Cellular hypersensitivity to UV-A: a clue to the aetiology of actinic reticuloid?

Fibroblasts cultured from six patients with actinic reticuloid (AR) showed striking cytopathic changes and inhibition of RNA synthesis after exposure to near-ultraviolet radiation that had no effect on normal and other photosensitive cell strains, such as those of xeroderma pigmentosum and Bloom syndrome. An abnormal pattern of DNA fragmentation was observed after doses insufficient to cause cytopathic effects. These results suggest a cellular defect in the prevention or repair of some damage caused by free radicals and other photoproducts. In order to explain the pathogenesis of AR, it is proposed that a deficiency in the cellular mechanisms dealing with oxygen radicals leads to the establishment of a vicious circle favouring the persistence of a lymphohistiocytic infiltrate and hence the chronic clinical course characteristic of the disease.