Outbreaks of polymorphic light eruption (PLE) typically occur in the spring and summer, but can occur at any time of the year when individuals are in areas of high sun exposure. Lesions appear on the skin several hours to days after sun exposure, often within 18-24 hours, and are localized to sun-exposed areas of the body, including the neck, chest, shoulders, forearms and shins, less commonly the face and trunk. The eruptions are accompanied by varying degrees of itching, occasionally a burning sensation or paresthesia. After sun exposure, the rash elements resolve within a few days to 1-2 weeks without scarring.

The eruptions show significant polymorphism, including small lichenoid papules or larger prurigo-like papules, polymorphic erythema or annular granulomas, eczematous eruptions, and urticarial eruptions.

The most characteristic eruptions are pink to red papules, 0.2 to 1 cm in diameter, on an erythematous background. Individual papules may coalesce to form plaques, sometimes clinically resembling the lesions of discoid lupus erythematosus because of their intense pruritus, and the skin of affected individuals is often characterized by excoriation and linear hemorrhagic crusts.

In about 1/3 of patients, the papular-vesicular eruptions on sun-exposed skin are often accompanied by moisturization, mimicking the clinical picture of eczema.

In addition to the cutaneous manifestations, about 1/4 of patients have actinic cheilitis of varying severity, accompanied by burning and pain.

The disease typically follows a chronic, relapsing course. During recurrences many patients show the same morphological type of eruptions. Polymorphous light eruption is characterized by the phenomenon of adaptation (hardening) - reduction of disease symptoms after repeated short-term exposure of the patient to the sun. This phenomenon is attributed to the development of skin tolerance to sunlight, and as a result, many patients with eruptions that first appear in spring or early summer do not experience recurrences later. In some patients, a few years may pass, resulting in a decrease in the severity of the recurrence or complete recovery.

The diagnosis of polymorphic light eruption is based on the patient's medical history, the presence of characteristic clinical symptoms of the disease, the results of phototesting, and laboratory tests.

Phototesting: To confirm the diagnosis, phototesting is performed using artificial sources of UVA and UVB radiation or sunlight simulators. Exposure is directed to areas of the skin that are free of eruptions (such as the back, abdomen, or inner forearm).

Photoprovocation tests are performed to induce PLE eruptions and determine the range of ultraviolet radiation that triggers the disease. However, these tests can be negative in 50% of patients. PLE eruptions are often induced by long-wave ultraviolet radiation (UVA range, wavelength 320-400 nm), less commonly by medium-wave ultraviolet radiation (UVB range, wavelength 280-320 nm), or a combination of medium- and long-wave ultraviolet radiation (UVA/B range, wavelength 280-400 nm). Skin photopatch testing is performed when a patient's sensitization to drugs or chemicals is suspected.

Laboratory tests: Complete blood count, urinalysis, and blood biochemistry may be performed. Antibody testing includes antinuclear antibody (ANA) titers, anti-double-stranded (native) DNA antibodies, anti-Sm antibodies, anti-Ro/SS-A antibodies, and anti-La/SS-B antibodies, among others, which are performed to rule out systemic lupus erythematosus (SLE). Porphyria testing examines the levels of porphyrins in blood plasma, erythrocytes, and urine and is performed to rule out porphyria.

• Systemic and discoid lupus erythematosus
• Erythropoietic protoporphyria
• Phototoxic and photoallergic reactions
• Skin conditions exacerbated by sunlight or ultraviolet light (atopic dermatitis, seborrheic dermatitis, erythema multiforme).
• Solar urticaria.
• Hydroa vacciniforme
• Chronic actinic dermatitis.
• Dermatitis herpetiformis

General Treatment Recommendations:

When eruptions occur, patients are advised to avoid or limit sun exposure, especially during the midday hours (11:00 am to 4:00 pm), and to apply sunscreen regularly. In most patients, these measures are sufficient to induce regression of the affected areas.

Topical corticosteroids are used as symptomatic therapy, but controlled studies confirming their efficacy are lacking. In cases of severe symptoms that cause significant discomfort to the patient, a short course of oral prednisone may be effective.

In cases of PLE recurrence and no response to sunscreen, it is recommended that patients undergo preventive treatment in early spring or early summer with narrow band ultraviolet therapy at a wavelength of 311 nm, broad spectrum medium wave ultraviolet therapy at a wavelength of 280-320 nm, or PUVA therapy.

Preventive phototherapy courses increase the tolerance of patients' skin to sunlight, thereby preventing flares in summer or reducing the severity of clinical manifestations during exacerbations. The protective effect of phototherapy can last for 6-8 weeks or longer. To maintain tolerance to sunlight throughout the summer, patients are advised to spend 1-2 hours per week in the sun without using protective measures. For a more permanent effect, preventive phototherapy courses are performed several times and repeated every spring.

Narrow band medium wave ultraviolet therapy with a wavelength of 311 nm is preferred to PUVA therapy because it shows similar efficacy with a better safety profile.

There is evidence for the efficacy of treating PLE with antimalarials, beta-carotene, and antioxidants. However, the limited evidence base does not allow definitive conclusions about the advisability of their use. In a placebo-controlled trial, a modest efficacy of preventive treatment with chloroquine and beta-carotene was observed, corresponding to a protection factor of 2. Hydroxychloroquine has been shown to reduce the clinical manifestations of the disease (burning, itching, and erythema) to a greater extent than chloroquine, but it also has limited efficacy. In a double-blind randomized trial, the efficacy of oral vitamin C and E, which have antioxidant properties, did not differ from placebo.

In severe cases, immunosuppressive drugs such as azathioprine or cyclosporine may be used as an alternative treatment.

Medication Therapy:

Topical corticosteroids.

Treatment should continue until the eruptions completely resolve.

• Mometasone furoate, cream, or ointment, applied topically 1-2 times daily, or
• Methylprednisolone acetate, cream, ointment, or emulsion, applied topically 1-2 times, or
• Alclometasone dipropionate, cream, or ointment, applied topically 1-2 times, or
• Betamethasone valerate, cream, or ointment, applied topically 1-2 times daily, or
• Betamethasone dipropionate, cream, or ointment, applied topically 1-2 times daily, or
• Fluticasone propionate, cream, or ointment, applied topically 1-2 times daily, or
• Hydrocortisone butyrate, cream, or ointment, applied topically 1-2 times daily, or
• Clobetasol propionate, cream, or ointment, applied topically 1-2 times daily.

Systemic corticosteroids.

• Prednisone, 25 mg orally per day for 4-7 days.

Non-Medication Therapy:

• Narrowband medium-wave ultraviolet therapy with a wavelength of 311 nm.
• Broad-spectrum medium-wave ultraviolet therapy (synonymous with selective phototherapy, wavelength 280-320 nm).
• PUVA therapy with oral photosensitizer.

Treatment Approach in the Absence of Treatment Efficacy:

• In the absence of effectiveness from the use of sunscreens, a course of medium-wave ultraviolet therapy or PUVA therapy is recommended.
• In the absence of effectiveness from medium-wave ultraviolet therapy, a course of PUVA therapy is recommended.
• In the absence of effectiveness from phototherapy and corticosteroid treatment, hydroxychloroquine or immunosuppressive drugs (azathioprine or cyclosporine) may be considered.

Preventive Measures:

• Patients are advised to avoid direct sunlight exposure and to wear protective clothing and headgear that shield them from sunlight.
• Regular use of broad-spectrum sunscreen with a high protection factor is necessary.
• Patients should be informed about the possibility of UV-A radiation penetration through windows.