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Polymorphic photodermatosis: causes, symptoms, diagnosis, treatment

 
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Last reviewed: 23.04.2024
 
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Polymorphic photodermatosis clinically combines the features of solar prurigo and eczema arising from exposure to the sun. Disease, in general, develops under the influence of UVB, sometimes UVA rays. The term "polymorphic photodermatosis" in 1900 was proposed by the Danish dermatologist Rash. He observed 2 patients in whom the clinical manifestations of the disease were very similar to solar eczema and solar prurigo. However, some scientists consider these diseases independent.

The term "polymorphic photodermatosis" is interpreted by scientists in different ways. For example, English dermatologists understand this disease as a disease that occurs in young children who have pink red papules hemispherical in shape, having a solid consistency, containing a yellowish vial on the surface (the rash is located in open and closed areas). The rash in the winter is subjected to a slight regression, but does not disappear at all. 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 the patients are girls) and is highly sensitive to sunlight.

Pathogenesis of polymorphic photodermatosis. The pathogenesis of the disease is not fully understood. According to some scientists, the appearance of the disease is of great importance for violations in the immune system. The blood of patients revealed an increase in the total content of T-lymphocytes, an increase in the skin of T-helpers compared to other cells. There was an increase in the blood of patients with B-lymphocyte and IgG-immunoglobulin content and an increase in neutrophil sensitization with respect to the protein. In the emergence of the disease, the endocrine and gastrointestinal system is of great importance. Simultaneous action of the above factors and 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 starts in the spring months. After 7-10 days after the action of the rays, the symptoms characteristic of this disease appear. One of the signs is the appearance on the open areas of the skin (face, neck, arms) of prurigious or vesicular rashes accompanied by itching. There are conjunctivitis and cheilitis. The disease occurs seasonally, the rash appears in the spring and summer months, decreases in autumn. Papules 0.2-1 cm in size, pink and red, are located on the erythematous skin. Fusing, they form plaques. As a result of severe itching on the skin there are excoriations and hemorrhagic crusts. In 1/3 of patients, there is papuloveziculosis rash, mocculation of the skin, and the clinical manifestation of the disease more closely resembles acute eczema.

The disease is characterized by a change in papular rash with vesiclesia. However, if the disease recurs and manifests itself with such morphological elements as erythema, pruriginous-lichenoid papules, excoriation, cortex, then it is possible to diagnose "solar prurigo". With a prolonged course of the disease, superficial dipigmental scars can be observed on the skin. One patient can see both pruriginous and eczematous lesions.

At the same time, on the skin of a patient there may be an urticarial and granulomatous rash. With the progression of the disease, the rash can spread to those parts of the body where the sun's rays do not reach.

In diagnosis and differential diagnosis, it is important to determine the minimum erythema dose, which is high for polymorphic photodermatosis.

Histopathology. Morphological changes are not specific. Acanthosis, spongiosis are detected in the epidermis, and in the dermis - an infiltrate consisting of leukocytes.

Differential diagnosis. Dermatosis should be distinguished from lupus erythematosus, erythropoietic protoporphyria, sarcoidosis, hydroa aestivalis.

The hereditary polymorphic photodermatosis of the American Indians described AR Birt, R. A. Davis in 1975. The disease is found among Indians in the Americas; begins in childhood. The ratio of sick women to men is 2: 1. Family cases of the disease account for 75% and it is assumed that it is transmitted dominantly by inheritance.

Dermatosis begins in the spring months, the rash is located only in areas prone to sunlight. In young children, the disease proceeds as an acute eczema on the skin of the face and is often associated with cheilitis (starts simultaneously).

An epidemiological survey of American Indians has shown that this dermatosis can contribute to the development of diseases such as streptococcal pyoderma, post-streptococcal glomerulonephritis.

Summer Prurigo Getschinson is a clinical form of polymorphic photodermatosis and is very rare. Dermatosis begins in adolescents and is manifested by the rash of nodules, on the surface of which there are vesicles. The rash is observed not only in open areas of the body, but also on the skin of the buttocks and lower legs. In winter, the morphological elements do not completely disappear. When conducting a phototest with UVB rays, 50% of the patients showed the appearance of nodules observed in polymorphic photodermatosis. Some dermatologists note that the summer Pruerigo of Getchinson is a form of hydroa aestivale, others refer it to polymorphic photodermatosis. However, the frequent appearance at the young age, on the surface of the nodules of the vesicle elements, a weak relationship between the rash and the effect of sunlight, the incomplete disappearance of the rash in winter, the presence of morphological elements in areas not affected by sunlight, distinguish it from polymorphic photodermatosis.

Treatment. It is recommended to protect patients from sunlight, the use of ointments and other photoprotective agents. Recommend vitamins (groups B, C, PP), antioxidants (alpha-tocopherol), methionine, thionicol. Use of antiplatelet drugs (delagil, once a day for 0.25 g 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, PUV therapy or phototherapy with UVB rays is performed, which yield positive results. The use of preventive PUVA therapy together with beta-carotene increases the effectiveness of treatment.

trusted-source[1], [2], [3], [4], [5]

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