risk of self-harm), and give the patient alert card. Spironolactone for FPHL is off-label — use preferably with specialist advice, and individualise renal function, potassium and blood pressure monitoring.

Done

Lifestyle

Non-Pharmacological Interventions & Psychological Support

Nutritional optimisation Treat confirmed iron, thyroid, B12 or folate abnormalities per standard guidance — there is no universal ferritin target for regrowth. Iron-rich diet (red meat, lentils, dark leafy greens). Vitamin C with iron enhances absorption. Avoid tea/coffee with iron-containing meals.

Avoid hair trauma Reduce tight hairstyles (ponytails, braids, extensions, buns) — all cause traction alopecia. Heat styling, bleaching, and chemical relaxers damage hair shaft. Advise: loose styles, wide-toothed combs on wet hair. Optional cosmetic advice: a silk pillowcase may reduce friction/breakage but does not treat follicular alopecia.

Gentle hair washing Wash according to scalp condition, hair type and preference, with a gentle shampoo. Air dry rather than heat dry. Seborrhoeic dermatitis (dandruff) worsens some alopecias — use ketoconazole 2% shampoo twice weekly if present.

Stress reduction Psychological stress is a proven telogen effluvium trigger via cortisol-mediated anagen-to-telogen shift. CBT, mindfulness, exercise all reduce cortisol. Address underlying stressors. Mental health support if severe anxiety/depression.

Psychological support Ask about distress, social avoidance, body-image concerns, anxiety, depression and suicidal thoughts where clinically indicated; validate the impact explicitly. Formal psychological intervention for moderate-to-severe distress (BAD 2024); assess suicide risk where appropriate. Refer to NHS Talking Therapies for CBT. Alopecia UK charity offers peer support, wigs advice, helpline. NHS wig provision available for alopecia totalis/universalis.

NHS wig provision NHS wigs for medically indicated alopecia (alopecia areata totalis, chemotherapy-induced) are supplied through a hospital referral (usually dermatology or oncology), not on an FP10. In England a set NHS charge applies unless the patient is exempt (for example a hospital inpatient or on a qualifying benefit); they are free in Scotland, Wales and Northern Ireland (NHSBSA). Some trusts offer vouchers towards human-hair wigs.

Sunscreen (discoid lupus) Photoprotection is sensible in discoid lupus; a UV trigger for FFA is not established. Daily SPF 50+ on scalp and face. Hat use strongly encouraged. Refer to occupational health if outdoor worker.

Platelet-rich plasma (PRP) PRP is not routinely recommended in NHS primary care; evidence is limited and protocols are heterogeneous. BAD 2024 found insufficient evidence to recommend PRP for alopecia areata. Discuss only as a private, non-standard option after explaining uncertainty and cost.

Hair loss carries a psychological burden equivalent to that of chronic pain — studies consistently show quality-of-life scores in alopecia areata patients comparable to patients with psoriasis and chronic eczema. Validating this impact explicitly in the consultation improves patient satisfaction and reduces re-consultation. Traction alopecia is preventable and reversible if caught early — becoming the most common alopecia in Black women in the UK, with cultural and social dimensions that require sensitive discussion. NHS wig prescribing is an entitlement that is significantly under-utilised — GPs should be aware of the process.

Done

Safety

Follow-Up, Monitoring & Safety-Netting

6–8 weeks

Review response to iron/thyroid replacement in TE — bloods improving? Review traction alopecia if advised to change hair practices. Monitor for minoxidil side effects (scalp irritation, facial hypertrichosis in women). Confirm tinea capitis treatment compliance and household contact screening.

3–4 months

Recheck ferritin/TSH in TE if being treated for deficiency or thyroid disease. Minoxidil: early response may be seen (reduced shedding before regrowth). Alopecia areata: reassess extent (SALT), brows/lashes, nails and distress; refer if severe, rapidly progressive or distressing. Hormone results review for FPHL.

6–12 months

TE density recovery may take 6–12 months or longer — if not resolving, reassess diagnosis (FPHL? chronic TE? ongoing trigger?). Pattern hair loss: photo documentation to assess treatment response. Annual review of all chronic alopecia medications.

Monitoring — Finasteride

No routine PSA monitoring is required solely for finasteride 1 mg — if PSA is clinically indicated, remember finasteride lowers PSA and interpretation needs appropriate adjustment. Counsel: sexual dysfunction may persist after stopping; stop and seek advice if low mood — the same day for suicidal thoughts; 999 or A&E if at immediate risk of self-harm (MHRA 2026). Annual erectile function and mood enquiry.

Monitoring — Spironolactone

Check renal function, potassium and BP before and during treatment — individualise frequency per local protocol. Avoid or use with great caution in CKD and with ACE inhibitors, ARBs, potassium supplements or other potassium-retaining medicines (hyperkalaemia risk). Adequate contraception required (teratogenic).

Safety-net same-day GP

Rapid progression of hair loss over days/weeks, new scalp ulceration or bleeding lesion, systemic symptoms developing (fever, weight loss, rash), painful boggy scalp swelling or pustules (especially in a child), suicidal thoughts on finasteride (stop it; 999 or A&E if at immediate risk of self-harm), worsening after treatment initiation

Re-refer if

Scarring features develop in previously non-scarring alopecia, pattern hair loss not responding after 12 months of minoxidil, alopecia areata becoming severe, rapidly progressive or distressing, new neurological symptoms in patient with SLE, ferritin/TSH corrected but no improvement after 6–12 months

The clinical response to iron replacement in TE can take 6–12 months or longer to manifest as visible hair regrowth — patients require clear explanation and support through this waiting period to prevent premature abandonment of treatment. Minoxidil "shedding" in the first 2–4 weeks of treatment (paradoxical telogen effluvium induction) frequently causes patients to discontinue — proactively warn about this. Finasteride lowers PSA levels — a man on finasteride with a PSA within the "normal" range may actually have an elevated underlying PSA. PSA interpretation in finasteride users therefore needs appropriate clinical adjustment — seek specialist advice if unsure.