[Beyond immunopathogenesis. Insulin resistance and "epidermal dysfunction"].

Insulin is a central player in the regulation of metabolic as well as non-metabolic cells: inefficient signal transduction (insulin resistance) not only represents the cornerstone in the pathogenesis of type 2 diabetes mellitus, but also drives atherosclerosis through inducing endothelial dysfunction. Last but not least epidermal homeostasis depends on insulin. We summarize the effects of insulin on proliferation and differentiation of human keratinocytes as well as the relevance of cytokine-induced insulin resistance for alterations in epidermal homeostasis characteristic for psoriasis.

[Co-morbidities in psoriasis vulgaris].

Epidemiologic data document not only a higher prevalence of joint involvement among psoriasis patients than previously thought, but also an association with numerous other diseases, including depression, smoking, alcoholism, Crohn's disease, and metabolic syndrome. The resulting increased cardiovascular mortality is of particular clinical importance, and its pathogenetic link as a complication of the psoriatic inflammation is well recognized. Thus, we need to re-invent the management of psoriasis: Dermatologists are not only the sentinel regarding the early diagnosis of psoriatic arthritis, but also of metabolic complications such as dyslipidemia or diabetes.