At present, vitiligo is the most common depigmenting skin disorder, characterized by clearly demarcated discolored patches of various shapes and sizes. Depigmentation results from the initial dysfunction and subsequent destruction of melanin-producing cells, called melanocytes, which are located in the basal layer of the epidermis and in hair follicles. This review concludes that the extent of repigmentation, regardless of the treatment method, is greatest in stable localized vitiligo patients. The aim of this review is to provide an overview of the clinical evidence for which the vitiligo treatment method (cellular or tissue) is more effective. The treatment relies on multiple factors, ranging from patient skin predisposition for repigmentation to the experience of the facility performing the procedure. Vitiligo is a significant problem in modern society. Although it is a typically asymptomatic and not life-threatening disease, it may have significant psychological and emotional impacts. Standard treatment relies on pharmacotherapy and phototherapy; however, the treatment of patients with stable vitiligo varies. The stability of vitiligo more than often implies the exhaustion of the potential for skin self-repigmentation. Thus, the surgical methods that distribute normal melanocytes into the skin are crucial elements of these patients’ therapy. The most commonly used methods are described in the literature, with an indication of their recent progress and changes. In addition, information on the efficiency of the individual methods at specific locations is compiled in this study, and the prognostic factors indicating repigmentation are presented. Cellular methods are the best therapeutic option for large-sized lesions; although they are more exorbitant than tissue methods, they benefit from more rapid healing times and presenting fewer side effects. Dermoscopy is a valuable tool used to assess the further course of repigmentation, where it is of great value to evaluate the patient prior to and following an operation.

Oxidative stress plays an important role in the development of vitiligo. The aim of our study was to assess the effect of oral vitamin supplementation with antioxidant activity on the effectiveness of the vitiligo treatment. The study group consisted of 46 patients suffering from nonsegmental vitiligo for over a year. Before and after the therapy, the clinical advancement of the disease (VASI) and impairment of quality of life (DLQI) were assessed in all patients, and the activities of selected antioxidant enzymes (SOD, CAT, and GPx), lipid peroxidation products (MDA), and vitamins A and E were determined. Each patient was randomly assigned to one of three therapeutic groups: FOTO (UVB therapy at 311 nm, 3x a week for 4 months), WIT (oral antioxidant supplementation‐vitamin A + E at a dose of 5000 IU of retinol and 400 mg of tocopherol), and FOTO + WIT (combination therapy). After the treatment, an increase in all antioxidant enzymes and a decrease in the concentration of malondialdehyde in patients were noted, regardless of the therapeutic method used. The greatest improvement in the repigmentation of skin lesions was achieved in patients treated with combined therapy (VASI −6.95 ± 4.69, p < 0.01, DLQI −1.90 ± 2.77, p = 0.011). The burden of patients with risk factors for oxidative stress turned out to be associated with a greater severity of the disease process, and a longer period of disease was positively correlated with a reduction in the quality of life in patients.

Knowledge about determinants of addiction in people taking addictive substances is poor and needs to be supplemented. The novelty of this paper consists in the analysis of innovative aspects of current research about relationships between determinants of addiction in Polish patients taking addictive substances and rare available data regarding the relationships between these factors from studies from recent years from other environments, mainly in Europe, and on the development of genetic determinants of physiological responses. We try to explain the role of the microelements Mn, Fe, Cu, Co, Zn, Cr, Ni, Tl, Se, Al, B, Mo, V, Sn, Sb, Ag, Sr, and Ba, the toxic metals Cd, Hg, As, and Pb, and the rare earth elements Sc, La, Ce, Pr, Eu, Gd, and Nd as factors that may shape the development of addiction to addictive substances or drugs. The interactions between factors (gene polymorphism, especially ANKK1 (TaqI A), ANKK1 (Taq1 A-CT), DRD2 (TaqI B, DRD2 Taq1 B-GA, DRD2 Taq1 B-AA, DRD2-141C Ins/Del), and OPRM1 (A118G)) in patients addicted to addictive substances and consumption of vegetables, consumption of dairy products, exposure to harmful factors, and their relationships with physiological responses, which confirm the importance of internal factors as determinants of addiction, are analyzed, taking into account gender and region. The innovation of this review is to show that the homozygous TT mutant of the ANKK1 TaqI A polymorphism rs 1800497 may be a factor in increased risk of opioid dependence. We identify a variation in the functioning of the immune system in addicted patients from different environments as a result of the interaction of polymorphisms.

Background and Aims: Androgenetic alopecia (AGA) is a prevalent condition. The treatment methods currently available for this condition have limited potential (minoxidil) and side effects with long‐term therapy that affect the physiology of the male population (5α‐reductase inhibitors). In recent years, there has been a considerable expansion in knowledge about the etiology of AGA, while current treatment methods appear to be outdated in light of new findings. Methods: A review of the latest publications on androgenetic alopecia concerning its etiology and genetics was conducted, with the aim of examining the molecular pathways associated with mutations in the following genes: The following genes were found to be implicated: AR (WNT/β‐catenin pathway), EDA2R (WNT/β‐catenin and proapoptotic pathways), HDAC9 (Treg pathway), PAX1 and FOXA2 (development pathways). This facilitated the development of a theoretical model for the treatment of AGA using the STEAP3 protein. Results: A theoretical model of AGA therapy has been designed using the STEAP3 protein to activate the inhibited WNT/β‐catenin pathway as a result of mutations in the AR and EDA2R genes. STEAP3 catalyses the conversion of Fe ³⁺ to Fe ²⁺ , which in turn facilitates the phosphorylation of GSK3β, resulting in its subsequent inactivation. This process culminates in the dissolution of the complex that hinders the transfer of β‐catenin to the cell nucleus. Conclusion: It is hypothesised that STEAP3‐based therapy has the potential to become an effective treatment for AGA, acting on the underlying cause of the disease (determined by the mutations described). It should be noted that all analyses presented in the following text constitute a theoretical model of AGA treatment using STEAP3 protein and its derivatives, and are not supported by laboratory and clinical studies. Nevertheless, they serve as an introduction to further in vitro, in vivo, and clinical trials.