Hair and nail disorders

• Hair loss and nail disease look alarming but are common and mostly not dangerous: alopecia areata touches up to about 2% of people at some point, androgenetic alopecia dominates hair loss in older adults, and onychomycosis affects around 5 to 6% of people worldwide. ^{[2] [8]}
• A single round bald patch in a young person is usually alopecia areata: a non-scarring, autoimmune condition where the follicle survives and hair can regrow on its own. ^{[1] [2]}
• Permanent hair loss (scarring alopecia) is a different disease: inflammation destroys the follicle and only early treatment stops progression. ^[6]
• Fungal nail infection is the most common nail disease; it is diagnosed by sampling (KOH, PAS stain or culture), not by appearance alone, and treated with oral terbinafine for 6 weeks for a fingernail and 12 weeks for a toenail. ^{[8] [12]}
• Nails are a window on the body: clubbing, Beau lines, koilonychia, splinter haemorrhages and Terry nails can point to heart, lung, liver, kidney or blood disease. ^[10]
• Chromic inflammation of the nail folds (paronychia) behaves like hand eczema, not like a yeast infection: barrier care comes first and topical corticosteroids beat antifungals. ^[11]

By the end of this page you should be able to:

1. Tell non-scarring from scarring hair loss, and name the common causes of each.
2. Recognise alopecia areata, androgenetic alopecia, telogen effluvium and the main scarring alopecias from history and scalp examination.
3. Diagnose onychomycosis with confidence and choose between systemic and topical antifungal therapy.
4. Read the nail signs of systemic disease and know how each is produced.
5. Manage paronychia (acute and chronic) sensibly.
6. Choose treatment for each condition according to severity, age and pregnancy status, and advise a low-resource patient.

Hair and nails are not cosmetic extras. Hair is part of how patients see themselves, and a sudden bald patch or a thick, yellow nail drags people into clinic frightened of cancer or systemic illness. Most of the time the explanation is simple, common, and treatable, and the doctor's skill is to know when it is simple and when it is not. The trick is to work backwards from structure. Non-scarring alopecia keeps the follicle, so regrowth is possible; scarring (cicatricial) alopecia destroys it and is permanent. The same logic runs in the nail: nail plate is produced by the matrix, so anything that damages the matrix distorts the nail that grows out afterwards, and anything that alters blood supply, drug delivery or organ function writes its message into the nail over months. This page covers the main conditions a student will meet: alopecia areata, androgenetic (pattern) hair loss, telogen effluvium, scarring alopecia, onychomycosis, chronic paronychia and the nail changes of systemic disease. ^{[2] [6] [8] [11]}

Non-scarring (non-cicatricial) alopecia keeps the follicle intact; the hair can regrow.

• Alopecia areata: an autoimmune attack on the hair follicle, producing patchy, total or universal hair loss. ^{[1] [2]}
• Androgenetic alopecia (male and female pattern hair loss): a genetically determined sensitivity of follicles to androgens, shrinking terminal follicles down to vellus size. ^[7]
• Telogen effluvium: diffuse shedding of resting (telogen) hair three to six months after a trigger. ^[5]
• Traction alopecia and trichotillomania: mechanical loss, classed as non-scarring early on but scarring if prolonged.
• Diffuse alopecia from drugs, endocrine disease and nutritional deficiency: usually non-scarring.

Scarring (cicatricial) alopecia irreversibly destroys the follicle and replaces it with fibrous tissue. Once gone, the follicle does not return. ^[6]

Classification of scarring alopecia is by the predominant inflammatory cell on biopsy: lymphocytic (lichen planopilaris and frontal fibrosing alopecia, chronic cutaneous lupus erythematosus, central centrifugal alopecia, pseudopelade), neutrophilic (folliculitis decalvans, dissecting cellulitis) and mixed. ^[6]

A nail disorder is a problem of the nail plate, matrix, bed or surrounding folds. Three groups matter here:

• Infection of the nail unit: onychomycosis (fungal), paronychia (bacterial/fungal inflammation of the fold), viral warts.
• Signs of systemic disease written into the nail plate by disease or drugs.
• Local nail dystrophy from psoriasis, lichen planus and trauma.

The nail grows at roughly 3.5 mm a month in a fingernail and 1.6 mm a month in a toenail, so any event leaves its mark for months as it grows out. ^[10]

• Alopecia areata affects up to about 2% of people globally, with childhood prevalence higher than in adults (around 1.9% vs 1.5%). Lifetime risk is roughly 1.7%. ^{[2] [6]}
• Alopecia areata is more common in women, particularly with late-onset disease. About 2 in 10 affected people have a family history. ^{[1] [2]}
• Androgenetic alopecia is the most common cause of hair loss overall: roughly 30% of Caucasian men by age 30 and about 80% of men by age 70; roughly 50% of women are affected, with onset rising sharply after 65 years (about 75% of women over 65). ^{[6] [7]}
• Onychomycosis affects about 5.5% of the world's population, rising to as much as 35% in people over 65 years. Toenail infection is seven to ten times more common than fingernail infection. ^[8]
• Scarring alopecia is uncommon but not rare: about 7% of patients seen in specialist hair loss clinics. ^[6]
• Nail signs are shaped by where disease strikes. Clubbing is most often an acquired thoracic problem (about 80% of simple clubbing) rather than congenital heart disease. ^[10]

Autoimmune: the hair follicle's immune privilege breaks down and Th1, Th2 and Th17 cytokines drive an attack on the bulb. Genes (strongest evidence for PTPN22) raise susceptibility; family history is present in about 1 in 5 cases. ^[2] Triggers reported in reviews include viral infections (Epstein-Barr, hepatitis B and C, swine flu), vaccines, major infection, stress, and major life events. ^[2] Strong links with atopic disease (about 1 in 4 has atopic dermatitis), thyroid disease, vitiligo and type 1 diabetes. ^{[1] [2]}

Polygenic predisposition plus dihydrotestosterone (DHT). Scalp affected regions have more androgen receptors and higher DHT; 5-alpha-reductase converts testosterone to DHT, which miniaturises the follicle. Androgen deficiency (as in type 2 5-alpha-reductase deficiency) spares men from pattern loss, which is why 5-alpha-reductase inhibitors work. ^[7]

Any serious "shock to the system": childbirth, acute or chronic illness with fever, surgery, accident, crash dieting or iron deficiency, endocrine disease (thyroid), drug changes, stopping the combined pill, jet lag, psychological stress. ^[5]

Unknown cause in most; some cases follow prior trauma or chemical straightening (central centrifugal alopecia), or are variants of lichen planus or lupus. Female, postmenopausal and African descent are strong associations for subtypes. ^[6]

Dermatophytes (90% of toenail, 75% of fingernail disease), non-dermatophyte moulds (about 10%) and yeasts. Predispose with tinea pedis, trauma, diabetes, peripheral vascular disease, psoriasis, immunosuppression, occlusive footwear, communal bathing and older age. ^[8]

Acute: minor trauma (manicure, nail biting, ingrown nail) introducing bacteria, most often Staphylococcus aureus or Streptococcus, with Pseudomonas in chronic wet exposure. ^[11]

Chronic: multifactorial hand dermatitis. Repeated wetting and irritants break the cuticle seal; Candida is commonly isolated but does not cause the disease and often clearing happens without eradicating it. Housework, food handling, healthcare work, diabetes, HIV therapy (indinavir) and other drugs (retinoids, EGFR inhibitors) predispose. ^[11]

Each follicle cycles through anagen (growth), catagen (involution) and telogen (rest). Anagen bulb sits deep, where the immune system does not see it. In alopecia areata that immune privilege collapses, CD8 and other lymphocytes attack the bulb, and anagen is arrested. The follicle miniaturises into a telogen-like state but survives in most cases, which is why regrowth is common. A normal follicle grows anagen hair for about 4 years and then rests for about 4 months, before the cycle restarts. ^[5] The pull test (grasp 50 to 60 hairs and pull) is positive when more than about 10% come away, signalling active disease. ^[2]">

DHT shortens anagen and shrinks the follicle; terminal hairs are replaced by vellus hairs, then the follicle becomes invisible. The frontal hairline is usually spared in women but not in men. ^[7]

A shock resets many follicles into telogen at once. Shedding is then delayed 2 to 4 months until the new anagen hair pushes out the dead club hair. Paradoxically, hair fall is a sign of regrowth beginning. ^[5]

Inflammation targets the bulge, where epithelial stem cells live; destroy the bulge and the follicle can never regenerate. Fibrosis replaces it with a smooth, shiny, pore-less patch. ^[6]

The nail plate is made by the matrix and grows out at 3.5 (fingernails) and 1.6 (toenails) mm a month. Anything that acutely injures the matrix halts growth and leaves a transverse groove (Beau line) or a divided plate (onychomadesis) that takes months to grow out. The nail bed and circulation colour the nail, so chronic disease changes the colour long before it changes thickness. ^{[9] [10]}

Fungi digest keratin in the nail plate. Deeper-seated infection, nail matrix involvement and dermatophytoma make it resistant; thickening and subungual hyperkeratosis follow chronic invasion. ^[8]

Chronic paronychia is a barrier failure disease: moisture and irritants breach the cuticle seal, then repeated inflammation fibroses the proximal nail fold, so drugs no longer penetrate. It is eczema of the nail fold. ^[11]

Sudden, well-circumscribed, smooth patches of non-scarring hair loss on the scalp, beard, eyebrows, eyelashes or body. Short "exclamation mark" hairs at the edge (pathognomonic) and black dots and yellow dots on trichoscopy. A positive pull test means active disease. Patients may report itching, burning or tingling. Nail pitting (fine, regular, grid-like) is present in up to about 30% of patients, more often in children (13.2 to 18.8%). ^[2]"> ^[3] Hair can initially regrow white or fine. ^[1]

Pearl: alopecia areata favours pigmented hair, so white hairs are left behind in a bald patch. ^[1]

Men: bitemporal recession, then vertex thinning, with the frontal hairline eventually moving back. Women: diffuse thinning of the crown with preservation of the frontal hairline (Ludwig pattern). Both present in middle age though men can start in their teens. ^[7]

Diffuse shedding across the whole scalp 2 to 4 months after a trigger. The scalp shows short hairs of normal thickness and no atrophic patches. A gentle pull test yields increased telogen hairs. Daily loss can be up to about 100 hairs normally; in telogen effluvium the ratio reverses and up to about 70% of hairs may enter telogen. It affects up to about half of the scalp hair in some cases. Chronic form affects otherwise healthy women 30 to 60 years old. ^[5]

The hallmark is permanent loss of follicular openings (pores) in a smooth, shiny, atrophic or hyperkeratotic patch. Symptoms (itching, burning, pain), pustules and crusting at the active edge, perifollicular erythema and tufting give clues. ^[6]

• Lichen planopilaris: itchy, multifocal or central patches with perifollicular scale and violaceous keratotic papules; often normal nails and oral lichen planus. The commonest cause of scarring alopecia (at least 1 in 10 cases). ^[6]
• Frontal fibrosing alopecia: band of recession along the frontal hairline in postmenopausal women; eyebrow loss common. ^[6]
• Chronic cutaneous lupus erythematosus: patches most active in the centre, with follicular plugging, atrophy and dyspigmentation; scalp and ears. ^[6]
• Central centrifugal cicatricial alopecia: central scalp thinning that spreads outward, almost exclusively in women of African descent. ^[6]
• Folliculitis decalvans: pustules, honey-coloured crust and tufting at the vertex; bacterial culture usually grows Staphylococcus aureus. ^[6]
• Dissecting cellulitis: fluctuant nodules and sinus tracts in young men of African descent. ^[6]

Yellow-white-brown discoloration, subungual hyperkeratosis, onycholysis and thickening (onychauxis). Usually one or several toenails, big toe first; tinea pedis often present. Pattern types: distal lateral subungual (commonest), white superficial, proximal subungual (mainly immunosuppression), endonyx and total dystrophic. Fingernail disease usually means immunosuppression or trauma unless there is concomitant toenail disease. ^[8]

Acute paronychia is a sudden, painful, hot, red, swollen posterior nail fold, sometimes with pus, after a minor injury; the lateral folds can be involved. ^[11]

Chronic paronychia is a red, swollen, sometimes tender nail fold that lasts more than 6 weeks, with loss of the cuticle, rounding and thickening of the nail fold, longitudinal grooving, and secondary nail plate discoloration. Thumbs and finger webs are common in wet-work. ^[11]

Time for a proper nail examination: the hand, the fingers at 90 degrees, the nail fold and the half-moon (lunula). Common systemic clues (adapted from the AAD public list and a clinical review): ^{[9] [10]}

Diagnosis is usually clinical. Useful additions:

• Pull test (grasp 50 to 60 close hairs and pull): positive if more than 10% come out in alopecia areata and telogen effluvium.
• Trichoscopy (dermatoscope): yellow and black dots, exclamation mark hairs, short vellus hairs and broken hairs in alopecia areata; regrowing fringes and diffuse miniaturisation in telogen effluvium or androgenetic alopecia. Yellow dots stand out in active disease and confirm follicles persist (they are lost in scarring alopecia).
• Scalp biopsy (punch biopsy, with transverse and vertical sections and a further sample for immunofluorescence) when the diagnosis is doubtful, scarring alopecia cannot be excluded or a solitary patch is resistant. Biopsy from the edge of a lesion for active scarring alopecia. ^{[2] [6]}
• Laboratory tests directed by the clinical picture: thyroid function, iron studies and vitamin D for alopecia areata; autoantibodies, FBC and inflammatory markers if chronic lupus, sarcoid or a connective tissue disease is suspected; tinea capitis (KOH and culture) in any child with patchy alopecia, to avoid a misdiagnosis of alopecia areata.
• Steroid and vitamin D substitution tests in acne and palmoplantar psoriasis are not needed here; links to established dermatology references should suffice. (Avoid inventing protocols.)
• Mental health: a dermatologist asks about impact, mood and distress in every alopecia areata case, because anxiety and depression are common in these patients. ^{[1] [2]}

Severity and assessment scores for alopecia areata:

• SALT (Severity of Alopecia Tool) score: area of scalp without terminal hair, expressed as a percentage. S1 1 to 24%, S2 25 to 49%, S3 50 to 74%, S4 75 to 99%, S5 100%. Tools also score eyebrows, eyelashes and nails. ^[2]
• ALODEX refines SALT.
• SALT 20 or less is now the accepted treatment success definition in clinical trials. ^[2]
• Eyelash/brow ClinRO scores and nail appearance scores are used alongside when the eyebrow, eyelash or nail loss matters. ^[2]

• Mycology before treatment is the rule: KOH wet mount (immediate and cheap, but it misses many infected nails), PAS-stained nail clipping (more sensitive), fungal culture (slower, but it identifies the organism) or PCR if available. Do not start oral antifungals without laboratory confirmation unless the clinical picture is obvious and the patient accepts the uncertainty. ^[8]
• Dermoscopy of the nail shows onychomycosis as spikes, "aurora borealis" stripes or a dermatophytoma.
• Nail biopsy for doubtful cases, particularly to separate onychomycosis from psoriasis, lichen planus and subungual tumour.
• Blood tests and imaging when a nail sign suggests systemic disease: FBC, iron studies, LFTs, renal function, inflammatory markers, chest radiograph for clubbing, autoimmune screen for suspected connective tissue disease or lupus.
• Skin biopsy of a suspected scarring alopecia (punch biopsies at the active edge, transverse and vertical sections, a further sample for direct immunofluorescence when distinguishing lupus from lichen planopilaris). ^[6]

Acute paronychia is a clinical diagnosis; swab pus for culture when the patient is immunocompromised or the infection is severe or recurrent. Imaging is rarely needed except to exclude subungual abscess or osteomyelitis in severe infection. ^{[11] [12]}

Androgenetic alopecia has no laboratory diagnostic criterion; diagnosis is clinical, graded by the Norwood-Hamilton (men) and Sinclair or Ludwig (women) scales. A useful rule: women with frontal recession, male-type patterns or accompanying signs of androgen excess (hirsutism, acne, oligomenorrhoea, deepening voice) merit endocrine assessment for polycystic ovary syndrome and other causes. ^[7]

Alopecia areata severity uses SALT bands; extensive loss (S4, S5) changes treatment. Onychomycosis severity is graded by clinical involvement (less than 50% of the nail, matrix or proximal involvement, dermatophytoma) which directly decides topical versus systemic therapy. ^{[8] [12]}

Principles: match treatment to severity and mechanism, set expectations early (hair regrowth takes months; nails take as long as a year), tailor to age and pregnancy, and not every patient needs or wants treatment.

Guideline landscape: the BAD living guideline (2024, updated as a living document) and the AAD's public treatment guidance both emphasise severity-based plans; NICE CKS summarises the same pathway for primary care. ^{[1] [3] [4]}

• Mild, patchy disease of recent onset: first choice in most centres is intralesional triamcinolone acetonide (5 mg per ml) into the bald patches, repeated every 4 to 6 weeks, with visible regrowth usually at 3 months and injection pain limiting it to adults. ^{[2] [3] [6]}
• Small patches: potent topical corticosteroids daily (often with vitamin D analogues such as calcipotriol) and later minoxidil 2% or 5% to maintain regrowth; in children this alone can suffice. ^{[1] [2] [3]}
• Eyebrows and eyelashes: intralesional corticosteroids for brows; prostaglandin analogues (bimatoprost) for lashes; artificial lashes and scalp cosmetic camouflage.
• Extensive or resistant disease: contact immunotherapy (diphenylcyclopropenone), applied weekly, with complete regrowth in roughly 43% and major regrowth (over 70%) in about 56% in pooled data; JAK inhibitors for severe disease. ^{[2] [3] [8]}
• JAK inhibitors (JAK1/2/3, TYK2): baricitinib approved for severe alopecia areata 12 years and older (2 to 4 mg once daily); ritlecitinib (JAK3 inhibitor) approved for 12 years and older with extensive hair loss (200 mg daily for 4 weeks then 50 mg); deuruxolitinib for adults; many agents used off-label. Regrowth rates of 20 to 50% by SALT 20 in trials; relapse on stopping is common. ^{[2] [3] [1] [7][12]}
• Systemic conventional immunosuppression (methotrexate 15 to 25 mg weekly, ciclosporin 5 to 6 mg per kg daily, azathioprine) is second-line for resistant disease and usually combined with corticosteroids; systemic corticosteroids (pulse or low-dose prednisolone) have initial response but high relapse. ^{[2] [6]}
• Camouflage matters as much as drugs: wigs, hair fibres, micropigmentation, semi-permanent eyebrows. The NHS Wig Charter (BAD and Alopecia UK) guides provision. ^[1]

Severity-based choice (BAD public guidance): under half the scalp lost with patches present for under a year, watch and treat lightly; extensive loss, contact immunotherapy or a JAK inhibitor. ^[3]

The two FDA-approved drug classes remain topical minoxidil and 5-alpha-reductase inhibitors; everything else is adjunct or second-line. ^[7]

• Minoxidil: 2% or 5% solution or 5% foam. Men use 5% solution or foam twice daily; women use 2% solution or 5% foam once daily. Efficacy window 6 to 8 weeks to start, 12 to 16 weeks to peak; continued use needed or benefit is lost. 5% beats 2% in both sexes. Oral minoxidil (0.25 to 5 mg once daily) is an emerging, well-tolerated alternative for patients with poor compliance or irritant contact dermatitis. ^[7]
• Finasteride 1 mg daily in men. Reduces progression and increases count; peak effect at 1 year, benefit accumulates to 5 years. Side effects (sexual dysfunction, gynecomastia, depression) in roughly 1% to 40% in different reports. Finasteride is teratogenic and labelled as such. ^[7]
• Dutasteride 0.5 mg daily (off-label for AGA) is more potent than finasteride, with benefits even in finasteride non-responders and similar sexual side effects. ^[7]
• Topical finasteride (0.25% solution or spray) gives similar hair counts to oral finasteride with one-hundredth the plasma concentration and fewer systemic effects; combination with minoxidil works better than either alone. ^[7]
• Women: finasteride off-label (higher doses around 2.5 to 5 mg) helps postmenopausal women; for premenopausal women prefer minoxidil (and topical antiandrogens such as spironolactone; not on the FDA-approved list) and exclude androgen excess, especially polycystic ovary syndrome. ^[7]
• Procedures: low-level laser therapy (600 to 1100 nm), microneedling with minoxidil, platelet-rich plasma and finally hair transplantation. Camouflage is the simplest solution and should be offered routinely. ^[7]

Usually self-correcting. Management is reassurance, gentle hair care, nutrition, iron, B12, folate and vitamin D correction, and treating the underlying trigger (thyroid disease, fever, drug change). ^[5] No drug has a strong primary indication. Chronic telogen effluvium in women can overlap with female pattern hair loss; rule out androgenetic alopecia. ^[5]

The goal is to stop further loss, not to regrow hair; early inflammation is the only chance. Treat before the patch stabilises, and biopsy early. ^[6]

• Lichen planopilaris / frontal fibrosing alopecia: potent topical corticosteroids and intralesional triamcinolone into active foci (10 mg per ml, repeat every 6 to 8 weeks); hydroxychloroqine (under 7.5 mg per kg daily) first-line systemically, with 6 to 12 weeks onset; oral prednisolone (25 to 40 mg for 2 to 4 months) for rapidly progressive disease; doxycycline 100 mg twice daily; mycophenolate 500 mg twice daily; ciclosporin or retinoids in refractory cases. Frontal fibrosing alopecia may respond to 5-alpha-reductase inhibitors (dutasteride) and topical calcineurin inhibitors in addition. ^{[6] [2][3]}
• Chronic cutaneous lupus: sun protection, topical and intralesional steroids (triamcinolone), hydroxychloroquine (around 400 mg in summer, reduced in cooler months, better effect if the patient does not smoke), oral corticosteroids for rapidly progressive disease, and mycophenolate, methotrexate, azathioprine or retinoids for resistant disease. ^[6]
• Central centrifugal cicatricial alopecia: stop traumatic hair practices; topical steroids; often stabilises once trauma stops. ^[6]
• Folliculitis decalvans: antiseptic shampoo, topical benzoyl peroxide or clindamycin for mild cases; oral antibiotics (rifampicin 300 mg twice daily plus clindamycin 300 mg twice daily for 3 months, with topical steroid) for severe or resistant disease; isotretinoin for refractory cases. ^[6]
• Dissecting cellulitis: isotretinoin 0.5 to 1 mg per kg daily for 6 to 11 months; intralesional steroids for residual nodules. ^[6]
• Surgery (scalp reduction and transplantation) only after the disease has been inactive for at least a year. ^[6]

Get a mycological diagnosis first (sample from the active proximal zone, after clipping the distal nail), then treat according to involvement. ^{[8] [12]}

Key doses (check your local formulary):

• Terbinafine: children under 25 kg, 125 mg once daily; 25 to 35 kg, 187.5 mg; over 35 kg, 250 mg; adults, 250 mg once daily. Course: 6 weeks fingernails, 12 weeks toenails. ^{[8] [12]}
• Itraconazole: children under 20 kg, 5 mg per kg daily; 20 to 40 kg, 100 mg; over 40 kg, 200 mg daily for 1 week per month; adults, 200 mg daily for 1 week per month for 3 to 6 months. ^{[8] [12]}
• Topical monotherapy is reasonable when less than 50% of the nail is involved without matrix disease and fewer than 3 nails are affected. ^[8]
• Topical agents: efinaconazole 10% and tavaborole 5% (both applied daily for many months), ciclopirox lacquer (12 years and older), amorolfine lacquer; urea 40% to soften thick nails. ^{[8] [12]}

Acute paronychia (under 6 weeks): warm soaks several times a day, keep the digit dry, oral antibiotics (directed against Staphylococcus aureus and skin flora) when there is cellulitis, and drainage of any abscess. Remove a painful ingrown nail spicule; oral antibiotics alone will not cure an abscess. ^[11]

Chronic paronychia (over 6 weeks): treat it like hand dermatitis, not a yeast infection. ^[11]

1. General measures come first and are the most effective part: avoid wet work, wash with soap sparingly, use emollients after washing, wear cotton-lined rubber gloves, keep nails short and stop manicuring. ^[11]
2. Topical corticosteroids (moderate to potent) are the first-line drug and beat antifungals. In a trial in chronic paronychia, a topical steroid cleared more nail folds than oral terbinafine or itraconazole. ^[11]
3. Topical tacrolimus 0.1% ointment is an alternative, with evidence of at least equal benefit to topical betamethasone 0.1%. ^[11]
4. Reserve antifungals (topical ciclopirox, or short oral courses) for culture-proven concomitant onychomycosis or for suspected Candida disease that does not respond. Systemic antifungals are of little value now. ^[11]
5. Surgery for recalcitrant disease: eponychial marsupialisation or en bloc excision of the proximal nail fold; en bloc excision plus nail avulsion does better than marsupialisation alone. The newer Swiss roll technique retains the nail plate. ^[11]
6. Always exclude psoriasis, vesicobullous disease, carcinoma (unilateral, ulcerated or treatment-resistant paronychia) and drug causes (retinoids, antiretroviral indinavir, EGFR inhibitors) before settling on a benign diagnosis. ^[11]

• Permanent hair loss and disfigurement from untreated scarring alopecia; 1 in 10 at the other extreme for severe alopecia areata. ^{[1] [6]}
• Infective endocarditis as a cause of splinter haemorrhages and Bywaters' lesions (small nail fold petechiae in rheumatoid vasculitis). ^[10]
• Recurrence of onychomycosis in 10 to 53% of cases, usually within 3 years, because the nail is a reservoir and tinea pedis persists. ^[8]
• Secondary bacterial infection (cellulitis, paronychia) on onychomycotic nails, especially with diabetes or immunosuppression. ^[8]
• Continued exposure of the hand in wet work leads to chronic paronychia and loss of the cuticle seal, which makes the disease recalcitrant. ^[11]
• Drug side effects: hepatotoxicity from oral antifungals (rare but real with terbinafine/itraconazole; check liver function in at-risk patients); teratogenicity of 5-alpha-reductase inhibitors and methodrexate; oral antifungal drug interactions (itraconazole with statins and antiarrhythmics). ^{[8] [12]}
• Psychological burden: anxiety, depression and impaired life quality follow hair loss; Alopecia UK and similar groups are worth recommending. ^[1]

• Alopecia areata: 4 out of 5 people with limited disease regrow within 1 year without treatment; about 1 in 10 with more than half the scalp lost or total loss achieve full recovery. The nails worsen prognosis. Relapses are common. ^{[1] [3]}
• Telogen effluvium is self-correcting in most, with shedding tapering over 6 to 9 months after the peak. ^[5]
• Scarring alopecia: hair does not regrow without early treatment; the disease usually slows and burns out spontaneously. ^[6]
• Onychomycosis clears with oral therapy but grows out only as the nail grows: 6 months for a fingernail, 12 to 18 months for a toenail. ^[12]
• Chronic paronychia resolves slowly; months are realistic. ^[11]

• Scalp protection: sun protection for bald areas, careful walking under low doors. ^[1]
• Alopecia areata: screen for thyroid disease and atopy; patients with autoimmune thyroid disease or vitiligo benefit from vigilance. Psychological support should be offered. ^{[1] [2]}
• Androgenetic alopecia: family history; treat androgen excess in women. ^[7]
• Onychomycosis: keep feet dry, wear non-occlusive shoes and absorbent socks, clip nails short, treat tinea pedis, treat affected household contacts; maintain therapy (topical weekly) for high-risk groups for up to 2 years after cure. ^[8]
• Chronic paronychia: primary prevention is the cure; protect hands, keep them dry and moisturise. ^[11]
• Systemic nail signs: clubbing warrants investigation for thoracic and gastrointestinal disease; isolated coated (Terry) nails in a young person warrants assessment for liver and cardiac disease. ^[10]

• Alopecia areata in children often regrows without treatment; dermatologists usually use topical (not intralesional) steroids because of pain. JAK inhibitors are licensed from 12 years of age. ^{[2] [3]}
• Alopecia areata nail changes are more common and often settle on their own in children. ^{[2] [3]}
• Onychomycosis in children responds better to topical therapy because nails grow faster and penetration is higher. ^{[8] [12]}
• Paronychia in infants often arises from teething digit sucking; keep the digit dry. ^[11]

• Treat alopecia areata conservatively in pregnancy (camouflage, watch, mild topical agents after discussion). Systemic agents and JAK inhibitors are avoided. ^[3]
• Oral antifungals are avoided in pregnancy; use topical agents and defer systemic treatment. Itraconazole is teratogenic. ^{[8] [12]}
• Finasteride and dutasteride are teratogenic: avoid in pregnancy and in women who could become pregnant without effective contraception. ^[7]
• Chronic paronychia antifungals in pregnancy: use topical corticosteroids; postpone systemic agents and surgery if possible. ^[11]

• Onychomycosis, at 35% in over-65s, is common and often combined with circulatory and neuropathic nail disease. Treat only if symptomatic. ^[8]
• Topical and oral treatments interact with polypharmacy; itraconazole is the biggest worry with statins and antiarrhythmics. ^{[8] [12]}
• Ram's horn nails need podiatry or dermatology to trim. ^[9]

• Proximal white onychomycosis should trigger an HIV assessment. ^{[8] [10]}
• Psoriasis remains an important cause of nail dystrophy (pitting, oil spots, onycholysis, subungual hyperkeratosis) and must not be missed as onychomycosis in a patient with psoriasis. ^{[8] [9]}

• Clinical diagnosis by distribution and morphology without technology: recognise scarring (loss of pores) versus non-scarring (follicles visible), and the exclamation mark hairs of alopecia areata.
• Local emollients plus potent topical corticosteroids and calcipotriol control most mild alopecia areata and are cheap. ^[1]
• Hydroxychloroquine, doxycycline and oral retinoids are low-cost systemic options for scarring alopecia; antiseptics and systemic antibiotics for folliculitis decalvans. ^[6]
• KOH microscopy is affordable and reliable for onychomycosis when cultures are not; oral terbinafine is off-patent. ^[8]
• Protect hands: barrier care costs almost nothing and beats drugs for chronic paronychia. ^[11]
• Mental health aspects of hair loss are neglected; support groups and clinical empathy go a long way. ^[1]

Many inflammatory skin diseases can look like scarring alopecia or nail psoriasis. The table lists the feature that usually separates each. ^{[2] [6] [8]}

• Common hair loss is common and usually not dangerous: alopecia areata affects up to about 2% of people, androgenetic alopecia dominates with age, and telogen effluvium follows a trigger by 2 to 4 months. ^{[2] [5] [7]}
• Hold the walking stick question first: is the hair loss scarring or non-scarring? Follicle surviving means regrowth possible; destroyed follicle means prevention only. ^[6]
• Alopecia areata is autoimmune, patchy and non-scarring; intralesional triamcinolone gives visible regrowth in months, and JAK inhibitors (baricitinib, ritlecitinib) are approved for severe disease from 12 years of age. ^{[2] [3] [6]}
• Late-onset patchy loss in children often needs no treatment; about 4 out of 5 limited cases regrow within a year. ^[1]
• Early hair in alopecia areata grows back white. ^[1]
• Androgenetic alopecia management rests on minoxidil and finasteride; minoxidil starts to work in 6 to 8 weeks and peaks at 12 to 16, and finasteride works best in men 1 mg daily with peak benefit at 1 year. ^[7]
• Scarring alopecia destroys the bulge and is permanent; treat early and biopsy active, untreated disease before it stabilises. ^[6]
• Onychomycosis is diagnosed by sampling, not appearance: KOH, PAS or culture before systemic therapy; terbinafine for 6 weeks (fingernails) or 12 weeks (toenails), itraconazole by weight if non-dermatophyte or intolerance. Topical treatment only when less than half the nail is affected, without matrix disease, in fewer than 3 nails. ^{[8] [12]}
• Nails report systemic disease: clubbing, Beau lines, koilonychia, Terry nails, half-and-half nails, Mees lines and yellow nail syndrome all carry a differential to work through. ^[10]
• Paronychia is hand-dermatitis with barrier failure; topical corticosteroids beat antifungals in chronic disease. Acute cases need drainage for an abscess and antibiotics only when there is cellulitis. ^[11]
• Pregnancy, childhood and immunosuppression each change the drug list; teratogenic drugs (5-alpha-reductase inhibitors, oral retinoids, itraconazole in pregnancy) must be avoided. ^{[7] [8] [12]}

Related topics listed by title (links will appear once those topics are verified): tinea and superficial fungal infections; atopic dermatitis; psoriasis; lichen planus; secondary syphilis; seborrhoeic dermatitis; systemic lupus erythematosus; polycystic ovary syndrome and androgen excess; rheumatoid arthritis and endocarditis; anaemia; iron deficiency; HIV infection; heart failure and ischaemic heart disease; liver cirrhosis and chronic kidney disease; hypothyroidism and hyperthyroidism; chronic skin conditions in pregnancy; emollients and topical corticosteroids; retinoids and 5-alpha-reductase inhibitors.

This page is educational and is not a substitute for clinical judgement or local guidelines. Medication doses and pathways change; check your local formulary.