Stefania Guida

Likelihood of finding melanoma when removing a Spitzoid-looking lesion in patients aged 12 years or older

BACKGROUND Dermoscopy improves the recognition of melanoma and Spitz nevus but occasionally melanoma may exhibit a symmetric pattern mimicking Spitz nevus. OBJECTIVE We sought to investigate the likelihood of finding melanoma when excising a symmetric Spitzoid-looking lesion in patients aged 12 years or older. METHODS This study included patients aged 12 years or older with symmetric, Spitzoid-looking lesions that were diagnosed histopathologically as Spitz nevus or melanoma. Demographic, clinical, and dermoscopic variables were included in the analysis. We used χ(2) for nonparametric comparisons. Crude odds ratios and 95% confidence intervals were calculated by univariate logistic regression. RESULTS Of 384 included lesions, 333 (86.7%) were histopathologically diagnosed as Spitz nevus and 51 (13.3%) as melanoma. The risk of melanoma significantly increased with increasing age, being 50% or higher after the age of 50 years. LIMITATIONS Limitations are retrospective design, exclusion of patients younger than 12 years, lack of detailed histopathologic data, and limited sample size. CONCLUSION Our results confirm the observation that melanoma may be dermoscopically indistinguishable from Spitz nevi, strongly suggesting that the only safe strategy not to miss melanoma is to excise all Spitzoid-looking lesions in patients aged 12 years or older.

Spitz naevi and melanomas with similar dermoscopic patterns: can confocal microscopy differentiate?

Differentiating Spitz naevi from melanomas can be difficult both clinically and dermoscopically. Previous studies have reported the potential role of in vivo reflectance confocal microscopy (RCM) in increasing diagnostic accuracy.

Aurora kinase B inhibition reduces the proliferation of metastatic melanoma cells and enhances the response to chemotherapy

BackgroundThe poor response to chemotherapy and the brief response to vemurafenib in metastatic melanoma patients, make the identification of new therapeutic approaches an urgent need. Interestingly the increased expression and activity of the Aurora kinase B during melanoma progression suggests it as a promising therapeutic target.MethodsThe efficacy of the Aurora B kinase inhibitor barasertib-HQPA was evaluated in BRAF mutated cells, sensitive and made resistant to vemurafenib after chronic exposure to the drug, and in BRAF wild type cells. The drug effectiveness has been evaluated as cell growth inhibition, cell cycle progression and cell migration. In addition, cellular effectors of drug resistance and response were investigated.ResultsThe characterization of the effectors responsible for the resistance to vemurafenib evidenced the increased expression of MITF or the activation of Erk1/2 and p-38 kinases in the newly established cell lines with a phenotype resistant to vemurafenib. The sensitivity of cells to barasertib-HQPA was irrespective of BRAF mutational status. Barasertib-HQPA induced the mitotic catastrophe, ultimately causing apoptosis and necrosis of cells, inhibited cell migration and strongly affected the glycolytic metabolism of cells inducing the release of lactate. In association i) with vemurafenib the gain in effectiveness was found only in BRAF(V600K) cells while ii) with nab-paclitaxel, the combination was more effective than each drug alone in all cells.ConclusionsThese findings suggest barasertib as a new therapeutic agent and as enhancer of chemotherapy in metastatic melanoma treatment.

Late paradoxical development of pyoderma gangrenosum in a psoriasis patient treated with infliximab

In July 2013 a 43-year-old Caucasian man presented to our outpatient Dermatology clinic with multiple extensive ulcerative lesions on the posterior aspects of both legs, which reportedly appeared some weeks before and had since rapidly extended. The lesions, which were very painful, had first developed as multiple erythemato-violaceous plaques which later became deeply ulcerated, showing irregular margins and a seropurulent bed. The patient suffered from severe psoriasis, for which he had been under [...]

Allergic contact dermatitis caused by Helichrysum italicum contained in an emollient cream.

A 69-year-old non-atopic woman presented with eczematous lesions on her legs, trunk, and upper limbs. The history revealed that, one month before the development of the eczema, she had been applying an emollient cream to her legs (BioEulen Pediatric Cream, Aboca, Sansepolcro, Italy) based on natural ingredients to treat a moderate xerosis. She was treated with topical corticosteroids (mometasone furoate) with a once-daily application for 2 weeks, and instructed to avoid further contact with the suspected topical product. Three months after the complete resolution of the lesions, she was patch tested with the Italian Society of Allergological, Occupational and Environmental Dermatology (SIDAPA) standard baseline series (Euromedical®, Calolziocorte, LC, Italy), with our ‘natural ingredients’ series (Firma®, Florence, Italy) (Table 1), and with the emollient cream ‘as is’. Patch tests were applied on the back, and left in place for 2 days with Finn Chambers® (diameter 8 mm; SmartPractice®, Phoenix, AZ, USA) on Scanpor® tape (Norgesplaster A/S, Vennesla, Norway). Readings were performed at D2 and D4. The reactions were classified according to the International Contact Dermatitis Research Group guidelines. Readings showed positive reactions (++) to Myroxylon pereirae and to the cream ‘as is’. Hence, we performed patch tests with the ingredients of the cream (Table 2), kindly provided by the manufacturer (Aboca). Patch tests gave positive reactions (++), at both D2 and D4, for the hydrophilic fraction and the lipophilic fraction of flowering tops of Helichrysum (Helydol®), both at 3% pet. Ten healthy volunteers were patch tested with both substances, with negative results.

Risk factors for recurrence after successful treatment of warts: the role of smoking habits

Several therapies have been proposed for cutaneous warts without results concerning factors affecting recurrences.

Paradigmatic cases of pigmented lesions: How to not miss melanoma.

A large number of cases of melanoma exhibit clinical and dermoscopic clues leading to the correct diagnosis; however, sometimes melanoma can mimic benign melanocytic and non‐melanocytic lesions. We present a small series of melanomas in which additional clues provided by confocal microscopy increased the index of suspicion and prompted us to perform an excisional biopsy. Practical rules that are useful in difficult‐to‐diagnose melanomas are discussed.

Sporadic melanoma in South-Eastern Italy: the impact of melanocortin 1 receptor (MC1R) polymorphism analysis in low-risk people and report of three novel variants.

Environmental and genetic risk factors are involved in the development of melanoma. The role of the melanocortin 1 receptor (MC1R) gene has been investigated and differences according to geographic areas have been described. To evaluate the role of some clinical and genetic risk factors in melanoma development, we performed a case–control study involving 101 melanoma patients and 103 controls coming from South-Eastern Italy (Puglia), after achieving informed consent. We confirmed the role of known clinical risk factors for melanoma. Furthermore, 42 MC1R polymorphisms were observed. Three of these variants (L26V, H232L, D294Y) were not previously reported in the literature. Their predicted impact on receptor function was evaluated using bioinformatic tools. We report an overall frequency of MC1R variants in our population higher than in Northern or Central Italy. The most common polymorphism found was V60L, that has been recently reported to spread among South Mediterranean population. This variant influenced phenotypic characteristics of our population while it did not impinge on melanoma risk. An increased risk of melanoma was associated with two or more MC1R variants, when at least one was RHC, compared to people carrying the MC1R consensus sequence or a single MC1R polymorphism. Interestingly, we observed an increased risk of melanoma in subjects with darker skin and lower nevus count, usually considered at low risk, when carrying MC1R polymorphisms.

Allergic contact dermatitis caused by Glycofilm® 1.5P contained in an anti-wrinkle cream.

A 78-year-old atopic woman presented with the appearance of eczematous lesions involving the face, neck, and trunk. Her history showed that the lesions developed 2 months after the daily application of an anti-wrinkle cream. She was treated with a daily application of topical corticosteroid (methylprednisolone aceponate) for 10 days, and at the same time she stopped applying the above-mentioned cream. One month after complete resolution of the dermatitis, she was patch tested with the Italian Society of Allergological, Occupational and Environmental Dermatology (SIDAPA) baseline series (Euromedical®, Calolziocorte, LC, Italy), with our cosmetics series, and with the anti-wrinkle cream ‘as is’. Patch tests were applied on the back, and left occluded for 2 days with Finn Chambers® (diameter 8 mm; SmartPractice®, Phoenix, AZ, USA) on Scanpor® tape (Norgesplaster A/S, Vennesla, Norway). The test readings were performed on D2 and D4. The reactions were classified according to the International Contact Dermatitis Research Group guidelines. Readings showed positive reactions (++) to colophonium and to the antiwrinkle cream ‘as is’. Hence, we performed patch tests with the ingredients of the cream (Table 1), which were provided by the manufacturer. Patch tests gave positive reactions, at both D2 and D4, to Glycofilm® 1.5P (Solabia, Pantin, France) (Fig. 1), an aqueous solution containing biosaccharide gum-4 (CAS no. 283602-75-5), and phenoxyethanol. Ten healthy volunteers were patch tested with Glycofilm® 1.5P and with the anti-wrinkle cream ‘as is’, and the results were negative.

The mitochondrial master regulator gene PGC1alpha in novel sporadic melanoma cell lines: correlations with BRAF mutational status

Background Metabolic reprogramming is commonly found in cancer but it is poorly understood in melanoma. Recent works [1,2] provided new insights concerning molecular mechanisms involved in mitochondrial biogenesis of melanoma. This work aims to find possible correlations between pathways involved in the onset and progression of the disease in order to provide supporting information in this field. In particular we studied the behaviour of the mitochondrial master regulator gene PGC1alpha in novel sporadic melanoma cell lines and its relations with BRAF mutational status.