Warts
Benign epidermal proliferations caused by human papillomavirus (HPV) infection. Extremely common, particularly in children and young adults. Most resolve spontaneously within 2 years. Treatment includes topical salicylic acid, cryotherapy, and observation. Genital warts (condylomata acuminata) are sexually transmitted and managed differently.
Key Facts
Human papillomavirus (HPV): >100 types; common warts (HPV 2, 4), plantar warts (HPV 1), genital warts (HPV 6, 11) Extremely common: affect ~10% of population; up to 30% of school-aged children Spontaneous resolution: ~65% resolve within 2 years without treatment (immune-mediated clearance) Salicylic acid 15–26%: first-line topical treatment — apply daily after paring; ~75% clearance at 12 weeks Cryotherapy (liquid nitrogen): second-line — every 2–3 weeks; ~70% clearance after multiple treatments Gardasil 9 (HPV vaccine): protects against HPV 6, 11, 16, 18, 31, 33, 45, 52, 58 — offered to all 12–13 year-olds in UK Black dots: thrombosed capillaries within wart — distinguishing feature from callus Immunosuppressed patients: extensive, treatment-resistant warts; increased risk of HPV-related malignancy
Overview
Key Facts
Cutaneous warts are one of the most common presentations in primary care dermatology. They are benign but can be cosmetically distressing and painful (plantar). Understanding that most resolve spontaneously is important to avoid overtreatment.
Epidemiology
- Prevalence: ~10% of general population; up to 30% of children
- Peak age: 12–16 years
- Equal sex distribution
- More common and persistent in immunosuppressed patients
- Genital warts: most common viral STI in UK
Aetiology
- HPV: double-stranded DNA virus; >100 types identified
- Common warts: HPV 2, 4, 27
- Plantar warts (verrucae): HPV 1, 2, 4
- Plane (flat) warts: HPV 3, 10
- Genital warts (condylomata acuminata): HPV 6, 11 (low-risk); HPV 16, 18 (high-risk — oncogenic)
- Transmission: direct skin contact, autoinoculation, fomites (swimming pools for plantar warts)
Pathophysiology
- HPV infects basal keratinocytes through micro-abrasions → viral DNA integrates or remains episomal → stimulates keratinocyte proliferation → epidermal hyperplasia (acanthosis, papillomatosis)
- Immune evasion: HPV downregulates MHC class I, interferon signalling → persistent infection
- Immune clearance: cell-mediated immunity eventually clears virus → spontaneous resolution in most cases
Clinical Presentation
Common Warts (Verruca Vulgaris)
- Firm, rough, dome-shaped papules with verrucous (cauliflower-like) surface
- Most common on hands, fingers, knees
- Black dots (thrombosed capillaries) visible on surface
- May be single or multiple; may coalesce
Plantar Warts (Verrucae)
- On soles of feet; pushed inward by weight-bearing → flat/endophytic
- Painful on lateral compression (callus is painful on direct pressure)
- Black dots visible after paring surface
- Mosaic warts: coalescent plantar warts
Plane (Flat) Warts
- Small (2–4 mm), flat-topped, skin-coloured or pink papules
- Often on face and dorsum of hands
- May be very numerous; Koebner phenomenon common
Genital Warts (Condylomata Acuminata)
- Flesh-coloured, soft, filiform or pedunculated papules
- Genital, perianal skin
- HPV 6, 11 (benign); screen for HPV 16, 18 co-infection
Red Flags
- Immunosuppressed patient with extensive/refractory warts — monitor for malignant transformation
- Rapidly growing, atypical, or pigmented lesion — consider SCC, amelanotic melanoma
- Genital warts in children — safeguarding assessment (may also be non-sexual transmission)
Differential Diagnosis
| Diagnosis | Key Features | Investigation |
|---|---|---|
| Seborrhoeic keratosis | Stuck-on, waxy, well-demarcated; elderly patients | Dermoscopy |
| Squamous cell carcinoma | Indurated, ulcerated, rapidly growing | Biopsy |
| Molluscum contagiosum | Pearly papules with central umbilication | Clinical |
| Callus/corn | No black dots, painful on direct pressure (not lateral) | Pare surface — no punctate bleeding |
| Amelanotic melanoma | Flesh-coloured nodule, irregular | Excision biopsy |
| Keratoacanthoma | Rapid growth, crateriform, central keratin plug | Excision biopsy |
Diagnosis / Investigation
Bedside
- Clinical diagnosis: usually straightforward; pare surface to reveal black dots
- Dermoscopy: frog-spawn pattern (black dots = thrombosed capillaries), absence of dermatoglyphics
Biopsy
- Not routinely required for typical warts
- Indicated if: atypical appearance, rapid growth, pigmented, immunosuppressed with treatment-resistant lesion
Bloods
- Not required for cutaneous warts
- HIV test: if extensive/refractory warts in at-risk patient
Special Tests
- HPV typing: not routine for cutaneous warts; relevant for genital warts and cervical screening
- STI screen: if genital warts — screen for co-existing STIs
Management
Non-Pharmacological
- Observation: first-line for children — majority resolve spontaneously within 2 years
- Patient education: benign condition, avoid picking/biting (autoinoculation)
- Occlusion with duct tape: anecdotal evidence; limited trial support
Pharmacological
- Salicylic acid 15–26% (Bazuka, Occlusal): first-line topical
- Pare wart, apply daily, cover; continue for up to 12 weeks
- Cure rate ~75% at 12 weeks
- Cryotherapy (liquid nitrogen): second-line — applied every 2–3 weeks; 2–3 freeze-thaw cycles per session
- Cure rate ~70% after 3–4 treatments
- Painful — less suitable for young children
- Topical formaldehyde 3% or glutaraldehyde 10%: for plantar warts
Genital warts (GUM clinic):
- Podophyllotoxin 0.5% cream/solution: patient-applied; BD for 3 days, repeat weekly for up to 4 cycles
- Imiquimod 5% cream: 3 nights/week for up to 16 weeks
- Cryotherapy or electrosurgery: clinic-based
Refractory/specialist:
- Intralesional bleomycin: specialist use for resistant warts
- Photodynamic therapy: limited evidence
- Cidofovir topical: specialist use in immunosuppressed
Referral Criteria
- Dermatology: diagnostic uncertainty, treatment-resistant, immunosuppressed
- GUM clinic: genital warts
- Safeguarding: genital warts in children
Prognosis
- ~65% of cutaneous warts resolve spontaneously within 2 years
- Treatment accelerates resolution but no treatment is 100% effective
- Recurrence common (~20–30%) even after successful treatment
- Immunosuppressed: persistent, extensive, treatment-resistant; increased malignant transformation risk
- Genital warts: 70–80% resolve with treatment; recurrence ~20–30%
- HPV vaccination: expected to dramatically reduce genital wart incidence (already seen in vaccinated populations)
Other Relevant Information
HPV Types and Associated Lesions
| HPV Type | Lesion | Risk |
|---|---|---|
| 1, 2, 4 | Common/plantar warts | Benign |
| 3, 10 | Plane warts | Benign |
| 6, 11 | Genital warts, laryngeal papillomatosis | Low-risk |
| 16, 18 | Cervical, anal, oropharyngeal cancer | High-risk (oncogenic) |
| 31, 33, 45, 52, 58 | Cervical cancer | High-risk |
Treatment Comparison
| Treatment | Efficacy | Advantages | Disadvantages |
|---|---|---|---|
| Salicylic acid | ~75% | Home-based, painless | Slow (12 weeks) |
| Cryotherapy | ~70% | Clinic-based, faster | Painful, scarring risk |
| Observation | ~65% at 2 years | No side effects | Slow |
| Imiquimod (genital) | ~50–75% | Immune-mediated | Local irritation |