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Background Dermatologists are at risk of body-fluid contamination during procedures. Objective We sought to determine the frequency of blood splash during procedural dermatology. Methods In all, 500 consecutive excisions were performed. Postoperatively, blood droplets on face shields and surgical gowns were counted. A survey regarding universal precautions during procedures was also conducted with members of the American College of Mohs Surgery (ACMS). Results Contamination from blood splashes during dermatologic procedures (Mohs micrographic surgery, excision, repair) occurred in 66.4%. Reconstruction type, anticoagulation use, wound location, and wound size correlated with a higher blood splash rate. Our survey showed that face shields and goggles are used inconsistently. Limitations The 4 participating dermatologists do not represent all practicing dermatologists. It may be possible to generalize the survey results directed at physicians in the ACMS. Conclusion Physician body-fluid contamination risk with procedural dermatology is clinically significant. Dermatologists and their assistants should wear preventive barriers during procedures to minimize the risk of viral transmission.

Ultraviolet irradiation represents a well-established treatment modality for inflammatory skin diseases. The aim of this study was to investigate the mechanisms of ultraviolet B radiation-induced keratinocyte insensitivity towards interferon-gamma. Flow cytometric analyses indicated that ultraviolet B radiation temporarily inhibits the interferon-gamma-induced activation of primary keratinocyte and HaCaT cells as measured by reduced intercellular adhesion molecule-1 (CD54) and HLA-DR upregulation. Western blot experiments have suggested that this is mediated by the ultraviolet B radiation-induced inhibition of signal transduction and transcription factor-1 phosphorylation. Neither interleukin-10 neutralization nor interleukin-10 addition had any effect on the ultraviolet B radiation-induced inhibition of interferon-gamma induced intercellular adhesion molecule-1 expression. Furthermore, the supernatant from ultraviolet B-irradiated cells failed to inhibit the interferon-gamma-induced CD54 and HLA-DR upregulation in nonradiated HaCaT cells. Moreover, irradiated cells from whom the supernatant was withdrawn 4 h after irradiation still showed a diminished interferon-gamma-induced response after 24 h. Thus, not soluble but intracellular factors might be involved in the ultraviolet B radiation-induced inhibition of interferon-gamma-induced keratinocyte activation. Therefore, we analyzed the expression of members of suppressors of cytokine-signaling (SOCS) molecules using real-time polymerase chain reaction. We found a fast and strong upregulation of SOCS1 and SOCS3 but not of SOCS2 after ultraviolet B radiation. Similarly, ultraviolet B radiation induced the expression of these particular SOCS molecules in lesional psoriatic skin. As SOCS molecules are known inhibitors of signal transduction and transcription factor phosphorylation, which is essential for interferon-gamma-induced intercellular adhesion molecule-1 and HLA-DR upregulation, this may explain the interferon-gamma unresponsiveness after ultraviolet B radiation.