Photodermatoses

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 1^st or 2^nd-degree burn.
• Epidemiology: particularly light-skinned individuals
• Etiology: excessive exposure to UVB radiation
• Pathophysiology: 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
• Clinical features
  • Primarily limited to exposed skin
  • Begins a few hours after exposure, with symptoms peaking after 12–24 hours; usually resolves within a week
  • Initially pruritus 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.
• Treatment
  • General: wet compresses, cooling ointments, and moisturizers ^[1]
  • Severe sunburn or large affected area
    • NSAIDs (e.g., diclofenac)
    • Wet antiseptic compresses
    • If blistering occurs: covering of the blisters, treatment of ruptured blisters with antiseptic ointment
• Prognosis
  • 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
• Prevention
  • 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
      • Zinc oxide effectively absorbs both UVA and UVB (also the active ingredient in barrier creams)
      • Trolamine salicylate, para-aminobenzoic acid, and vitamin E only absorb UVB radiation
  • Sun-protective measures for infants and children ^[2]
    • Avoid sun exposure: shade, protective clothing (e.g., lightweight long pants, long-sleeved shirts, brimmed hats shading the neck, sunglasses with UV protection)
    • Avoid the use of sunscreen in infants < 6 months
      • Higher risk of contact dermatitis and photosensitivity in infants
      • If adequate clothing and/or shade are unavailable, a minimal amount of waterproof sunscreen with at least 30 SPF should be applied to small areas (e.g., face, hands).
    • For children, the use of oil-based emulsions of inorganic filters (e.g., zinc oxide, titanium dioxide) is recommended due to low sensitization and irritation potential.

The use of sunscreen is not recommended in infants < 6 months. Avoiding sunlight exposure is the most effective measure to protect children and infants from sunburn.

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.

“UVA tAns the skin and UVB Burns it.”

References:^[1][3][4][5]

• Definition: acquired photodermatosis; characterized by a pathological response to UV exposure (also known as a sun allergy)
• Epidemiology: most frequently occurring idiopathic photodermatosis
• Pathophysiology
  • Most likely a cell-mediated immune response resembling delayed-type hypersensitivity reaction
  • Presumably caused by reaction to autoantigens that arise from UV exposure
• Clinical features
  • Symptoms typically present a few hours to days after the first high-intensity UV exposure in the spring or the summer.
  • Rash
    • Erythema, papules, plaques, vesicles; typically pruritus
    • Manifold skin efflorescence varying from patient to patient
  • 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).
• Diagnostics
  • Usually clinical diagnosis
  • Provocative phototesting: occurrence of lesions is provoked by selective UV radiation
  • Skin biopsy
• Treatment
  • Avoid UVA exposure
  • If exposed: sun protection; sunscreen
  • Habituation (4–6 weeks before more intense UV exposure)
  • Local glucocorticoid therapy for acute skin inflammation and pruritus
  • Possibly antihistamines to reduce itching

References:^[6]

Drug-induced phototoxic reactions

• Short description: non-allergic photosensitivity reaction due to certain drug metabolites
• Etiology: tetracyclines (especially doxycycline), thiazides, sulfonamides, amiodarone, fluoroquinolones, retinoids, psoralens, NSAIDs, griseofulvin, grazoprevir
• 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
• Clinical features
  • Severe sunburn-like rash, possibly with vesicles or bullae
  • Occurs within minutes to hours of sun exposure
  • Localization: sun-exposed areas of the skin
• Diagnostics: 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
• Clinical features
  • Localization: sun-exposed areas of the skin (most often the extremities)
  • Rash
    • Stripe-like or reticulate rash; 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
• Diagnostics: patch or photopatch testing, skin biopsy, or provocative phototesting
• Treatment: photoprotective measures, oral corticosteroids, and, in some cases, immunosuppressive agents (azathioprine)

Berloque dermatitis

• Occurs with low light exposure and fragrance application (which includes bergamot oil)
• Direct transition to hyperpigmentation without previous inflammatory phase

References:^[7][8]

• 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
  • The skin changes are limited to areas that were exposed to UVA radiation and were in contact with the photosensitizing agent.
  • Efflorescence: erythema and papules, rarely vesicles
• Diagnostics
  • Patient history
  • Photopatch test
    • Initially, the minimal erythema dose (MED) is determined to establish the patient's general light sensitivity (through UVA and UVB exposure).
    • Then, specific test substances are applied to each side of the back and remain there for 24 hours.
    • The initial reading upon application is recorded, followed by exposure of one side to UVA light. Additional readings occur 24, 48, and 72 hours after exposure.
    • The non-exposed side is used as a control.
    • A visible reaction on the exposed side but not on the control side indicates a photoallergic reaction. If a reaction occurs on both sides for the same test substance, then it is most likely a light-independent allergic contact dermatitis.
• Management
  • Avoid the specific photosensitizing agent.
  • Sun protection: protective clothing and/or sunscreen
  • During acute phase: topical glucocorticoids

• 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
• Management: photohardening , carotenoids, photoprotective measures

• 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
  • Severe, persistent, eczematous eruption with distinct lichenification, itching, scales, and erosions
  • Persistent light reactivity (PLR) to visible UVB (with or without UVA) light
• Management: photoprotective measures, emollients, topical corticosteroids, oral or topical Immunosuppressants