BackgroundIt has been reported that treatment of DENV-infected cultures with Lovastatin (LOV), can affect viral assembly. The objective of this study was to evaluate the effect of LOV on the survival rate and viremia levels of DENV-2-infected AG129 mice.Methodology/Principal FindingsMice were inoculated with 1×106 plaque-forming units (PFU/ml) of DENV-2 and treated with LOV (200 mg/kg/day). Pre-treatment with one or three doses of LOV increased the survival rate compared to untreated mice (7.3 and 7.1 days, respectively, compared to 4.8 days). Viremia levels also decreased by 21.8% compared to untreated mice, but only in the group administered three doses prior to inoculation. When LOV was administered after viral inoculation, the survival rate increased (7.3 days in the group treated at 24 hpi, 6.8 days in the group treated at 48 hpi and 6.5 days in the group treated with two doses) compared to the untreated group (4.8 days). Interestingly, the serum viral titer increased by 24.6% in mice treated at 48 hpi with a single dose of LOV and by 21.7% in mice treated with two doses (at 24 and 48 hpi) of LOV compared to untreated mice. Finally histopathological changes in the liver and spleen in infected and untreated mice included massive extramedullary erythropoiesis foci and inflammatory filtration, and these characteristics were decreased or absent in LOV-treated mice.Conclusions/SignificanceOur results suggest that the effect of LOV on viremia depends on the timing of treatment and on the number of doses administered. We observed a significant increase in the survival rate in both schemes due to a delay in the progression of the disease. However, the results obtained in the post-treatment scheme must be handled carefully because this treatment scheme increases viremia and we do not know how this increase could affect disease progression in humans.

Because of rising cocaine consumption and levamisole adulteration frequency, levamisole-adulterated cocaine-induced vasculitis/vasculopathy is becoming more common. Detailed characterization of skin involvement coupled with multiple antibody positivity is essential for a diagnosis. Renal involvement is frequent, clinically and histologically heterogeneous, and potentially serious.

Pancreatic disorders, such as chronic or acute pancreatitis, and carcinoma may be infrequently accompanied or preceded by panniculitis or polyarthritis. This triad is known in the literature as the pancreatitis, panniculitis, and polyarthritis syndrome. Although the pancreatic disease of pancreatitis, panniculitis, and polyarthritis syndrome usually includes pancreatitis, here we review the literature with report of 1 additional case of polyarthritis and panniculitis occurring in the presence of pancreatic carcinoma. Given that the diagnosis is often difficult when abdominal symptoms are absent, knowledge of the association between panniculitis and polyarthritis with pancreatic disease may lead to a prompt diagnosis and management. The histopathology of the skin lesions can be a valuable clue for focusing attention to a pancreatic disease.

Cutaneous T-cell lymphomas (CTCL) result from the infiltration and proliferation of a population of T cells in the skin, inducing changes in the activity of both T cells and surrounding skin cells. In the CTCL microenvironment, cell interactions mediated by cell signaling pathways are altered. Defining changes in cell signaling enables to understand Tcell deregulations in the CTCL microenvironment and thus the progression of the disease. Moreover, characterizing signaling networks activated in CTCL stages can lead to consider new molecular biomarkers and therapeutic targets. Focusing on mycosis fungoides (MF), the most frequent variant of CTCL, and S ezary syndrome (SS), its leukemic variant, this review highlights recent molecular and genetic findings revealing modifications of key signaling pathways involved in (1) cell proliferation, cell growth, and cell survival such as MAP kinases and PI3K/Akt; (2) immune responses derived from TCR, TLR, JAK/STAT, and NF-kB; and (3) changes in tissue conditions such as extracellular matrix remodeling, hypoxia, and angiogenesis. Alterations in these signaling networks promote malignant Tcell proliferation and survival, T-cell migration, inflammation, and suppression of immune regulation of malignant T cells, making a skin microenvironment that allows disease progression. Targeting key proteins of these signaling pathways, using molecules already available and used in research, in clinical trials, and with other disease indications, can open the way to different therapeutic options in CTCL treatment.

Becker's nevus syndrome is part of the epidermal nevus syndromes and has been described with a phenotype that includes Becker's nevus, ipsilateral breast hypoplasia, and variable skeletal malformations. It is more frequent in males than in females (5 : 1) but is more relevant in females. The diagnosis is clinically based and the skin lesion must be present and no other numbered criteria have been established, but with more criteria being present the possibility of the diagnosis is higher. Regarding the treatment of breast hypoplasia, the use of antiandrogen medication has demonstrated adequate clinical response in a dose of 50 mg/day of spironolactone.