Photodermatoses: Clinic, diagnosis and treatment
Medical review by Dr. Pierre Schneider, Dermatologist, Saint-Louis Hospital, France.
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Dr. Pierre Schneider
Related topics
- Photoprotection
Key messages:
- Photodermatoses are a group of skin disorders caused by an abnormal reaction of the skin to sunlight or other light sources1.
- Symptoms may include redness, itching, blistering, pain or burning1.
- Photodermatoses can be caused by excessive exposure to sunlight, photosensitive medication or genetic diseases1.
- Photodermatoses can be classified according to their origin and symptoms, and treatment may include taking medication, applying special sunscreen and avoiding sun exposure1.
- 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 areas1-3.
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).
Good to know:
There are also so-called "idiopathic" photodermatoses for which it is known that they all require solar irradiation to occur, but the precise pathophysiology remains unknown.
Photodermatoses by Photosensitization3-5
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.
Good to know:
- In the context of photosensitization dermatoses, only the most evocative aspects have been described as well as the molecules most often incriminated in one of the two mechanisms (phototoxicity or photoallergy).
- However, it is important to remember that many agents, by contact or during systemic administration, can induce both types of reactions.
- The list of inducing agents is long and growing every day.
Photodermatoses by Photosensitivity3,6-10
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 exploration4, 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.
Good to know:
- Photobiological exploration consists of exposing the skin to a specific light source, such as a UVB or UVA lamp, to evaluate the skin's reaction.
- This exposure can be done directly on the affected area or on a control area.
All Photodermatoses Benefit from External Photoprotection13
Clothing
- Long sleeve tops.
- Long trousers.
- Glasses.
- Headgear.
Sun Protection
- SPF (sun protection factor) 50+ balanced against UVB and UVA, water resistant, sweat resistant and with good photostability. In the form of cream for the face and neckline, milk or spray for the body, stick for lips and scars.
- Application should be regular during the day when outdoors, ideally every 2 hours.
According to the Pathologies13
Photodermatoses with Photosensitization
- Discontinuation of triggering contact or systemic photosensitizers.
- Often, a level 2 local corticosteroid therapy is prescribed for 15 days.
Photodermatoses with Photosensitivity
- Effective external photoprotection is the only recourse in photoaggravated dermatoses and dermatoses with deficient skin protection systems.
- In photosensitivity due to metabolic abnormalities:
- In porphyria cutanea tarda, bloodletting and synthetic antimalarials are used.
- In pellagra and pellagra syndromes: intake of vitamin PP, B1, B2, B6, tryptophan, depending on the deficits and dietary rebalancing.
Idiopathic Photodermatoses
- Benign summer light eruption: PUVA therapy or UVB TL-01 phototherapy in increasing doses in the 6 weeks preceding the departure on vacation (10 to 15 sessions).
- Polymorphic light eruption: PUVA therapy or UVB TL-01 phototherapy started in late winter or early spring or synthetic antimalarials.
- Juvenile spring eruption: level 2 local steroid therapy for 10 days.
Basic Rules of Good Interaction with the Sun14
- Avoid exposure during the hottest hours (12:00 to 4:00 pm).
- Systematically apply a sun protection adapted to the type of skin and outside conditions. The strength of the sun protection (SPF and IP UVA) should match the strength of the sunlight (polar, tropical) as well as matching skin sensitivity (fair skin, children...).
- Apply sun protection 20 minutes before exposure, then every 2 hours.
- Reapply the product after each swim.
- The application of sunscreen should allow for safe exposure but should not, under any circumstances, encourage prolonged exposure.
- Never expose children under 1 and up to 3 years of age.
- The use of a parasol is possible provided that it is made of anti-UV fabric and that one keeps in mind that it does not protect from reflected radiation, not negligible on the sand.
- Beware of the apparent protection of clouds: they allow a very large quantity of UV rays to pass through. Beware also of a windy atmosphere on land or on a boat which cancels out the infra-red alarm signal (sensation of heat which encourages you to take shelter from the sun).
- Remember that the reflection of the sun's rays off the sand and water increases the amount of UV received.
- Ban exposure to artificial UVA rays in a tanning booth, which has been shown to increase the risk of skin cancer.
Tips for Preventing Summer Light Eruption14
- Prepare your skin for the sun, 15 days before exposure to the sun and throughout the sun exposure by using a food supplement containing fish oils, rich in omega-3 fatty acids, carotenoid pigments and other antioxidant ingredients.
- Apply a sunscreen with an SPF of no more than 30 throughout the exposure period to allow the tanning process to take place, which has a UVA protection equivalent to the SPF (recommended coefficient: SPF30 / IP UVA 30), as UVA rays play a fundamental role in triggering lucitis.
- This recommendation does not apply to milky skin (phototype I, redheads) and extreme sun conditions (polar, tropical) which require a very high SPF 50+ protection.
- Lehmann P et Schwarz T. Photodermatoses: diagnosis and treatment. Dtsch Arztebl Int. 2011 Mar;108(9):135-41.
- Adamski H. Actualités des photodermatoses. Réalités Thérapeutiques en Dermato-Vénérologie n° 277_Décembre 2018
- Chader H et Gacem H. Impact de l’irradiation solaire sur la santé. Batna J Med Sci 2020;7(2):151-8.
- Béani JC. Les photosensibilisations graves. Ann Dermatol Venereol. 2009 Jan;136(1):76-83.
- Montgomery S et Worswick S. Photosensitizing drug reactions. Clin Dermatol. 2022 Jan-Feb;40(1):57-63.
- Arora H, Chacon AH, Choudhary S, McLeod MP, Meshkov L, Nouri K, Izakovic J. Bloom syndrome. Int J Dermatol. 2014 Jul;53(7):798-802.
- Bergqvist C et Ezzedine K. Vitiligo: A Review. Dermatology. 2020;236(6):571-592
- Black JO. Xeroderma Pigmentosum. Head Neck Pathol. 2016 Jun;10(2):139-44.
- Hołubiec P, Leończyk M, Staszewski F, Łazarczyk A, Jaworek AK, Rojas-Pelc A. Pathophysiology and clinical management of pellagra - a review. Folia Med Cracov. 2021 Sep 29;61(3):125-137.
- Dawe R. An overview of the cutaneous porphyrias. F1000Res. 2017 Oct 30;6:1906.
- Ledo E. Photodermatosis. Part I: Photobiology, photoimmunology, and idiopathic photodermatoses. Int J Dermatol. 1993 Jun;32(6):387-96.
- C. Piérard-Franchimont, M. Caucanas, P. Quatresooz, G.E. Piérard. Identification d’une dermatose provoquée par la lumière. Rev Med Liège 2011; 66 : 12 : 643-647
- Gozali MV, Zhou BR, Luo D. Update on treatment of photodermatosis. Dermatol Online J. 2016 Feb 17;22(2):13030/qt1rx7d228.
- Risques solaires, ce qu’il faut savoir pour que le soleil reste un plaisir. [Accessed on 22/03/2023] www.prevention-soleil.fr
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