in the body following sunlight exposure, in a genetically susceptible person. It is also thought that skin microbiome or microbial elements could be involved in pathogenesis of the disease UV exposure PLE can be provoked by UVA or UVB (chief cause of sunburn) rays, meaning it can be triggered even by sunlight through glass. UV-A is a major constituent of sunlight, can pass through glass, is relatively resistant to sunscreen and can cause light eruption without sunburn. Artificial UV light sources from tanning units and phototherapy treatment units can also trigger PLE. About three-quarters of patients acquire PLE after UV-A exposure only, one-tenth after UV-B exposure only, and the rest after a combination of UV-A and UV-B exposure. People vary in the amount of sun exposure needed to trigger the rash. Oxidative stress Oxidative stress and the modification of the redox status of the skin has been implicated in the expression of PLE. Photosensitizer It has been suggested that an undefined endogenous or exogenous photo-allergen may trigger a delayed immune reaction resulting in PLE. Genetics Half of patients have a family history of PLE, demonstrating a clear genetic influence. Oestrogen effect The preponderance in women with a decline in severity following menopause has been thought to be associated with oestrogen effects, A natural fall in oestrogens may account for the tendency to remit after the menopause. Diagnosis The diagnosis of PLE is typically made by assessing the history and clinical observations. Any investigations are usually to exclude other conditions, particularly lupus and porphyria. Blood tests are usually normal. However, positive antinuclear antibody and extractable nuclear antigen (anti-Ro/La) in low titre may be found, even in the absence of other criteria to suggest a diagnosis of lupus erythematosus. If clinical findings suggest a possibility of porphyria, urinary and red cell porphyrin screening may be performed and are negative in PLE. Photoprovocation tests are usually not required but may be undertaken by specialised centres in winter. When a decision to undertake this is made, a small area of the frequently affected skin is exposed to varying doses of UVA and minimal erythema dose (MED) (amount of UV radiation that will produce minimal redness of skin within a few hours following exposure) of broadband UVB for three consecutive days. An examination of the skin to detect the rash is made, however, up to 40% have false negative responses. Biopsy findings Depending on the