Sun protection, sunburn and seborrhoeic keratosis

• Ultraviolet (UV) radiation is the main cause of skin cancer, skin ageing and sunburn. UVB, with its shorter wavelength, is the principal cause of sunburn and stimulates vitamin D production; UVA penetrates more deeply and drives photoageing, while a tan is simply a sign that the skin has been damaged.
• The safest way to use the sun is to limit strong exposure, use shade and clothing, and apply a broad-spectrum, water-resistant sunscreen of SPF 30 or higher generously, 15 to 30 minutes before going out and again regularly every two hours.
• Sunburn is a superficial first-degree burn that usually settles within a week. Care is symptomatic: cool the skin, use an emollient, drink extra water, take ibuprofen or aspirin if needed, and never burst blisters.
• Vitamin D can normally be made with small, non-burning exposures; people who must avoid the sun can use supplements, about 10 to 25 micrograms per day, rather than deliberate sunbathing.
• Seborrhoeic keratosis is a very common, benign, warty skin tumour that becomes more frequent with age and is harmless on its own. An abrupt eruption of many new itchy lesions (the sign of Leser-Trelat) can be a clue to an internal cancer and deserves cancer screening.
• Actinic keratosis is a rough, scaly patch produced by chronic sun damage and is a recognised precursor of squamous cell carcinoma.

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

1. Explain the difference between UVA, UVB and UVC, and what each does to skin and eyes.
2. Assign a patient to a skin phototype and connect it with sunburn and skin cancer risk.
3. Advise on shade, clothing and sunscreen choice and application, including for water exposure and for babies and children.
4. Manage an acute sunburn, including when it needs medical review.
5. Explain the vitamin D trade-off and give safe advice to someone who avoids the sun.
6. Recognise seborrhoeic keratosis and its variants, distinguish them from actinic keratosis, melanoma and other mimics, and manage suspicious or symptomatic lesions.
7. Recognise the sign of Leser-Trelat and say which cancers it associates with and what screening follows.

UVB is the primary cause of sunburn and stimulates the skin to make vitamin D. UVA penetrates deep into the dermis and affects connective tissue and blood vessels, producing the gradual loss of elasticity that we see as photoageing.^[1] Both wavelengths contribute to photoageing and to skin cancer risk.^[1][6]

Skin is classified into six phototypes by its response to sun: whether it burns and whether it tans.^[2]

A sunscreen's sun protection factor (SPF) is the multiple by which it delays sunburn compared with unprotected skin. Current dermatology guidance advises a broad-spectrum sunscreen (UVA and UVB) with an SPF of at least 30, and one that is water resistant.^[3][4]

Actinic keratosis is a different, sun-damage lesion: a rough, scaly patch of dysplastic keratinocytes on sun-exposed skin, and a recognised precursor of squamous cell carcinoma.^[2][3]

The sign of Leser-Trelat is not a single lesion but an abrupt eruption of multiple, often itchy, seborrhoeic keratoses in association with an underlying internal malignancy.^[8] It has no standardised or quantified diagnostic criteria; the practical definition is a rapid increase in the number or size of lesions, with tumour screening warranted once it is suspected.^[7][8]

Skin cancer is the most common cancer in fair-skinned populations, with between 2 and 3 million non-melanoma skin cancers and 132,000 melanomas occurring worldwide each year.^[2] Risk rises with phototype I and II: pale, freckled skin, blue or green eyes, fair or red hair, and a tendency to burn rather than tan.^[2]

Seborrhoeic keratoses are extremely common in adults and increase steadily with age, reaching a peak at about 60 years.^[7] They occur in all skin colours, but the small variant called dermatosis papulosa nigra, which appears as multiple tiny papules on sun-exposed skin, is more frequent in people of African or Asian descent and in women, occurring in about 10% of African-American people with a positive family history in up to 85% of cases.^[7]

Actinic keratosis becomes common in fair-skinned older adults with cumulative sun exposure and is a marker of field cancerisation on sun-damaged skin.^[2][3]

The cause of all these conditions is ultraviolet radiation, but the pattern of exposure differs.

• For melanoma, high intermittent exposure and early sunburns are the important risk, alongside many atypical moles and a family history. For squamous cell carcinoma, cumulative lifetime UV dose matters, with actinic keratosis forming as a precursor. For basal cell carcinoma, long repeated exposure on sites such as the ears, face, neck and forearms is the pattern.^[1][2]
• People of colour have much lower skin cancer risk and need more solar UV to make adequate vitamin D, which can make deficiency more likely at high latitudes. Excessive UV exposure still damages every skin type, and the risk of eye damage and heatstroke is the same for everyone.^[1][2]
• For seborrhoeic keratosis, chronic (especially UV) skin ageing and genetic susceptibility are the main drivers. Mutations of fibroblast growth factor receptor 3 and signalling molecules are common in these lesions but do not imply malignant change; even acquired oncogenic mutations in benign seborrhoeic keratosis do not increase proliferative activity.^[7]
• Patients with solid organ transplants have a markedly increased risk of both squamous cell carcinoma and basal cell carcinoma, with ultraviolet radiation as the dominant factor; fair skin, male sex and older age add further risk.^[3] For them sun protection is advised all year round at SPF 50.
• Drugs and illnesses that cause photosensitivity (for example some diuretics, tetracyclines, retinoids and tanning-bed use) can lower the sunburn threshold and need individualised advice. Medications that are photosensitising produce reactions at a small dose of UV.

Sunburn begins when UVB photons are absorbed by epidermal cells. Keratinocytes release RNA, which activates Toll-like receptor 3 and nuclear factor kappa B (NFkB), leading to production of pro-inflammatory cytokines including interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha). At higher doses UVB triggers apoptosis in keratinocytes, the "sunburn cells" with pyknotic nuclei. UVB photons are also absorbed by DNA, producing cyclobutane pyrimidine dimers; failure of repair can mutate proto-oncogenes and tumour-suppressor genes. UVA adds carcinogenic risk by generating reactive oxygen species. The visible erythema is a downstream sign; DNA damage can occur before the erythema threshold is reached.^[1]

Melanin is the skin's principal filter. Eumelanin is photo-protective, absorbing UV and dissipating it as heat; pheomelanin affords less protection and is itself photo-toxic, generating reactive oxygen species when exposed to UVA. Darker skin makes more eumelanin, which is the main reason phototypes V and VI tolerate much higher exposure before burning, though not before DNA injury.^[6]

A suntan provides a sun protection factor of only 2 to 4 and gives no protection against long-term UV damage, including skin cancer.^[1]

UVB also suppresses the skin's immune response to antigens through changes in the distribution and activity of skin and immune cells, adding another route to carcinogenesis. Cumulative UV dose relates more to squamous cell carcinoma, while intermittent intense exposure and sunburn relate more to melanoma.^[2][6]

Vitamin D is the one benefit of UV. UVB converts 7-dehydrocholesterol in skin to previtamin D3, which isomerises to vitamin D3. People with little sun exposure, dark pigmented skin living at high latitudes, traditionally veiled people, housebound older adults and those whose vitamin D metabolism is abnormal are at risk of deficiency. Sufficient synthesis is achieved by healthy people exposing the face, hands and arms uncovered and without sunscreen two to three times a week for about half the time it would take unprotected skin to develop a sunburn, about 12 minutes for a sensitive (phototype II) person when the UV index is 7.^[1]

Seborrhoeic keratosis pathogenesis is not completely understood but it is considered a mark of skin ageing, particularly chronic UV exposure, with a UV-inducible mutational signature. It strongly expresses amyloid precursor protein, and FGFR3 and PIK3CA mutations are common. These lesions do not transform to malignancy.^[7]

In the sign of Leser-Trelat the mechanism is thought to be tumour-secreted cytokines and growth factors from an underlying neoplasm, causing the abrupt appearance of many seborrhoeic keratoses, most often in gastric, colorectal and breast cancer. New targeted cancer drugs such as cytarabine, docetaxel, gemcitabine and PD-1 inhibitors can inflame pre-existing warts and produce a pseudo-Leser-Trelat sign, in which treatment can continue.^[7][8]

After overexposure the skin is red, warm, swollen and tender within 3 to 5 hours, with discomfort peaking at 12 to 36 hours. Severe burns blister and may be complicated by dehydration and secondary infection. Systemic symptoms such as fever, nausea and headache suggest a severe burn.^[5][6]

This presents gradually with wrinkling, sagging and bags, most marked where the skin has been chronically sun-exposed, and is irreversible.^[1]

Lesions are waxy, slightly greasy plaques or papules with a stuck-on look, ranging from a few millimetres to several centimetres, in colours from yellowish through tan to dark brown or black. They may have a warty surface covered by a keratotic film, may be pruritic, and often show "horn cysts" on close inspection. They favour the trunk and forehead, and may become irritated, infected or bleed if rubbed.^[7]

The histological subtypes include hyperkeratotic, acanthotic, reticular or adenoid (more common in sun-exposed areas and often hyperpigmented), clonal, irritated, melanoacanthoma and a verrucous type with keratoacanthoma-like features.^[7]

Dermatosis papulosa nigra presents as multiple tiny papules on sun-exposed areas in phototypes III or darker, especially women, often with a family history.^[7]

These are raised, rough, pink or red spots with a raw, sandpaper feel on sun-exposed skin (face, bald scalp, neck, ears, backs of hands and forearms). They may be easier to feel than to see.^{[3] [2]}

Examine all skin, including the scalp, ears, neck and backs of hands, and ask about sunburn history, tanning-bed use, occupation, hobbies and immune status. For suspected seborrhoeic keratosis, use dermoscopy to look for fissures and ridges, hairpin vessels with a white halo, comedo-like openings and milia-like cysts, which distinguish it from melanoma.^[7]

Clinical mimics of severe sunburn include scalds and other superficial burns, phototoxic and photoallergic drug rashes, polymorphic light eruption and lupus photosensitivity.

Seborrhoeic keratosis and sunburn are clinical diagnoses. Tests serve to exclude mimics, confirm complications or screen for associated cancer. A diagnosis of the sign of Leser-Trelat is based on the abrupt appearance of multiple seborrhoeic keratoses with a malignancy, rather than on any single laboratory cut-off.^[7][8]

Get out of the sun, ideally indoors. Take frequent cool baths or showers, then gently pat the skin dry. Apply an emollient such as aloe vera or soy while the skin is still damp, or use calamine lotion or a colloidal oatmeal bath. Take aspirin or ibuprofen for pain and swelling. Drink extra water, because a sunburn draws fluid to the skin surface. If the skin blisters, this is a second-degree burn: do not pop blisters, keep them clean and protect them with petroleum jelly.^[5][6]

Sunburn is usually a first-degree, superficial burn that peaks at 12 to 24 hours and clears within about a week.^[6] For pain, both topical and systemic NSAIDs such as aspirin, ibuprofen and indomethacin are useful because UV exposure raises prostaglandin E2 and contributes to erythema; NSAIDs may reduce erythema for 24 to 36 hours. Topical and systemic corticosteroids, regardless of timing, strength or dose, H1 and H2 antihistamines, antioxidants, aloe vera and vitamins have shown little or no effect on recovery time in a systematic review of 40 trials.^[6]

The single most reliable measures are behavioural: stay out of strong sun between 11 am and 3 pm, seek shade, and cover skin with a wide-brimmed hat, close-weaved long sleeves and sunglasses. Babies and young children should be kept out of direct sunlight. Avoid indoor tanning devices, which raise skin cancer risk at all ages.^[3]

When direct exposure cannot be avoided, apply sunscreen liberally to all uncovered skin 15 to 30 minutes before going out, ideally twice. Reapply every two hours, and straight after swimming, sweating or towel-drying, even with water-resistant products, which remain water resistant for only 40 or 80 minutes.^[3][4]

A sunscreen should be broad spectrum (UVA and UVB), have an SPF of at least 30, and be water resistant.^[4] Choose 5 UVA stars or the UVA circle logo for strong UVA protection. SPF 50 is advised all year round for people who are immunosuppressed after an organ transplant. Reapply as above; never use sunscreen to stay out longer or in place of shade and clothing.^[3][4]

For people with black or dark brown skin, routine sun protection is rarely needed in temperate climates, but it is important with photosensitivity, vitiligo, lupus, a high skin cancer risk, immunosuppression or residence in very sunny climates; reflection from snow, sand and water and high altitude can all increase UV exposure.^[3]

Babies and young children should be kept out of direct sunlight. From spring to autumn children need shade, covering clothing, hats and at least SPF 30 sunscreen. Vitamin D intake should be ensured as advised locally.^[3]

Do not sunbathe to top up vitamin D: at the point where skin begins to redden, vitamin D has already reached its optimum and continuing exposure only adds cancer and ageing damage. Small non-burning exposures make enough vitamin D, and people who avoid the sun can use supplements of about 10 to 25 micrograms per day, together with oily fish, eggs, meat and fortified margarine and cereals, with monitoring of serum 25-hydroxyvitamin D if needed.^[3][1]

There is often no need to treat seborrhoeic keratosis. Removal is requested for cosmetic, irritation or diagnostic reasons. Options include cryosurgery (most commonly used), shave excision, electrodessication, curettage or a combination of these, and laser (Er:YAG and CO2 give high clearance, with less hyperpigmentation than cryosurgery). In one trial total clearance was achieved with Er:YAG laser in all lesions compared with 68% with cryotherapy. HP40, a 40% hydrogen peroxide topical solution, clears some lesions, with the best response on the face (clear or near-clear in 65%) followed by the trunk and then the extremities; an aqueous nitric-zinc complex has also shown complete clearance in most treated lesions. Topical agents such as diclofenac, imiquimod, vitamin D analogues and dobesilate have only case-report or negligible evidence.^[7]

Lesions that are inflamed, bleeding, ulcerated or sufficiently irritated should be biopsied or excised to exclude malignancy before treatment.^[7]

Dermoscopy aids both diagnosis and follow-up; if dermoscopy is unavailable, a low threshold for biopsy of atypical lesions is wise. Melanoma can mimic seborrhoeic keratosis, especially in pigmented tumours, so any changing, asymmetric or multi-coloured lesion needs histology.^[7]

Because eruptive seborrhoeic keratoses can announce a hidden tumour, the sudden appearance of multiple pruritic lesions calls for cancer screening rather than cosmetic removal: start with a careful history and examination, and target imaging and age-appropriate endoscopy toward the sites most reported (stomach, colon, rectum, then breast, lymphoma and lung).^[7][8] The sign has been described in young people with cancer, which supports it as a real paraneoplastic phenomenon rather than a chance association in the elderly.^[8] Pseudo-Leser-Trelat from chemotherapy does not mean the underlying treatment has failed; treatment can continue.^[7]

Actinic keratoses are managed by dermatology, usually with cryotherapy, topical agents (such as 5-fluorouracil or imiquimod), photodynamic therapy, curettage or, where needed, excision, alongside strict sun protection and regular skin checks.^[3]

• Severe sunburn: blistering, dehydration and secondary infection. Repeated sunburns, particularly in childhood and adolescence, markedly increase the risk of melanoma, and lifetime UV dose increases the risk of squamous cell carcinoma.^[2][6]
• Photoageing is irreversible and accumulates even without burning.^[1]
• Skin cancers arise on sun-exposed sites; a high number of atypical moles is the strongest melanoma risk factor.^[2]
• Seborrhoeic keratosis rarely causes problems other than irritation, infection, bleeding or cosmetic concern, and it does not become malignant.^[7]
• Actinic keratosis may progress to invasive squamous cell carcinoma if untreated.^[2]
• Severe eye damage can follow UV overexposure (photokeratitis, pterygium, cataract, eye cancer), so the same protective advice covers eye protection.^[1]
• High, intermittent UV exposure also suppresses skin immunity, reducing defence against certain diseases.^[1]

Sunburn settles completely within about a week with no scarring beyond the epidermal peeling.^[6] Seborrhoeic keratosis is benign and, once removed, the individual lesion does not recur; the appearance of new lesions with age is expected. Actinic keratosis may be successfully eradicated and usually does not progress. The outcome in the sign of Leser-Trelat depends on stage of the underlying malignancy, which is why early recognition matters.^[7][8]

• Limit strong sun between 11 am and 3 pm, and follow the shade, clothing and sunscreen approach for planned exposures.^[3]
• Avoid sunbeds and indoor tanning completely.^[3]
• Apply broad-spectrum SPF 30+ sunscreen liberally to all exposed skin daily as routine, with SPF 50 year-round for transplant recipients and others with high skin cancer risk.^[3]
• Examine your skin about once a month and report any new or changing moles or patches; an annual check with a clinician is advised for those at increased risk.^[3]
• Treat actinic keratoses early and review sun-damaged skin regularly.^[3]
• Ensure vitamin D needs are met without deliberate sunbathing: small non-burning exposures or supplements of 10 to 25 micrograms per day.^[3][1]

• Babies and children. Keep babies and young children out of direct sunlight. Older children need shade and covering clothing with at least SPF 30 sunscreen from spring to autumn. Their skin burns easily and early sunburns raise lifetime skin cancer risk. Vitamin D intake should be ensured as advised locally.^[3]
• People with darker skin. Routine sun protection is rarely needed in temperate climates, but photosensitivity, vitiligo, lupus, immunosuppression, genetic predisposition and residence in very sunny climates are exceptions. They need more UV to maintain vitamin D and are more prone to deficiency at high latitudes.^[1][3]
• Older adults. Vitamin D synthesis declines with age, so housebound or veiled people need supplementation and serum monitoring. Seborrhoeic keratoses accumulate with age but remain benign. Skin cancers are more likely to have been seeded by decades of earlier exposure.^[1][3]
• Immunosuppressed patients. Organ transplant recipients need SPF 50 all year round, regular dermatological review, and early treatment of actinic keratoses and skin cancers.^[3]
• Pregnancy. No skin-cancer-specific change is needed beyond sensible sun protection and avoidance of overheating; if sun avoidance is necessary, ensure vitamin D intake.^[3]

Clothing, shade and hats are the cheapest and most reliable protection and cost almost nothing. Sunscreens are a supplement, not a substitute. Vitamin D can be protected by fortified foods and supplements where sunlight is scarce or unsafe. For seborrhoeic keratosis, dermoscopy may be unavailable, so enlarge the role of clinical diagnosis and low-threshold biopsy or excision of atypical lesions; simple cryotherapy or blade excision is feasible where trained staff and basic equipment exist. Lesions that bleed, ulcerate or grow need referral to exclude malignancy.

• UV radiation is the main cause of skin cancer, photoageing and sunburn, and damage can accumulate without a single severe burn.
• UVB causes sunburn and makes vitamin D; UVA penetrates more deeply and drives photoageing. A tan offers only an SPF of 2 to 4 and is a sign of damage.
• Limit strong sun between 11 am and 3 pm, and use shade, clothing and a broad-spectrum water-resistant sunscreen of at least SPF 30, applied 15 to 30 minutes before and every two hours.
• Sunburn is a superficial first-degree burn that settles within about a week; manage it with cool compresses or baths, emollients, fluids and NSAIDs. Corticosteroids, antihistamines and vitamins add little.
• Vitamin D needs are met by small non-burning exposures; those who avoid the sun should use 10 to 25 micrograms per day of supplement rather than sunbathe.
• Fair skin and phenotypes I and II carry the highest skin cancer risk; darker skin is more vitamin D deficient at high latitudes.
• Seborrhoeic keratosis is extremely common and benign, increasing with age; lesions that are irritated, bleeding or atypical need biopsy.
• Dermoscopy distinguishes seborrhoeic keratosis from melanoma and actinic keratosis, which is a precursor of squamous cell carcinoma.
• An abrupt eruption of multiple itchy seborrhoeic keratoses may be the sign of Leser-Trelat and calls for screening for stomach, colorectal, breast, lymphoma and lung malignancy.
• Immunosuppressed and transplant patients need SPF 50 all year and regular skin checks; babies and young children need strict sun avoidance.
• For people with black or dark brown skin, routine sun protection is rarely needed in temperate climates, but the exceptions matter.