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Psoriasis vulgaris occurs with a prevalence of up to 2% in childhood and adolescence. In most cases, diagnosis can be made clinically. We report about a pediatric patient with psoriasis vulgaris who posed a diagnostic challenge due to uncharacteristic manifestation. The most important differential diagnoses of various forms of psoriasis vulgaris as well as actual treatment recommendations in childhood and adolescence are discussed.Die Psoriasis vulgaris tritt mit einer Prävalenz von bis zu 2 % im Kindes- und Jugendalter auf. Größtenteils wird die Diagnose klinisch gestellt. Wir berichten über einen pädiatrischen Patienten, welcher uns aufgrund der für eine Psoriasis vulgaris eher untypischen Lokalisation vor eine diagnostische Herausforderung stellte. Diskutiert werden die wichtigsten Differenzialdiagnosen der verschiedenen Psoriasisformen sowie die aktuellen Therapieempfehlungen im Kindes- und Jugendalter.

Although most acute skin wounds heal rapidly, non-healing skin ulcers represent an increasing and substantial unmet medical need that urgently requires effective therapeutics. Keratinocytes resurface wounds to re-establish the epidermal barrier by transitioning to an activated, migratory state, but this ability is lost in dysfunctional chronic wounds. Small-molecule regulators of keratinocyte plasticity with the potential to reverse keratinocyte malfunction in situ could offer a novel therapeutic approach in skin wound healing. Utilizing high-throughput phenotypic screening of primary keratinocytes, we identify such small molecules, including bromodomain and extra-terminal domain (BET) protein family inhibitors (BETi). BETi induce a sustained activated, migratory state in keratinocytes in vitro, increase activation markers in human epidermis ex vivo and enhance skin wound healing in vivo. Our findings suggest potential clinical utility of BETi in promoting keratinocyte re-epithelialization of skin wounds. Importantly, this novel property of BETi is exclusively observed after transient low-dose exposure, revealing new potential for this compound class.

High titers of anti-vimentin antibodies after transplantation are known to be associated with poor long-term graft survival. Vimentin is an intracellular protein which is present in different isoforms in the cell. In a previous study with sera from hemodialysis patients on the kidney transplantation waiting list we could show that only a 49 kDa and a 60 kDa isoform are recognized by patients' anti-vimentin antibodies while the other isoforms remain undetected. However, it is still unclear whether antibodies against this intracellular protein can bind to intact cells. Here we show that vimentin can be present on the cell surface under certain conditions. Lymphocytes from healthy volunteers were used as a model for allogeneic cells. We could show by immunofluorescence microscopy, flow cytometry and Western blot experiments that concanavalin A (Con A) activated lymphocytes express a 49 kDa vimentin isoform on their cell surface while the 60 kDa isoform remains inaccessible from the outside. This expression is associated with an increased binding of sera from hemodialysis patients which were positive for anti-vimentin antibodies. These results suggest that cell activation enhances binding of anti-vimentin antibodies to intact cells which might contribute to chronic allograft nephropathy.