We report a case of a 50-year old female presenting with a giant tumor on the volar aspect of the third finger of the left hand, a thorough clinical and paraclinical evaluation followed by surgical resection resulted in a benign lipoma with an uneventful postoperative course. We present this case due to its rare location and repercussion in the decision making process when other more common similar pathologies with varying prognosis are conceived.

BackgroundOverexpression of type I interferon (IFN-I)-induced genes is a common feature of systemic lupus erythematosus (SLE) and its experimental models, but the participation of endogenous overproduction of IFN-I on it is not clear. To explore the possibility that abnormally increased IFN-I receptor (IFNAR) signaling could participate in IFN-I-induced gene overexpression of SLE, we examined the phosphorylation status of the IFNAR-associated signaling partners Jak1 and STAT2, and its relation with expression of its physiologic inhibitor SOCS1 and with plasma levels of IFNα and IFN-like activity.Methodology/Principal FindingsPeripheral blood mononuclear cells (PBMC) from SLE patients with or without disease activity and healthy controls cultured in the presence or in the absence of IFNβ were examined by immunoprecipitation and/or western blotting for expression of the two IFNAR chains, Jak1, Tyk2, and STAT2 and their phosphorylated forms. In SLE but not in healthy control PBMC, Jak1 and STAT2 were constitutively phosphorylated, even in the absence of disease activity (basal pJak1: controls vs. active SLE p<0.0001 and controls vs. inactive SLE p = 0.0006; basal pSTAT2: controls vs. active and inactive SLE p<0.0001). Although SOCS1 protein was slightly but significantly decreased in SLE in the absence or in the presence of IFNβ (p = 0.0096 to p<0.0001), in SOCS1 mRNA levels were markedly decreased (p = 0.036 to p<0.0001). IFNβ induced higher levels of the IFN-I-dependent MxA protein mRNA in SLE than in healthy controls, whereas the opposite was observed for SOCS1. Although there was no relation to increased serum IFNα, active SLE plasma could induce expression of IFN-dependent genes by normal PBMC.Conclusions/SignificanceThese findings suggest that in some SLE patients IFN-I dependent gene expression could be the result of a low IFNAR signaling threshold.

Lipomas are benign mesenchymal tumors that develop in areas of abundant adipose tissue. Due to the fatty composition of the breast, difficulties in diagnosis, treatment, and reconstruction are often encountered. We report a case of a 55-year-old female with a giant tumor of the right breast that comprised most of its mass, causing breast asymmetry. A thorough preoperative evaluation, followed by an uneventful difficult surgical resection and reconstruction, resulted in diagnosis of a benign lipoma. The case prompted this report because of its challenging size, location, diagnosis, and reconstructive solution.