Photodermatoses: Clinic, diagnosis and treatment

• The constant element is the localization of photodermatoses on the exposed skin with a clear limitation by the clothing protection. However, not all exposed skin is necessarily affected.
• The rash may extend secondarily to covered areas but always predominates in exposed areas^1-3.

Two mechanisms can be Triggered in the Occurrence of Photodermatoses

Photosensitization

• It is a phenomenon induced by the presence of a photosensitizing substance in the skin and its contact with solar radiation, which activates it.
• These substances reach the skin by internal (medication) or external routes (topical medication and most often contact with plants).
• This photosensitization is expressed in two ways: phototoxicity (sunburn type) and photoallergy, which is much rarer.
• This is a subject-specific reaction that requires prior sensitization.

Photosensitivity

• Photosensitivity is the overreaction of the skin to bright light or ultraviolet (UV) light.
• This concerns photoaggravated and photo-triggered dermatoses where the mechanisms are most often unknown (lupus erythematosus).
• Dermatoses in which photosensitivity is part of the signs of the disease, either due to a deficiency in the skin protective systems (albinism or xeroderma pigmentosum) or related to the presence of metabolic abnormalities: presence of porphyrins (porphyria cutanea tarda or PCT) or vitamin deficiency (vitamin PP and vitamin B in pellagra).

Photodermatoses by Photosensitization^3-5

Phototoxic Contact Dermatitis (PTCD)

• Meadow Grass Dermatitis:
  • Appearance 24 to 48 hours after contact with plants on wet skin during sunbathing, of erythematous, papulovesicular or bullous lesions, often linear or reproducing the pattern of grasses or leaf veins.
  • These plants contain psoralens. The lesions evolve towards a residual pigmentation.

• Plant Dermatitis:
  • Equivalent to meadow grass dermatitis.
  • Contact occurs when pulling weeds or mowing the lawn.
• Berloque Dermatitis:
  • Corresponds to the use of cologne, eau de toilette, refreshing towels...containing bergamot essence or other photoreactive essences responsible for pigmentations reproducing the application of the product, often in runs for liquid products, which can persist for months, even years.
  • The neck and neckline are frequently affected.

Systemic Phototoxicity

Phototoxic Reaction:

• It is a "super sunburn" in reaction to a specific medication.
• It manifests itself with an acute erythema of the uncovered areas, sometimes accompanied by oedema and bullae, frequently leaving residual pigmentation.
• There is a risk of persistent photosensitization (a few months to 2 years) despite the discontinuation of the responsible drug.
• Most commonly incriminated medication:
  • Cyclines: The reaction is dose dependent. It is safe to take 100 mg of doxycycline in the evening in the treatment of acne during the summer.
  • Quinolones.
  • Phenothiazines: in patients receiving high doses above 300 mg per day.
  • Tricyclic antidepressants.
  • Amiodarone: erythematous eruption, of the "super sunburn" type, affecting uncovered skin parts with a clear limitation by clothing protection. The reaction appears within 2 months to 2 years after the beginning of the treatment and disappears within 4 months of stopping taking the medication.

Photoallergic Contact Dermatitis

• Contact to certain plants: chrysanthemum for example.
• Taking medication such as ketoprofen: present in anti-inflammatory creams and responsible for many years of severe photoallergies.
• Use of sunscreen: currently, benzophenone, a filter used in sunscreen products, has a cross-reaction with ketoprofen.

Systemic Photoallergy

• Triggered by sulfonamides: hypoglycemic and especially diuretic including chlorothiazide, hydrochlorothiazide and furosemide. The usual appearance is an acute eczema of the uncovered skin parts, which usually regresses within 8 days after stopping the medication.

Photodermatoses by Photosensitivity^3,6-10

Photoaggravated Dermatoses

In those dermatoses, exposure to sunlight either triggers the disease, causes new lesions to appear on the exposed skin, or aggravates pre-existing lesions. The most frequent are:

• Lupus erythematosus (discoid or systemic).
• Recurrent herpes, especially of the upper lip.
• Rosacea.
• Acne vulgaris.
• Actinic lichen planus.
• Some genodermatoses: Bloom syndrome (BSyn), Cockayne syndrome, Rothmund-Thomson syndrome.

Dermatoses with sensitivity due to a deficiency in the protective system

A deficiency in the skin’s protective system can lead to a phototoxic reaction and can be complicated by multiple early onsets of skin cancers.

• Abnormalities in melanin formation and distribution:
  • Oculocutaneous albinism (OCA) with congenital generalized hypochromia affecting the epidermis, hair and eyes.
  • Vitiligo: very frequent circumscribed hypomelanosis with the presence of well-limited milky-white achromic naevus surrounded by peripheral hyperpigmentation.
  • Dermatoses with deficiency of DNA repair systems: xeroderma pigmentosum (XP).

Dermatoses with Photosensitivity Due to Metabolic Anomalies

• Cutaneous porphyrias: hereditary diseases related to a specific enzyme deficiency in the liver or bone marrow. Cutaneous porphyria tarda is the most common porphyria. The enzyme deficiency is hepatic, revealed by toxic factors: alcohol, medication, especially estrogen plus progestin contraceptives. It is characterized by:
  • The presence of bubbles on the back of hands and fingers, triggered by sun exposure leaving scars.
  • Skin fragility.
  • Greyish pigmentation of the face with occasional temporo-malar hypertrichosis in the form of long blackish hairs.

• Pellagra:
  • It is due to multiple vitamin deficiencies: vitamin PP mainly but also vitamins B1, B2 and B6 and tryptophan.
  • These deficiencies were previously linked to poverty, lack of food intake.
  • Currently: alcoholism, digestive malabsorption and certain medication (isoniazid or INH).
  • It is a skin condition triggered by the sun in the form of a reddish-purple erythema.
  • The lips are affected (dryness and cracking), the tongue (smooth, reddish-glazed edges), the digestive tract (abdominal pain and diarrhea) and neuropsychological disorders ranging from confusion to dementia.

• Pellagroid erythema: only the dermatological appearance of pellagra, without the other symptoms.

Idiopathic Photodermatoses¹¹

Idiopathic photodermatoses all require solar irradiation to manifest but the pathophysiology remains unknown.

Benign Summer Light Eruption (BSLE) or "Sun Allergy”

• Very frequent.
• It is more common in young women (between 25 and 35 years old).
• It appears within a few hours (less than 12 hours) after intense and prolonged exposure to bright sunlight on the first or second day of a seaside vacation.
• It is most often polymorphic, papular, papulovesicular or pseudo-urticarial, very pruritic.
• It affects the neckline, shoulders, upper limbs but always avoids the face.
• The eruption evolves spontaneously towards regression in about fifteen days without any sequelae.
• It recurs in the following years under the same conditions of sun exposure.
• It usually disappears after a few years.

Polymorphic Light Eruption (PLE)

• It can start at any age, there is no gender preponderance and there is a family history.
• The beginning of the eruption takes place in spring (March-April).
• It is triggered by a short duration (10 minutes to 3 hours) of exposure in everyday conditions (on a clear or overcast day).
• The face and the most exposed areas (neckline, forearms, etc.) are constantly affected.
• It is very pruritic with a burning sensation.
• The appearance of the rash is multifaceted, most often with small papules of 1 to 2mm in diameter, but also eczema-like, prurigo-like, with large papules, or with a maculonodular or patchy appearance, sometimes urticarial.
• Lip involvement (cheilitis) and ocular sensitivity are often present.
• It evolves in flare-ups, punctuated by sun exposure until the end of the Summer, and recurrence is usual each spring, with in some cases a worsening of the symptoms.

Juvenile Spring Eruption

• It affects children from 5 to 12 years of age with a male predominance, linked to the hairstyle off clearing around the ears.
• It always appears in the spring when exposed to the sun on a cold morning.
• It affects the ears (the free margin of the auricle), with papulo-edematous lesions, then papular and vesicular.
• It is pruritic and disappears spontaneously without sequelae in 15 days.

Rare Photodermatoses

• Solar urticaria.
• Hydroa vacciniforme.
• Actinic pseudolymphoma.

The diagnosis is based on asking questions to the patient, observing the appearance of the lesions, their histology, as well as the results of the photobiological exploration^{4, 12}:

• Positive diagnosis is usually established by the observation of the role of light in the onset of the rash and the involvement of the areas of uncovered skin.
• This makes it easy to exclude heat-related dermatitis, contact dermatitis of the face, and infectious dermatitis of the face (erysipelas, malignant staphylococcal disease).
• Questioning looks for the use of a substance known to be photosensitizing.
• The clinical examination establishes the semiological characteristics of the rash which then confirms the photoallergy in an exogenous photosensitization or specifies the specific characters of each idiopathic lucitis.