CRP Levels as a Prognostic Factor in Mycosis Fungoides.

Mycosis Fungoides (MF) and Sézary syndrome (SS) are the most common forms of cutaneous T-cell lymphomas. Few validated prognostic factors have been reported in MF/SS, especially when compared with non-cutaneous lymphomas. Increased C-reactive protein (CRP) levels have recently been associated with poor clinical outcome in various malignancies. The aim of this study was to evaluate the prognostic significance of serum CRP levels at diagnosis in patients with MF/SS. This retrospective study included 76 patients with MF/SS. Stage was assigned according to the ISCL/EORTC guidelines. The follow-up period was 24 months or more. Disease course and response to treatment were determined using quantitative scales. Wilcoxon's rank test and multivariate regression analysis were used to analyze the data. Increased CRP levels correlated significantly with advanced stages (Wilcoxon's test, P>0.0001). Furthermore, increased CRP levels were associated with a lower treatment response rate (Wilcoxon's test, P=0.0012). Multivariate regression analysis showed that CRP is an independent predictor of advanced clinical stage at diagnosis.The present data suggest that elevated CRP levels could serve as a useful prognostic factor in MF/SS and may assist in guiding treatment choices.

FOXP3 Predicts Response to Treatment in Mycosis Fungoides.

BACKGROUND: The role of the T-regulatory cells (Tregs) marker forkhead box Protein 3 (FOXP3) in mycoses fungoides (MF) pathogenesis is unclear and the results of previous studies are inconclusive. OBJECTIVE: We aimed at ascertaining the possibility that FOXP3 expression may serve to predict MF stage and response to therapy. PATIENTS AND METHODS: Immunohistochemistry staining for FOXP3 was performed on 30 skin biopsies from patients with MF, and FOXP3 expression level was quantitatively graded. Disease stage, progression, and response to treatment were determined based on clinical and imaging evidence, and association with FOXP3 expression was assessed. RESULTS: FOXP3 expression in the dermis correlated with poor response to treatment (P=0.047). A negative non-significant relationship between epidermal FOXP3 expression and clinical stage severity was observed (P=0.17). CONCLUSIONS: Dermal FOXP3 expression in MF lesions could be used to predict response to treatment in patients with MF.

1064-nm Q-switched fractional Nd:YAG laser is safe and effective for the treatment of post-surgical facial scars.

Post-surgical facial scars are often associated with unaesthetic outcome. Treatment of these scars using various lasers could be beneficial; however, the use of the Q-switched fractional (QSF) 1064-nm neodymium-doped yttrium aluminum garnet (Nd:YAG) laser has yet to be evaluated for this indication. Our objective was to determine the safety and efficacy of a QSF-Nd:YAG laser for the treatment of post-surgical facial scars. Eleven (5 male, 6 female) patients who underwent facial surgery with significant scarring were treated using the QSF-Nd:YAG laser. Scars were exposed to 600-1200 mJ/stacked pulses (12-24 mJ per pixel), emitted at a rate of 10 Hz for up to 2 passes per treatment session, receiving overall 3-6 treatments. Patient follow-up was 3 months. Scars' photographs were blindly assessed by two dermatologists, who graded them on a scale of scar severity from 1 to 5 (1 = least severe, 5 = most severe) before and after treatment. A blinded before/after recognition of these photographs was also performed. Patient satisfaction was assessed 3 months post-treatment and graded on a scale of 1-5 (1 = not satisfied, 5 = very satisfied). Pain perception and adverse effects were also evaluated. Patients demonstrated a decrease in scar severity score by a mean of 1.57 points (p = 0.0005). A blinded before/after recognition was correct in 86.5% of the cases. Pain and adverse effects were mild and transient. Patient satisfaction was high (4.2). QSF-Nd:YAG laser is a safe and effective modality for the treatment of post-surgical facial scars.

[PIGMENTED BASAL CELL CARCINOMA AND IONIZING RADIATION].

AIMS: This study aimed at demonstrating whether the histological and clinical manifestations of pigmented basal cell carcinoma are different among those who were previously treated with ionizing radiation for ringworm infection. BACKGROUND: Ionizing radiation is known to cause increased morbidity among those who are chronically exposed. Basal cell carcinoma in known to be related to ionizing radiation however, the characteristics of pigmented BCC in relation to ionizing radiation are poorly described. METHODS: The study included the demographics and characteristics of 23 patients with pigmented BCC who were treated for ringworm with ionization radiation and a control group of 21 patients that had not been treated with ionizing radiation. All the cases treated between the years 2005-2015 were included in the study. The data was analyzed with a SPSS program. RESULTS: Among the patients who were treated with ionizing radiation the percentage of the tumors that were well differentiated was 34.8%, much higher than those who were not treated with ionizing radiation - 14.3%. In addition, the average age for those who were treated with ionizing radiation was 66 compared to 73 in the group that weren't treated with radiation. DISCUSSION: Pigmented basal cell carcinoma is a rare variant of BCC and it has characteristics that are quite dissimilar among patients treated with ionizing radiation. However, more studies are needed in order to strengthen the results.

[SYSTEMIC REVIEW OF EOSINOPHILIC DERMATOSES PATIENTS TREATED WITH TNF-Α INHIBITORS AND USTEKINUMAB].

AIMS: This study aims to critically review the pros and cons of biological drugs as treatments and triggers of eosinophilic dermatoses. BACKGROUND: Eosinophilic dermatoses syndromes are rare diseases with a prominent eosinophilic infiltration mechanism. These syndromes have several known treatments with limited success. Several physicians worldwide suggested possible advantages of using specific biological drugs, which are different from eosinophil targeted biotherapies as treatments for eosinophilic dermatoses syndromes. Others considered these drugs as possible triggers. METHODS: Articles published in the last 30 years containing relevant key words were reviewed using PubMed and Medline. Associations between Infliximab, Adalimumab, Etanercept, TNF alpha inhibitors and Ustekinumab to Eosinophilic Dermatoses syndromes were reviewed. RESULTS: Our search revealed an association between 17 eosinophilic dermatoses patients and the drugs of interest. Out of 5 Wells' syndrome cases, four patients had an outbreak of the disease following treatment and one improved by the treatment. Six cases of Eosinophilic Fasciitis mostly had a positive reaction to the treatment. More associations were found among 4 cases of Churg-Strauss syndrome, one case of Granuloma Faciale and 1 case of Eosinophilic Pustular Folliculitis. CONCLUSIONS: TNF alpha inhibitors and Ustekinumab may have a role in the treatment of eosinophilic dermatosis syndromes. These drugs may act as triggers among Wells' syndrome patients. Further investigation is needed.

The Role of Desmoglein 1 in Gap Junction Turnover Revealed through the Study of SAM Syndrome.

An effective epidermal barrier requires structural and functional integration of adherens junctions, tight junctions, gap junctions (GJ), and desmosomes. Desmosomes govern epidermal integrity while GJs facilitate small molecule transfer across cell membranes. Some patients with severe dermatitis, multiple allergies, and metabolic wasting (SAM) syndrome, caused by biallelic desmoglein 1 (DSG1) mutations, exhibit skin lesions reminiscent of erythrokeratodermia variabilis, caused by mutations in connexin (Cx) genes. We, therefore, examined whether SAM syndrome-causing DSG1 mutations interfere with Cx expression and GJ function. Lesional skin biopsies from SAM syndrome patients (n = 7) revealed decreased Dsg1 and Cx43 plasma membrane localization compared with control and nonlesional skin. Cultured keratinocytes and organotypic skin equivalents depleted of Dsg1 exhibited reduced Cx43 expression, rescued upon re-introduction of wild-type Dsg1, but not Dsg1 constructs modeling SAM syndrome-causing mutations. Ectopic Dsg1 expression increased cell-cell dye transfer, which Cx43 silencing inhibited, suggesting that Dsg1 promotes GJ function through Cx43. As GJA1 gene expression was not decreased upon Dsg1 loss, we hypothesized that Cx43 reduction was due to enhanced protein degradation. Supporting this, PKC-dependent Cx43 S368 phosphorylation, which signals Cx43 turnover, increased after Dsg1 depletion, while lysosomal inhibition restored Cx43 levels. These data reveal a role for Dsg1 in regulating epidermal Cx43 turnover.