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Polymorphic photodermatosis: causes, symptoms, diagnosis, treatment
Last reviewed: 07.07.2025

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Polymorphic photodermatosis clinically combines the features of solar prurigo and eczema caused by sun exposure. The disease mainly develops under the influence of UVB, sometimes UVA rays. The term "polymorphic photodermatosis" was proposed in 1900 by the Danish dermatologist Rash. He observed 2 patients whose clinical manifestations of the disease were very similar to solar eczema and solar prurigo. However, some scientists consider these diseases to be independent.
The term "polymorphic photodermatosis" is interpreted differently by scientists. For example, English dermatologists understand this disease as a disease that occurs in small children, who develop pink red papules of a hemispherical shape, having a hard consistency, containing a yellowish vesicle on the surface (the rash is located on open and closed areas). The rash undergoes a slight regression in winter, but does not disappear completely. In the scientific literature of South America, polymorphic dermatosis is included in the number of hereditary diseases. It occurs mainly in Indian families (80% of patients are girls) and is manifested by high sensitivity to sunlight.
Pathogenesis of polymorphic photodermatosis. The pathogenesis of the disease has not been fully studied. According to some scientists, disorders in the immune system are of great importance in the development of the disease. An increase in the total content of T-lymphocytes, an increase in T-helpers in the skin compared to other cells were found in the blood of patients. An increase in the content of B-lymphocytes and IgG immunoglobulins and an increase in the sensitization of neutrophils in relation to protein are noted in the blood of patients. The endocrine and gastrointestinal systems are of great importance in the development of the disease. The simultaneous action of the above factors and the high sensitivity of the patient to sunlight accelerate the development of the disease.
Symptoms of polymorphic photodermatosis. The disease occurs between 10-30 years and most often in women. It usually begins in the spring months. 7-10 days after exposure to rays, symptoms characteristic of this disease appear. One of the signs is the appearance of pruritic or vesicular rashes on exposed areas of the skin (face, neck, hands), accompanied by itching. Conjunctivitis and cheilitis are observed. The disease is seasonal, the rash appears in the spring and summer months, and decreases in the fall. Papules 0.2-1 cm in size, pink-red in color, are located on erythematous skin. Merging, they form plaques. As a result of severe itching, there are excoriations and hemorrhagic crusts on the skin. In 1/3 of patients, papulovesicular rash, weeping skin are observed, and the clinical manifestation of the disease is more reminiscent of acute eczema.
The disease is characterized by the change of papular rash to vesiculosis. However, if the disease recurs and manifests itself with such morphological elements as erythema, pruriginous-lichenoid papules, excoriation, crust, then the diagnosis of "solar prurigo" can be made. With a long course of the disease, superficial dipigment scars can be observed on the skin. In one patient, both pruriginous and eczematous lesions can be seen.
At the same time, urticarial and granulomatous rashes may be found on the patient's skin. As the disease progresses, the rash may spread to those areas of the body that are not exposed to sunlight.
In diagnostics and differential diagnostics, it is important to determine the minimum erythemal dose, which is high for polymorphic photodermatosis.
Histopathology. Morphological changes are not specific. Acanthosis and spongiosis are detected in the epidermis, and an infiltrate consisting of leukocytes is found in the dermis.
Differential diagnosis. Dermatosis should be distinguished from lupus erythematosus, erythropoietic protoporphyria, sarcoidosis, hydroa aestivalis.
Hereditary polymorphic light eruption of American Indians was described by A. R. Birt, R. A. Davis in 1975. The disease occurs among Indians in North and South America; it begins in childhood. The ratio of affected women to men is 2:1. Familial cases of the disease make up 75% and it is assumed that it is transmitted dominantly by inheritance.
Dermatosis begins in the spring months, the rash is located only on areas exposed to sunlight. In small children, the disease occurs as acute eczema on the skin of the face and is often associated with cheilitis (it begins at the same time).
An epidemiological study of American Indians showed that this dermatosis can contribute to the development of diseases such as streptococcal pyoderma and poststreptococcal glomerulonephritis.
Summer prurigo of Hutchinson is a clinical form of polymorphic photodermatosis and is very rare. The dermatosis begins in adolescents and is manifested by a rash of nodules with vesicles on the surface. The rash is observed not only on exposed areas of the body, but also on the skin of the buttocks and shins. In winter, morphological elements do not completely disappear. When conducting a phototest with UVB rays, 50% of patients showed the appearance of nodules observed in polymorphic photodermatosis. Some dermatologists note that summer prurigo of Hutchinson is a form of hydroa aestivale, others attribute it to polymorphic photodermatosis. However, the frequent appearance at a young age, on the surface of the nodules of vesicular elements, a weak connection between the rash and the action of sunlight, incomplete disappearance of the rash in winter, the presence of morphological elements in areas not exposed to sunlight, distinguish it from polymorphic photodermatosis.
Treatment. It is recommended to protect patients from sunlight, use ointments and other sunscreens. Vitamin therapy (groups B, C, PP), antioxidants (alpha-tocopherol), methionine, thionicol are recommended. The use of antipyretic drugs (delagyl, 0.25 g once a day for 5 days) gives good results. The use of beta-carotene together with xanthaxanthin increases the effectiveness of treatment. In order to prevent polymorphic photodermatosis in early spring and during remission, PUVA therapy or phototherapy with UVB rays is carried out, which give positive results. The use of preventive PUVA therapy together with beta-carotene increases the effectiveness of treatment.
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