Seborrhoeic Keratosis
Summary
Seborrhoeic Keratosis (SK) is the most common benign tumour of the skin, originating from keratinocytes in the stratum basale. Often described as the "barnacles of ageing," they typically appear after age 30 and increase in number and size with age. They vary widely in appearance but characteristically present as "stuck-on," waxy, hyperpigmented papules or plaques with a verrucous (wart-like) surface. They have zero malignant potential themselves but can clinically mimic melanoma or pigmented basal cell carcinoma.
Key Facts
- Definition: Benign epidermal neoplasm caused by clonal expansion of mutated keratinocytes.
- Prevalence: Near universal (>90%) in population over age 60.
- Mortality/Morbidity: Strictly benign - cosmetic concern or irritation only.
- Key Management: Reassurance is first-line. Removal via cryotherapy or curettage if irritating.
- Critical Threshold: Sudden eruption of hundreds of lesions (Sign of Leser-Trélat) requires cancer screening.
- Key investigation: Dermoscopy (cerebriform pattern, milia-like cysts) is usually diagnostic.
Clinical Pearls
The "Stuck-On" Appearance: SKs often look like a piece of wax or clay has been pressed onto the skin. You can often peel or pick at the edge, distinguishing them from melanocytic naevi which are part of the skin.
Dermatosis Papulosa Nigra (DPN): A variant seen in darker skin types (Fitzpatrick IV-VI), presenting as multiple small, dark papules on the face and neck (think Morgan Freeman). These are histologically SKs but smaller.
The "Ugly Duckling" in Reverse: While a melanoma is the "ugly duckling" (different from other moles), an SK is often the "ugly duckling" in a field of moles because it looks so disordered and warty, yet is perfectly safe.
Why This Matters Clinically
The primary importance of SK lies in the differential diagnosis. A deeply pigmented SK can look identical to a nodular melanoma to the naked eye. Recognizing diagnostic features of SK allows clinicians to confidently reassure patients and avoid unnecessary excision of benign lesions, whilst ensuring true malignancies are not dismissed as "just a wart."
Incidence & Prevalence
- Incidence: Increases steadily with age.
- Prevalence:
- <30 years: Rare (except DPN variant).
- >40 years: 30-50% prevalence.
- >70 years: >90% of individuals have at least one SK.
- Trend: Stable.
Demographics
| Factor | Details |
|---|---|
| Age | Disease of ageing. Peak prevalence 50-80 years. |
| Sex | Males = Females. |
| Ethnicity | More common in Caucasians than Asian/African populations (though DPN is common in African descent). |
| Geography | Potential link to UV exposure, so slightly higher in sunny climates (Australia/NZ). |
Risk Factors
Non-Modifiable:
- Age: The strongest predictor.
- Genetics: Validated familial tendency (autosomal dominant inheritance pattern proposed for multiple SKs).
- Skin Type: Fitzpatrick I-III (fair skin) have higher burden of typical SKs.
Modifiable:
- UV Exposure: While SKs occur in sun-protected areas (unlike Solar Keratoses), cumulative sun damage correlates with higher numbers.
- Friction: Areas of repeated friction (belt line, bra strap) often develop SKs ("irritated SKs").
| Risk Factor | Strength of Association |
|---|---|
| Age > 50 | Strong |
| Family History | Moderate |
| UV Exposure | Weak/Debated |
Mechanism
Step 1: Somatic Mutation
- FGFR3 Mutation: Activating mutations in the Fibroblast Growth Factor Receptor 3 gene are found in >80% of SKs.
- PIK3CA Mutation: Found in ~50%.
- This drives constitutive activation of cell signaling pathways (Ras/MAPK/Akt) leading to proliferation.
Step 2: Clonal Expansion
- Benign proliferation of immature keratinocytes.
- Accumulation of melanin pigment within the keratinocytes (making them brown/black) even though they are not melanocytes.
Step 3: Horn Cysts Formation
- The proliferation creates invaginations of the epidermis filled with keratin.
- When seen from above (dermoscopy), these keratin plugs appear as "pseudo-horn cysts" or "comedo-like openings."
Classification of Variants
| Variant | Definition | Clinical Features |
|---|---|---|
| Common SK | The classic type. | Stuck-on, warty, tan to black. |
| Dermatosis Papulosa Nigra | Facial variant in pigmented skin. | Multiple small (1-5mm) brown papules on cheeks/neck. |
| Stucco Keratosis | Lower leg variant. | Small white/grey "stuck-on" papules on ankles/feet. |
| Irritated SK | Inflamed lesion. | Red, crusted, bleeding (mimics SCC or pyogenic granuloma). |
| Melanoacanthoma | deeply pigmented. | Jet black, mimicking melanoma. |
Anatomical/Physiological Considerations
They spare the palms and soles (glabrous skin) entirely. They are ubiquitous on the trunk ("Christmas Tree" pattern following Blaschko's lines sometimes) and face/scalp.
Symptoms
Typical Presentation:
Atypical Presentations:
Signs
Red Flags
[!CAUTION] Red Flags — Sign of Leser-Trélat
- The sudden, explosive onset of numerous (dozens to hundreds) of pruritic seborrhoeic keratoses.
- Association: Internal malignancy, most commonly Gastric Adenocarcinoma or Colon Cancer.
- Action: Urgent referral for systemic malignancy screening (Gastroscopy/Colonoscopy/CT).
Structured Approach
General:
- Total Body Skin Exam: SKs are rarely solitary. Look for the "company they keep" - finding multiple typical SKs elsewhere supports the diagnosis of a questionable lesion.
Specific Lesion Examination:
- Palpation: Runs finger over it. It should feel elevated and rough compared to surrounding skin.
- Pick Test: Gentle picking at the edge often lifts a greasy scale (unlike melanocytic naevi).
Dermoscopy (The Gold Standard)
Dermoscopy increases diagnostic accuracy significantly.
| Feature | Description | Sensitivity/Specificity |
|---|---|---|
| Milia-like Cysts | Bright white round clods (keratin pearls). | High Spec |
| Comedo-like Openings | Dark brown/black irregular crypts (keratin plugs). | High Spec |
| Fissures & Ridges | "Cerebriform" or "Brain-like" appearance. | Classic Feature |
| Hairpin Vessels | Loops of vessels surrounded by white halos. | Common in irritated SK |
| Moth-eaten Border | Concave bite-like notches at the edge. | Distinct from melanoma's streak border |
First-Line (Bedside)
- Dermoscopy: As detailed above. Often sufficient for diagnosis without biopsy.
Biopsy (Histopathology)
Indicated only if diagnostic uncertainty exists (e.g., cannot rule out melanoma).
| Technique | Indication | Note |
|---|---|---|
| Shave Biopsy | Flat or pedunculated lesions | Ideally "Scoop" shave to get base. |
| Curettage | Typical SKs | Sample is often fragmented (less good for path). |
| Excision | Suspected Melanoma | Do NOT shave a suspected melanoma. Excision with 2mm margin. |
Laboratory Tests
- None required for isolated SK.
- If Leser-Trélat suspected: FBC, LFTs, CEA, Faecal Occult Blood.
Imaging
- No imaging indicated for the skin lesions themselves.
Management Algorithm
(See Section 2 for ASCII)
Conservative Management
Reassurance:
- "This is a benign barnacle of ageing."
- "It will not turn into cancer."
- "Insurance usually does not cover removal unless inflamed/bleeding."
Medical Management
Topical treatments are generally ineffective, though some niche uses exist.
| Drug Class | Drug | Dose | Note |
|---|---|---|---|
| Keratolytic | Urea Cream 40% | Twice daily | Can flatten thick lesions. Poor efficacy. |
| Caustic | H2O2 (Eskata) | In-office application | FDA approved (USA) but expensive and limited use. |
Surgical/Procedural Management (Removal)
1. Cryotherapy (Liquid Nitrogen)
- Technique: 5-10 second freeze. 1-2mm halo.
- Pros: Quick, cheap, no injected anaesthetic needed.
- Cons: Hypopigmentation (white spot) risk is high. Not suitable for legs (poor healing).
2. Curettage & Cautery
- Technique: Local anaesthetic. Scrape off with sharp spoon (curette). Cauterize base.
- Pros: Tissue for pathology. Excellent cosmetic result.
- Cons: Requires LA injection.
3. Shave Excision
- Technique: Scalpel blade used to slice lesion flush with skin.
- Pros: Best for flat lesions. Good histology specimen.
- Cons: Scarring potential.
Disposition
- Discharge: Vast majority.
- Derm Refer: If diagnosis unclear (Rule Out Melanoma) or for complex cosmetic removal (e.g., on face).
Immediate (Post-Procedure)
| Complication | Incidence | Presentation | Management |
|---|---|---|---|
| Pain/Blistering | 100% (Cryo) | Expected response | Vaseline/Dressing |
| Infection | Low | Redness, pus | Topical antibiotic (Mupirocin) |
Early (Weeks)
- Recurrence: Incomplete removal (common with Cryo) leads to re-growth.
- Pyogenic Granuloma: Rare vascular overgrowth at site of curettage.
Late (Months)
- Post-Inflammatory Hypopigmentation: White mark where lesion was. Very common after Cryo. Patients must be warned ("Would you rather a brown wart or a white flat spot?").
- Scarring: Hypertrophic scarring (especially on chest/shoulders).
Natural History
- SKs persist indefinitely. They do not spontaneously resolve.
- They tend to grow slowly thicker and darker over years.
- New lesions appear continuously.
Outcomes with Treatment
| Variable | Outcome |
|---|---|
| Cure Rate | High (>0%) with Curettage/Shave. Lower with Cryo. |
| Cosmesis | Generally good, but pigmentary change is common. |
| Malignancy Risk | ~0% (A true SK does not become cancer). |
Prognostic Factors
Not applicable for benign lesions.
Key Guidelines
- British Association of Dermatologists (BAD) — Guidelines for the management of Seborrhoeic Keratoses. Emphasizes reassurance and non-intervention.
- DermNet NZ — Seborrhoeic Keratoses. Gold standard online resource for clinical features.
Clinical Distinctions (The "Collision" Lesion)
- Collision Tumour: Occasionally, a Melanoma or BCC can grow inside or colliding with an SK.
- Evidence: Histopathological studies show this is rare but possible. This is why "blind" destruction (Cryo) of atypical lesions is discouraged. if not 100% sure, BIOPSY.
Evidence Strength
| Intervention | Level | Key Evidence |
|---|---|---|
| Dermoscopy validity | 1a | Meta-analyses showing superior dx accuracy over naked eye |
| Cryotherapy | 2b | Standard of care |
What is a Seborrhoeic Keratosis?
It is a harmless skin growth that is incredibly common as we get older. We often call them "senile warts" or "wisdom spots." It is basically a build-up of skin cells that pile up on the surface like a barnacle on a ship. They are NOT caused by the sun, and they are NOT skin cancer.
Why does it matter?
They don't matter for your health, but they can be annoying. They can catch on bra straps or belts, become itchy, or bleed if scratched. The main reason to see a doctor is just to double-check it isn't a bad mole, especially if it is dark black.
How is it treated?
Most of the time, we leave them alone. If one is bothering you or looks unsightly:
- Freezing (Cold Spray): We spray it with liquid nitrogen. It creates a scab and falls off in a week or two.
- Scraping: We numb the skin and gently scrape it off. This usually heals very well.
What to expect
- If we remove it, you might be left with a white mark or a small scar.
- You will likely get more of these spots as you get older. This is normal.
- They do not turn into cancer.
When to seek help
- If a spot bleeds without being scratched.
- If it changes shape or colour very quickly.
- If you suddenly get dozens of them appearing all at once over a few weeks.
Primary Guidelines
- Hafner C et al. Seborrheic keratoses: molecular pathogenesis and clinical management. G Ital Dermatol Venereol. 2024;159(4):365-374. PMID: 39077983
- Wollina U. Seborrheic Keratoses - The Most Common Benign Skin Tumor of Humans. Open Access Maced J Med Sci. 2018;6(11):2270-2275. PMID: 30559863
Further Resources
- DermNet NZ: Seborrhoeic keratoses
- Primary Care Dermatology Society (PCDS): Seborrhoeic Keratosis
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.