The main aim of the paper was to simulate the drug release by a multifractal theoretical model, as a valuable method to assess the drug release mechanism. To do this, drug delivery films were prepared by mixing poly(vinyl alcohol boric acid) (PVAB) and diclofenac (DCF) sodium salt drug in different mass ratios from 90/10 to 70/30, in order to obtain drug delivery systems with different releasing rates. The different drug content of the three systems was confirmed by energy-dispersive spectroscopy (EDAX) analysis, and the encapsulation particularities were investigated by scanning electron microscopy (SEM), atomic force microscopy (AFM), and polarized optical microscopy (POM) techniques. The ability of the PVAB matrix to anchor the DCF was assessed by Fourier transform infrared (FTIR) spectroscopy. The in vitro release of the diclofenac sodium salt from the formulations was investigated in biomimetic conditions (pH=7.4 and 37°C) by UV-Vis spectroscopy, measuring the absorbance of the drug at 275 nm and fitting the results on a previously drawn calibration curve. An estimation of the drug release kinetics was performed by fitting three traditional mathematical models on experimental release data. Further, the drug delivery was simulated by the fractal theory of motion, in which the release dynamics of the polymer-drug complex system is described through various Riccati-type “regimes.” To explain such dynamics involved multifractal self-modulation in the form of period doubling, quasiperiodicity, intermittency, etc., as well as multifractal self-modulation of network type. Standard release dynamics were explained by multifractal behaviors of temporary kink type. The good correlation between the traditional mathematical models and the new proposed theoretical model demonstrated the validity of the multifractal model for the investigation of the drug release.

Atopic dermatitis (AD) is a chronic skin disorder associated with significant quality-of-life impairment and increased risk for allergic and non-allergic comorbidities. The aim of this review is to elucidate the connection between AD and most common comorbidities, as this requires a holistic and multidisciplinary approach. Advances in understanding these associations could lead to the development of highly effective and targeted treatments.

Psoriasis is a chronic multisystem inflammatory disease associated with a plethora of comorbidities including metabolic syndrome, cardiovascular disease, hypertension, diabetes, hyperlipidemia, obesity, anxiety, depression, chronic kidney disease, and malignancy. Advancement in unveiling new key elements in the pathophysiology of psoriasis led to significant progress in the development of biologic agents which target different signaling pathways and cytokines involved in the inflammatory cascade responsible for the clinical manifestations found in psoriasis. Currently available novel therapeutic options for moderate-severe psoriasis include tumor necrosis factor alpha inhibitors, inhibitors of the interleukin 17, and inhibitors of the interleukin 23. Nevertheless, concerns have been raised with respect to the possible risks associated with the use of biologic therapy requiring close collaboration between dermatologists and physicians of different specialties. Our aim was to perform an in-depth literature review and discuss the potential risks associated with biologic therapy in patients with psoriasis and concurrent diseases with a focus on the influence of novel therapeutic agents on liver function in the context of hepatopathies, particularly viral hepatitis. A multidisciplinary teamwork and periodic evaluation of psoriasis patients under biologic therapy is highly encouraged to obtain an accurate management for each case.

Dermatofibroma (DF) or fibrous histiocytoma is one of the most frequent benign cutaneous soft-tissue lesions, characterized by a post-inflammatory tissue reaction associated with fibrosis of the dermis. Clinically DFs have a polymorphous clinical aspect from the solitary, firm, single nodules to multiple papules with a relatively smooth surface. However, multiple atypical clinicopathological variants of DFs have been reported and, therefore, clinical recognition may become challenging, leading to a more burdensome identification and sometimes to misdiagnosis. Dermoscopy is considered an important tool in DFs diagnosis, as it improves diagnostic accuracy for clinically amelanotic nodules. Although typical dermoscopic patterns are most frequently seen in clinical practice, there have also been some atypical variants described, mimicking some underlying recurrent and sometimes harmful skin afflictions. Usually, no treatment is required, although an appropriate work-up may be necessary in specific cases, such as in the presence of atypical variants or a history of recent changes. This narrative review’s aim is to summarize current evidence regarding clinical presentation, positive and differential diagnosis of atypical dermatofibromas and also to raise awareness about the importance of specific characteristics of atypical variants to better differentiate them from malignant conditions.

The occurrence of both melanoma and glioma was first suggested by the observation of a familial association between these conditions, which was later confirmed by the description of the melanoma–astrocytoma syndrome, an extremely rare, inherited affliction in which people have an increased risk of developing melanoma and nervous system tumors. Taking into consideration the common embryologic precursor, the neuroectoderm, it was hypothesized that this syndrome is associated with a genetic disorder. While some families with germline CDKN2A mutations are prone to develop just melanomas, others develop both melanomas and astrocytomas or even other nervous-system neoplasms. Herein, we report the case of a 63-year-old male patient with no personal or family history of malignancy who had primary melanoma followed by glioblastoma. Our case report suggests that the occurrence of both melanoma and glioblastoma is most likely not coincidental but instead linked to genetic mutations of common embryologic precursors or signaling pathways.