Medical expert of the article
New publications
Skin lesions caused by ultraviolet rays (photodermatosis): causes, symptoms, diagnosis, treatment
Last reviewed: 23.04.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Ultraviolet radiation (UV) can get on the skin naturally in sunlight and with artificial UV-irradiation with special lamps (medical fotarii and UV lamps of industrial purpose).
In the human skin there are many substances that are natural chromophores, capable of absorbing ultraviolet radiation. These include keratin proteins, hemoglobin erythrocytes, melanin, nucleic acids, lipoproteins, porphyrins, aromatic amino acids (tyrosine, tryptophan, histidine). As a result of excessive absorption by these natural chromophore UVA and UVB, phototraumatic reactions, or solar dermatitis (solar "burn") develop, the severity of which is directly proportional to the intensity and time of exposure to UV radiation on the skin. Of undoubted importance is the natural color of the human skin.
There are also photodynamic skin reactions caused by the accumulation of photosensitizers in the skin - substances that increase its sensitivity to ultraviolet radiation. Separate obligate and facultative photosensitizers, which can be exo- or endogenous.
The obligate exogenous photosensitizers include solid hydrocarbons of oil, coal, photocoumarins (found in clover and buckwheat plants, in many essential oils, for example in 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. Connecting with iron, they form a hemoconstituent part of hemoglobin, contained in red blood cells. The liver is the main organ involved in the metabolism of porphyrins. If the function of the liver cells is disturbed, normal metabolism of porphyrins can be disturbed and later skin porphyria may develop, a disease whose skin manifestations are provoked by ultraviolet rays. This photodermatosis reveals a deficiency of uroporphyrinogenecarboxylase in the liver cells, which is promoted by chronic alcohol intoxication, exposure to hexachlorobenzene and estrogens (when taking a number of hormonal contraceptives and estrogen preparations).
In the blood, the level of uroporphyrins increases, which are deposited on the skin and sharply increase its sensitivity to ultraviolet rays. Porphyrins in the skin play the role of UVA and UVB accumulators that drive the damage to cellular structures, the formation of free radicals and oxygen molecules, the development of an inflammatory reaction.
Under the influence of ultraviolet rays in the skin, photo-allergic reactions are possible, due to:
- exogenous photosensitizers (chromium salts, some detergents, long-term topical steroids);
- endogenous photosensitizers (tetraethyl lead poisoning included in leaded gasoline, taking tetracycline drugs, barbiturates, sulfonamides, etc.).
Symptoms of photodermatosis. Phototractive reactions are manifested by a clinic of simple acute or chronic dermatitis. With a single intense insolation after 4-6 h develops erythema irradiated area of the skin (I degree of injury), against which can form painful blisters with serous contents (II degree of dermatitis). Bullous lesions are most often observed in the area of the shoulder and upper third of the back, i.e. In the localizations of maximum exposure to UVL, where you form acute sun dermatitis, or "sunburn". Under the influence of prohibitively high doses of UV with irradiation with artificial sources of ultraviolet irradiation, the development of necrosis of the epidermis and dermis (III degree of dermatitis) is possible.
When chronic exposure to sunlight on the exposed areas of the skin, chronic sun dermatitis is formed. Most often this is observed in people who spend a lot of time in the sun (builders, sailors, agricultural workers). On the back surface of the neck, hands and even on the face is formed persistent pigmentation, lichenification, desquamation, telangiectasia and fissures. Possible rapid formation of skin dystrophy and various skin lesions.
Photodynamic reactions are manifested in open areas of the skin with erythematous and bullous rash, and the dose of ultraviolet radiation can be insignificant, but its destructive effect is enhanced by photosensitizers accumulated in the skin.
Late skin porphyria is characterized by the formation on the face, the back of the hands of blisters on the erythematous base. These rashes are provoked by UVL and minor mechanical injuries. Bubbles are opened with the formation of erosions and superficial ulcers that heal atrophic scars. An itch disturbs. Similar reactions are repeated seasonally, in the spring-summer period. When resolving the rash, hyperpigmentation foci may remain. The face of these patients is gradually pigmented, the soft tissues of the orbit sink ("failing" eyes). The patients look older than their years. The urine of patients has a bright orange color, when viewed under a fluorescent lamp in UV rays, the urine glows bright pink.
Photo-allergic reactions are polymorphic and can be manifested by microvesicles on the background of edematous erythema ("solar eczema"), blisters ("solar urticaria"), gray-papules as a nodular prurigo ("sun prurigo").
The diagnosis of phototravmatic, photodynamic and photoallergic reactions is based on the history (presence of sun exposure or UV rays, clear seasonality of the lesion), localization of lesions in open areas of the skin.
Principles of therapy and prevention. Active photoprotection is shown. Therapy is similar to contact dermatitis therapy.
[