Sunlight and the skin

Controversy exists about the adverse effects of UV radiation exposure on the skin. However, damage can occur in four ways:
1 UVB (medium wavelength 280-310 nm) reaching the earth’s surface is increased by depletion of the stratospheric ozone layer. Synthetic chlorofluorocarbons e.g. some aerosols and refrigerators reaching this zone further compromise this important barrier function. A 1% decrease in the ozone layer has increased UVB levels at the earth’s surface by 2% with a concomitant rise in non-melanoma skin cancer of 2%. Increased levels of UVB are now being recorded in Europe. 2 Increased use of UVA (long wavelength 310-400 nm) for recreational tanning may expose individuals to more than five times the amounts reaching the earth’s surface at the equator. UVB is also generated in varying amounts by UVA lamps increasing the potential to cause skin cancer.
3 UVA accelerates skin ageing changes, augments the effects of UVB and penetrates into the dermis. It can affect the Langerhans cell, damage connective tissue and trigger photosensitivity diseases.
4 Evidence now exists that UV radiation affects immune responses in the skin in animals and humans and may have an effect on more general immunoreactivity. The effects of UV light on the skin may be beneficial or damaging. The formation of vitamin D from sterol precursors in the skin is dependent on sunlight, and UV light exposure may be used with benefit in the treatment of chronic skin conditions such as acne, eczema and psoriasis.
Damaging effects, however, occur with chronic irradiation, giving rise to changes in connective tissues that produce ageing, wrinkling, altered texture, dryness and changes in skin pigmentation. Epidermal changes include hyperkeratosis, dysplasia and malignancy.


These can be divided into:
• Eruptions in which sunlight has a primary role
• Diseases in which sunlight is a trigger or an exacerbating factor

Primary photosensitivity

Polymorphic light eruption

The term ‘polymorphic’ refers to the difference in the morphology of the eruption between one patient and another. The lesions tend, however, to be monomorphic in anyone individual.
Lesions are usually papulovesicular. Eczema, urticarial plaques or purpuric changes are less common. The rash is seen after a few hours of sun exposure and is inost common on the chest and arms, the backs of the hands or lower legs. The eruption usually occurs in spring and early summer and improves as summer progresses and the skin ‘hardens’. Fair-skinned individuals are most commonly affected by intense sunlight but those who have previously tanned easily and are of a darker complexion can also be affected. The papules may be associated with weeping and intense pruritus lasting for 5-10 days. The reaction can most readily be produced in the clinic or laboratory using high-intensity UV light at a wavelength of 320–420 nm. Pretreatment during spring-time with 12-18 treatments of PUV A may prevent the disease. Hydroxychloroquine given in doses of 400 mg daily for 2-3 weeks before and during sun exposure may prevent attacks. Topicalcorticosteroids such as betamethasone and high-factor sun-blo cking creams (factors 15-30) also help to minimize the disease.

Hutchinson’s summer prurigo

This rare disease usually has its onset before puberty. It affects both exposed and unexposed skin and may last throughout the year. Lesions are often excoriated and the necrotic papules may be quite disfiguring. The wavelengths responsible are usually in the sunburn range (290-320 nm). Sunscreen creams should be used but these do not offer sufficient protection in most cases. (3-Carotene given by mouth may help a few patients. Actinic reticuloid (chronic actinic dermatitis) This is a rare condition affecting older men in which the gross thickening, coloration and texture of exposed skin may resemble lymphomatous infiltration, both clinically and on microscopy. Many patients have had eczema previously and a significant proportion of these patients alsohave a positive patch test to materials such as rubber or  plants.
Clinical features include eczematous and purpuric lesions on non-exposed skin such as the legs, arms and trunk. Light sensitivity may be such that during active phases of the disease the only respite for patients is found in a darkened room. Protective clothing, sun-barrier creams, systemic steroid therapy, azathioprine, cytotoxic drugs and hydroxychloroquine may be required in combination to produce improvement.

Secondary photosensitivity

Topical agents

The application of perfumes (e.g. those contaimng bergaptine), sulphonamides and antimicrobial agents e.g. halogenated salicylanilides) may produce photosensitive reactions. The latter group of compounds have largely been withdrawn.
Plant extracts such as psoralens, commonly found in the family Umbelliferae, are used in photo chemotherapy (PUVA therapy). However, phytophotodermatitis may occur when the leaves of such plants (e.g. giant hogweed, wild parsley) abrade the skin surface. Psoralen compounds are absorbed into the skin and then activated by natural long-wavelength UV radiation. The linear configuration of the lesions should provide the clue to diagnosis.

Systemic agents

Systemic agents associated with photosensitivity include tetracyclines (chiefly chlortetracycline), thiazides (frusernide), phenothiazines, psoralens and retinoids.

Disease states

Sunlight can exacerbate SLE. Antibodies produced against DNA denatured by UV light form immune complexes in the skin and other organs. In porphyria, porphyrins deposited in the skin are activated by UV light.

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