The cause of<unk>  is not yet understood, but several factors may be involved. It is thought to be due to a type IV delayed-type hypersensitivity to an allergen produced 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<unk>  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<unk><unk>  without sunburn. Artificial UV<unk>  sources from tanning units and phototherapy treatment units can also trigger<unk> . About three-quarters of sufferers acquire<unk>  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<unk> . Photosensitizer It has been suggested that an undefined endogenous or exogenous photo-allergen may trigger a delayed immune reaction resulting in<unk> . Genetics Half of sufferers have a family history of<unk> , 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.
Polymorphous light eruption
Lichenoid eruption
Acneiform eruption
Papuloerythroderma of Ofuji
Streptococcal intertrigo
Granulomatous facial dermatitis
Drug eruption
Poikiloderma of Civatte