Several studies indicate that IFN-γ facilitates systemic inflammation during endotoxin-induced shock. However, the pathobiology of IFN-γ in clinically relevant models of septic shock, such as CLP, is not well understood. In this study, the role of IFN-γ in the pathogenesis of CLP-induced septic shock was evaluated by examining IFN-γ production at the tissue and cellular levels. The impact of IFN-γ neutralization on systemic inflammation, bacterial clearance, and survival was also determined. Following CLP, concentrations of IFN-γ in plasma and peritoneal lavage fluid were low in comparison with concentrations of IL-6 and MIP-2, as was IFN-γ mRNA expression in liver and spleen. The overall percentage of IFN-γ+ splenocytes was <5% after CLP and not statistically different from control mice. Intracellular IFN-γ was present in a large proportion of peritoneal exudate cells after CLP, primarily in infiltrating myeloid cells and NK cells. i.p. myeloid cell activation was decreased in IFN-γKO mice, and plasma concentrations of IL-6 and MIP-2 were significantly lower in IFN-γKO mice and in mice treated with anti-IFN-γ compared with controls, but bacterial clearance was not affected. IFN-γKO mice were resistant to CLP-induced mortality when treated with systemic antibiotics. However, neutralization of IFN-γ with blocking antibodies did not improve survival significantly. These studies show that IFN-γ facilitates the proinflammatory response during CLP-induced septic shock. However, neutralization of IFN-γ did not improve survival uniformly.

This unique case presentation is representative of the variability seen in the presentation of CHE and highlights the importance of considering CHE on the clinical and histologic differential of vascular tumors.

Zinc deficiency may result from either a congenitally inherited defect of zinc absorption or is acquired secondarily from a variety of factors affecting dietary zinc intake, absorption, or loss. We report a case of acquired zinc deficiency secondary to gastric bypass surgery that resulted in vulvar cutaneous manifestations of delayed onset, with failure to clear after oral supplementation with zinc. The patient experienced improvement of symptoms only after administration of intravenous zinc supplementation. Upon review of the current literature, it is thought that the patient's original suboptimal response to oral supplementation and improvement after receiving intravenous zinc were related to the intentional surgical alteration and bypass of the absorptive capacity of the duodenum and jejunum. With the current prevalence of obesity and availability of surgical weight loss therapies, it is important to be mindful of the resulting nutritional deficiencies, their clinical manifestations, and factors affecting the efficacy of therapeutic approaches as seen in this case.

We report a case of a 51-year-old Hispanic woman who presented with a several year history of multiple flesh colored papules of cosmetic concern on the nose and medial cheeks (Figure 1). Biopsies revealed fibrofolliculoma and trichodiscoma. The patient was referred for genetic testing and was found to be positive for the FLCN gene defect, confirming a diagnosis of Birt-Hogg-Dubé syndrome. Further work-up with screening renal ultrasound and CT scan of the thorax and abdomen was unrevealing. For treatment of these skin lesions, dermasanding was attempted initially with only minimal benefit. She subsequently had multiple lesions treated with hyfrecation (also known as electrodessication or cautery) at a low setting and was very pleased with the results (Figure 2). Importantly, there has yet to be a recurrence of lesions two years status-post hyfrecation.