Actinic Reticuloid–an Idiopathic Photodermatosis With Cellular Sensitivity to Near Ultraviolet Radiation

Long wavelength UV radiations (320–400 nm) cause persistent inhibition of RNA synthesis and marked cytopathic changes in fibroblasts from patients with actinic reticuloid (AR) but not in those from patients with Bloom syndrome or xeroderma pigmentosum. Furthermore, the AR cells show abnormal DNA fragmentation when they are irradiated at temperatures compatible with enzyme activity. Germicidal UVR (ca. 95% 254 nm) stimulates DNA repair synthesis and inhibits DNA replication to a normal extent in the AR cells. Thus, actinic reticuloid, a severe photodermatosis, characterised by skin sensitivity to UV‐B, UV‐A and part of the visible spectrum and by infiltrates reminiscent of mycosis fungoides, is a human disease with in vitro cellular sensitivity to UV‐A and, to our knowledge, is also the first to be reported. We advance the hypothesis that inefficient cellular neutralisation of free radicals may explain the cellular phenotype of actinic reticuloid and contribute to the establishment of a vicious circle that would favour the chronic clinical course and persistent lympho‐histiocytic skin infiltrates characteristic of the disease.