Creation of thick, scaling erythematous plaques that can persist for decades is a characteristic clinical finding in patients with psoriasis. Probingbeneath the skin surface reveals chronic inflammation, altered epidermal keratinocyte (KC) differentiation, KC hyperplasia, prolonged KC survival, elevated telomeraselevels, and dermal-based angiogenesis. Moreover, many, if not most, patients are or have been repeatedly exposed to various carcinogens (eg, anthralin,crude coal tar, UV light, and psoralen–UV-A [PUVA]), and/or systemic immunosuppressive agents (eg, corticosteroids and cyclosporine). Given theseclinical, pathologic, and treatment considerations, it would be expected that psoriatic plaques would be "hot spots" for sites of various cancer development,including squamous cell carcinoma, basal cell carcinoma, and malignant melanoma. Therefore, it would not be so much a question of whether skin cancer would develop in patients with psoriasis, but rather when the increased skin cancer susceptibility would startto manifest in these patients. Astonishingly, such tumors do not often, if ever, develop within psoriatic plaques,1-4 nordo their precursor lesions appear to occur with any frequency, as exemplified by the relative paucity of actinic keratosis, dysplastic nevi, and lentigomaligna. In this issue of the ARCHIVES, Paltiel et al,5 after studying 460 adults with plaque-type psoriasis and 738 control patients withoutpsoriasis but with other inflammatory dermatoses (atopic or contact dermatitis), concluded that psoriasis actually may protect against a common skin cancerprecursor, actinic keratosis (Figure 1).
Nickoloff BJ. The Skin Cancer Paradox of Psoriasis: A Matter of Life and Death Decisions in the Epidermis. Arch Dermatol. 2004;140(7):873–875. doi:10.1001/archderm.140.7.873
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