We investigated the capacity of 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] to protect human keratinocytes against the hazardous effects of ultraviolet B (UVB)-irradiation, recognized as the most important etiological factor in the development of skin cancer. Cytoprotective effects of 1,25(OH)(2)D(3) on UVB-irradiated keratinocytes were seen morphologically and quantified using a colorimetric survival assay. Moreover, 1,25(OH)(2)D(3) suppressed UVB-induced apoptotic cell death. An ELISA, detecting DNA-fragmentation, demonstrated that pretreatment of keratinocytes with 1,25(OH)(2)D(3) 1 microM for 24 h reduced UVB-stimulated apoptosis by 55-70%. This suppression required pharmacological concentrations 1,25(OH)(2)D(3) and a preincubation period of several hours. In addition, 1,25(OH)(2)D(3) also inhibited mitochondrial cytochrome c release (90%), a hallmark event of UVB-induced apoptosis. Furthermore, we demonstrated that 1,25(OH)(2)D(3) reduced two important mediators of the UV-response, namely, c-Jun-NH(2)-terminal kinase (JNK) activation and interleukin-6 (IL-6) production. As shown by Western blotting, pretreatment of keratinocytes with 1,25(OH)(2)D(3) 1 microM diminished UVB-stimulated JNK activation with more than 30%. 1,25(OH)(2)D(3) treatment (1 microM) reduced UVB-induced IL-6 mRNA expression and secretion with 75-90%. Taken together, these findings suggest the existence of a photoprotective effect of active vitamin D(3) and create new perspectives for the pharmacological use of active vitamin D compounds in the prevention of UVB-induced skin damage and carcinogenesis.

Dermatophytic infections of the skin, hairs and nails are very common and are very variable in aspect. In skin, inflammatory symptoms are often absent, but in other cases they may be very pronounced, in particular when caused by zoophilic dermatophytes. In onychomycosis, it is very difficult to make the differential diagnosis with other causes of onychodystrophy on purely clinical grounds; indeed, even in case of fungal infection, the causative agent can be suspected on clinical grounds only in a minority of cases. The clinical presentation of skin infections, infections of the scalp and beard, and the nails are presented more in detail.

Contact allergy to topical corticosteroids occurs more frequently than previously supposed. Cross-allergic phenomena are common. On the basis of a review of the literature and our own patch test data on 15 patients, we conclude that positive patchtests to corticosteroids occur approximately six to seven times more frequently in well-defined groups of structurally-related substances than between corticosteroids of different groups. An analogous substitution pattern on the steroid D-ring or the carbon side chain (C20, C21) seems to have a significant influence on the association of positive patchtest results. This is not the case for other structural variables, such as the presence of a double bond in the steroid A-ring or fluoride substitutions on the B-ring. The effect of other factors such as concomitant sensitization and steroid metabolism in the skin on the development of a corticosteroid polyallergy are analysed, and the specificity and sensitivity of cross-allergy phenomena are evaluated. These are important in the selection of a topical steroid in the future treatment of a corticosteroid sensitive patient.

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