- Clinical science
Photodermatoses consist of a variety of skin conditions that develop as a result of exposure to ultraviolet radiation (UVR) or visible light. The most common photodermatosis in the US is sunburn (dermatitis solaris), an inflammatory reaction that occurs after excessive UV exposure. This acute photodermatitis may potentially affect anyone, with a third of all adults and two-thirds of all children in the USA being affected at least once per year (lighter-skinned individuals are affected more frequently and severely). Other forms of photodermatoses include polymorphous light eruption (PLE) and phototoxic reactions. Polymorphous light eruption (PLE) is a delayed photosensitivity disorder involving pruritic rashes caused by exposure to ultraviolet A (UVA) radiation during the summer months. Lesions may vary from patient to patient; however, spontaneous resolution (on cessation of sun exposure) is often a unifying trait. Phototoxic reactions are patterned, inflamed eruptions of erythema and vesicles caused by contact with photosensitizing agents (like psoralen) and subsequent sun exposure. Diagnosis of these conditions is usually established on the basis of a thorough history and a full skin examination. Additionally, phototesting and/or photopatch testing are often utilized. Measures such as avoiding the sun, sun protective clothing, and sunscreen are the mainstay of therapy. Additional symptomatic treatment with cool compresses, emollients, and oral analgesics may be prescribed depending on the severity of symptoms.
- Definition: acute inflammatory skin response to UVR; , which is limited to the area of exposure. Sunburn (or dermatitis solaris) is often classified as a 1st or 2nd-degree burn.
- Epidemiology: particularly light-skinned individuals
- Etiology: excessive exposure to UVB radiation (wavelength: 280–320 nm)
- Pathogenesis: UV radiation → apoptosis of keratinocytes in the epidermis and release of inflammatory markers (including chemokines, prostaglandins) → inflammation of the dermis hours after exposure
- Primarily limited to exposed skin
- Begins a few hours after exposure, with symptoms peaking after 12–24 hours; usually resolves within a week
- Initially pain, then redness and swelling and
- Blisters may occur in severe cases of sunburn; if larger areas are affected, general symptoms (e.g., fever) may arise.
- Avoid sun exposure
- Protective clothing
Sunscreen with adequate SPF
- Applied at least 30 minutes prior to sun exposure
- Reapplied after 2–3 hours, exposure to water (swimming), and/or sweating
- The most effective active ingredients block UVA and UVB radiation
- Zinc oxide effectively absorbs both UVA and UVB
- Trolamine salicylate, Para-aminobenzoic acid, and Vitamin E only absorb UVB radiation
A severe sunburn with blistering (corresponding to a second-degree burn) that affects over 10% of an adult's body surface (or more than 5% in children) may result in a capillary leak and ultimately lead to hypovolemic shock!
- Definition: : acquired photodermatosis characterized by a pathological response to UV exposure; (also known as a sun allergy)
- Epidemiology: most frequently occurring idiopathic photodermatosis
- Most likely a cell-mediated immune response resembling delayed-type hypersensitivity
- Presumably caused by reaction to autoantigens that arise from UV exposure (especially UVA, less so UVB)
- Symptoms typically present a few hours to days after the first high intensity UV exposure in the spring or the summer.
- Without continuous sun exposure: resolves within a week
- Common sites involved: sun-exposed areas
- The symptoms usually recur annually; (always at the same anatomical sites and after first sun exposure).
- Usually clinical diagnosis
- Provocative phototesting: occurrence of lesions is provoked by selective UV radiation
- Skin biopsy
- Avoid UVA exposure
- If exposed: sun protection; sunscreen → combination of UV filters and antioxidants (α-glucosylrutin)
Habituation (4–6 weeks before more intense UV exposure)
- Slowly increasing full body exposure to UVB radiation; possibly systematic PUVA (psoralen and ultraviolet A) treatment in severe cases
- Local glucocorticoid therapy for acute skin inflammation and pruritus
- Possibly antihistamines to reduce itching
Drug-induced phototoxic reactions
- Short description: non-allergic photosensitivity reaction due to certain drug metabolites
Pathophysiology: drug metabolites interact with UV light (usually triggered by UVA) → free radical release → direct tissue or cell injury → severe rash
- occurs without pre-sensitization to the drug
- Etiology: tetracyclines (especially doxycycline), thiazides, sulfonamides, fluoroquinolones, retinoids, psoralens, NSAIDs, griseofulvin.
- Clinical features:
- Diagnosis: history of drug exposure, phototesting and/or photopatch testing, skin biopsy
- Treatment: Discontinuation of offending drug (if feasible), photoprotective measures, symptomatic treatment (see sunburn)
- Short description: photosensitivity reaction to plant-based products
- Epidemiology: more common from early summer until fall
- Pathophysiology: skin contact with photosensitizing agents (psoralen) from a plant → phototoxic reaction upon UVA exposure
- Localization: sun-exposed areas of the skin; (most often the extremities)
- Stripe-like or reticulate efflorescence; ; usually correlates to plant shape or forms a brush pattern resembling handprints or fingerprints
- 24–48 hours after contact: redness and blistering; most severe after three days
- Resolution after 2–4 weeks with hyperpigmentation that may be visible for months
- Itching, burning pain
- Diagnosis: patch or photopatch testing, skin biopsy, or provocative phototesting
- Treatment: photoprotective measures, oral corticosteroids, and, in some cases, immunosuppressive agents (azathioprine)
- Occurs with low light exposure and fragrance application (which includes bergamot oil)
- Direct transition to hyperpigmentation without previous inflammatory phase
- Short description: a specific substance (photosensitizing agent) in combination with UVA exposure causes an allergic reaction after previous sensitization
- Etiology: Possible photosensitizing agents include fragrances, ingredients in sunscreen products, preservatives, and drugs.
- Pathophysiology: T-cell mediated delayed hypersensitivity (Type IV) after epicutaneous or oral contact with photosensitizing agents
- Clinical features
- Patient history
- Photopatch test
- Avoid the specific photosensitizing agent.
- Sun protection: protective clothing and/or sunscreen
- During acute phase: topical glucocorticoids
- Short description: very rare chronic photodermatitis characterized by a vesiculopapular rash of the skin
- Epidemiology: mostly children
- Clinical features: livid red erythema with serous-filled and hemorrhagic, umbilicated bullae that heal with varioliform scarring
- Treatment: photohardening , carotenoids, photoprotective measures
- Short description: rare, photoallergic reaction that is associated with a persistent eczematous rash and presence of photosensitivity
- Etiology: can occur following chronic episodes of photoallergic contact dermatitis
- Clinical features:
- Treatment: photoprotective measures, emollients, topical corticosteroids, oral or topical Immunosuppressants