Skin lesions caused by ultraviolet rays (photodermatoses): causes, symptoms, diagnosis, treatment

Ultraviolet radiation (UV) can reach the skin naturally as part of sunlight and through artificial UV irradiation with special lamps (medical phototherapy lamps and industrial UV lamps).

Human skin contains many substances that are natural chromophores capable of absorbing ultraviolet radiation. These include keratin proteins, erythrocyte hemoglobin, melanin, nucleic acids, lipoproteins, porphyrins, aromatic amino acids (tyrosine, tryptophan, histidine). As a result of excessive absorption of UVA and UVB by these natural chromophores, phototraumatic reactions, or solar dermatitis (sunburn), develop, the severity of which is directly proportional to the intensity and time of exposure of the skin to UV radiation. The natural color of human skin is of undoubted importance.

There are also photodynamic reactions of the skin caused by the accumulation of photosensitizers in the skin - substances that increase its sensitivity to ultraviolet radiation. There are obligatory and facultative photosensitizers, which can be exogenous or endogenous.

Obligate exogenous photosensitizers include solid hydrocarbons of oil, coal, photocoumarins (found in plants - clover and buckwheat, in many essential oils, such as bergamot, including those used in perfumery). The main obligate endogenous photosensitizers are porphyrins. Porphyrins are produced by the bone marrow and also enter the body with food. When combined with iron, they form the heme component of hemoglobin contained in erythrocytes. The liver is the main organ involved in the metabolism of porphyrins. When the function of liver cells is impaired, the normal metabolism of porphyrins may be disrupted and late cutaneous porphyria may develop - a disease whose skin manifestations are provoked by ultraviolet rays. In this photodermatosis, a deficiency of uroporphyrinogen decarboxylase is detected in liver cells, which is facilitated by chronic alcohol intoxication, exposure to hexachlorobenzene and estrogens (when taking a number of hormonal contraceptives and estrogenic drugs).

The blood increases the level of uroporphyrins, which are deposited on the skin and sharply increase its sensitivity to ultraviolet rays. Porphyrins in the skin act as UVA and UVB accumulators, which leads to damage to cellular structures, the formation of free radicals and oxygen molecules, and the development of an inflammatory reaction.

Under the influence of ultraviolet rays, photoallergic reactions are possible in the skin, caused by:

• exogenous photosensitizers (chromium salts, some detergents, long-term topical steroids);
• endogenous photosensitizers (poisoning with tetraethyl lead, which is part of leaded gasoline, taking tetracycline drugs, barbiturates, sulfonamides, etc.).

Symptoms of photodermatoses. Phototraumatic reactions are manifested by the clinical picture of simple acute or chronic dermatitis. With a single intensive insolation, erythema of the irradiated skin areas develops after 4-6 hours (grade I lesion), against which painful blisters with serous contents may form (grade II dermatitis). Bullous lesions are most often observed in the shoulder area and upper third of the back, i.e. in localizations of maximum exposure to UV radiation, where acute solar dermatitis, or "sunburn", is formed. Under the influence of extremely high doses of UV radiation when irradiated with artificial sources of ultraviolet radiation, necrosis of the epidermis and dermis may develop (grade III dermatitis).

Chronic solar dermatitis develops with chronic exposure of exposed skin areas to sunlight. This is most often observed in people who spend a long time in the sun (builders, sailors, agricultural workers). Stable pigmentation, lichenification, peeling, telangiectasias and cracks develop on the back of the neck, hands and even on the face. Rapid formation of skin dystrophy and various skin neoplasms is possible.

Photodynamic reactions manifest themselves on exposed areas of the skin as erythematous and bullous rashes, and the dose of ultraviolet radiation received may be insignificant, but its destructive effect is enhanced by photosensitizers accumulated in the skin.

Late cutaneous porphyria is characterized by the formation of blisters on an erythematous base on the face and back of the hands. These rashes are provoked by UV radiation and minor mechanical injuries. The blisters open with the formation of erosions and superficial ulcers that heal with atrophic scars. Itching is a concern. Such reactions are repeated seasonally, in the spring and summer. When the rash resolves, foci of hyperpigmentation may remain. The face of such patients gradually becomes pigmented, the soft tissues of the eye sockets become sunken ("sunken" eyes). Patients look older than their years. The urine of patients is bright orange, when examined under a fluorescent lamp in UV rays, the urine glows bright pink.

Photoallergic reactions are polymorphic and can manifest as microvesicles against the background of edematous erythema (“solar eczema”), blisters (“solar urticaria”), and gray papules similar to nodular prurigo (“solar prurigo”).

The diagnosis of phototraumatic, photodynamic and photoallergic reactions is made based on anamnesis data (presence of exposure to the sun or UV lamp rays, clear seasonality of the lesion), localization of lesions on exposed areas of the skin.

Principles of therapy and prevention. Active photoprotection is indicated. Therapy is similar to that of contact dermatitis.

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