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. 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
- Pathogenesis: UV radiation → DNA mutations → 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 and pain, then redness and swelling
- Blisters may occur in severe cases of sunburn; if larger areas are affected, general symptoms (e.g., fever) may arise.
- Slight sunburn: transition to hyperpigmentation, followed by peeling of the skin ∼ 1 week later
- Severe sunburn with blistering: possibly nonmelanocytic scarring
- UV radiation (both UVA and UVB) contributes to visible aging of the skin (e.g., wrinkles, pigmentation heterogeneity)
- Increased risk of skin cancer
- Avoid sun exposure
- Protective clothing
Sunscreen with adequate SPF (a measurement of how much protection a sunscreen provides; SPF values indicate the fraction of ultraviolet rays, specifically UVB, that are absorbed by the sunscreen)
- 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
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.
To remember the effects of different types of UV radiation, think “UVA tAns the skin and UVB Burns it.”
- Definition: acquired photodermatosis; characterized by a pathological response to UV exposure (also known as a sun allergy)
- Epidemiology: most frequently occurring idiopathic photodermatosis
- 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
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, amiodarone, fluoroquinolones, retinoids, psoralens, NSAIDs, griseofulvin, grazoprevir
- 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)
Phytophotodermatitis (dermatitis pratensis)
- 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)
- 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