Vitiligo is a chronic skin disorder characterised by the loss of melanocytes and subsequent skin depigmentation. Although many theories have been proposed in the literature, none alone explains the pathogenesis of vitiligo. Oxidative stress has been identified as a potential factor in the pathogenesis of vitiligo. A growing body of evidence suggests that antioxidant therapies may offer a promising approach to managing this condition. This review summarises the potential mechanisms of oxidative stress and the types of melanocyte death in vitiligo. We also provide a brief overview of the most commonly studied antioxidants. Melanocytes in vitiligo are thought to be damaged by an accumulation of reactive oxygen species to destroy the structural and functional integrity of their DNA, lipids, and proteins. Various causes, including exogenous and endogenous stress factors, an imbalance between prooxidants and antioxidants, disruption of antioxidant pathways, and gene polymorphisms, lead to the overproduction of reactive oxygen species. Although necroptosis, pyroptosis, ferroptosis, and oxeiptosis are newer types of cell death that may contribute to the pathophysiology of vitiligo, apoptosis remains the most studied cell death mechanism in vitiligo. According to studies, vitamin E helps to treat lipid peroxidation of the skin caused by psoralen ultra-violet A treatment. In addition, Polypodium leucotomos increased the efficacy of psoralen ultra-violet A or narrow-band ultraviolet B therapy. Our review provides valuable insights into the potential role of oxidative stress in pathogenesis and antioxidant-based supporting therapies in treating vitiligo, offering a promising avenue for further research and the development of effective treatment strategies.

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.

E-health offers new opportunities for self-management, health and social care and access to health information. Over the last decade, the use of e-health solutions by patients, healthcare providers, professionals and citizens has increased significantly. This article provides an overview of e-health innovations in Poland, Spain, Romania and Estonia, focussing on the digital development of healthcare services. It outlines the concept of e-health and the innovative solutions the countries listed have introduced in this area. They all face challenges such as the cost of implementing new technologies, data access and the security of patient data. As a result, there is a constant need for coordinated collaboration, legislation and clear guidelines for the use of technology in healthcare. The lessons learnt from these countries are helping to shape the digital future of healthcare in Europe. In Poland, the Ministry of Health oversees the eHealth Centre, which has made remarkable progress in the field of eHealth services such as the Internet patient account, electronic prescriptions and electronic referrals. The biggest challenges include financing innovation and improving digital skills. Poland has also recently introduced the no-fault system as an alternative compensation system for medical errors, modelled on similar systems in Denmark and Sweden. Technological progress is driving the transformation of the Spanish healthcare system, which is particularly evident in the area of telemedicine and innovative healthcare systems. The Spanish Digital Health Strategy lines up with broader national initiatives. Despite challenges such as underfunding, Romania has introduced digital healthcare with the Health Electronic Record since 2014. As an absolute pioneer in the digitalisation of healthcare in Europe, Estonia is proud of its achievements in the digitalisation of healthcare data and services. The Estonian eHealth Foundation and the nationwide health information system are an example of seamless integration and set a benchmark for comprehensive digital healthcare.

To assess the determinants of lipid parameters in primary care patients without diagnosed cardiovascular disease (CVD), a cross-sectional study was conducted during 2018–2019 with a total of 200 patients. The following lipid parameters were measured: total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), small, dense LDL (sdLDL-C), and lipoprotein (a) (Lp(a)). Predictors of elevated and adequately controlled lipid parameters were assessed with logistic regression analysis. Older age was related to higher risk of TC ≥ 6.2 mmol/L [OR 1.03 (95% CI 1.0–1.05)], sdLDL-C ≥ 1.0 mmol/L [OR 1.05 (95% CI 1.0–1.1)], and decreased risk of Lp(a) ≥ 50 mg/dL [OR 0.97 (95% CI 0.94–0.99)]. Patients with diabetes mellitus (DM) had increased probability of TG ≥ 2.25 mmol/L [OR 3.77 (95% CI 1.34–10.6)] and Lp(a) ≥ 50 mg/dL [OR 2.97 (1.34–6.10)] as well as adequate control of TG and Lp(a). Higher material status was related to lower risk of TC ≥ 6.2 mmol/L [OR 0.19 (95% CI 0.04–0.82)] and LDL-C ≥ 3.6 mmol/L [OR 0.33 (95% CI 0.12–0.92)]. High BMI was related to increased [OR 1.14 (95% CI 1.02–1.29)], and female gender [OR 0.33 (95% CI 0.12–0.96)] and hypertension [OR 0.29 (95% CI 0.1–0.87)] to decreased risk of TG ≥ 2.25 mmol/L [OR 1.14 (95% CI 1.02–1.29)]. Taking lipid-lowering drugs (LLD) was associated with LDL-C < 2.6 mmol/L [OR 2.1 (95% CI 1.05–4.19)] and Lp(a) < 30 mg/dL [OR 0.48 (95% CI 0.25–0.93)]. Physical activity was related to LDL-C < 2.6 mmol/L [OR 2.02 (95% CI 1.02–3.98)]. Higher abdominal circumference was associated with decreased risk of TG < 1.7 mmol/L [OR 0.96 (95% CI 0.93–0.99)]. Elevated lipid parameters were related to age, gender, material status, BMI, history of DM, and hypertension. Adequate control was associated with age, education, physical activity, LLD, history of DM, and abdominal circumference.

Diabetes and obesity have been recognized as confirmed risk factors for the occurrence of liver fibrosis. Despite the long-standing acknowledgment of “diabesity”, the simultaneous existence of diabetes and obesity, scholarly literature has shown limited attention to this topic. The aim of this pilot study was to assess the prevalence of liver fibrosis among individuals with diabetes (specifically those who are obese) in order to identify the key factors associated with hepatofibrosis and determine the most important associations and differences between patients with and without liver fibrosis. The research included a total of 164 participants (48.17% had comorbid obesity). Liver elastography (Fibroscan) was performed on these individuals in addition to laboratory tests. Liver fibrosis was found in 34.76% of type 2 diabetes patients; male gender almost doubled the risk of hepatofibrosis (RR 1.81) and diabesity nearly tripled this risk (RR 2.81; however, in degree III of obesity, the risk was elevated to 3.65 times higher). Anisocytosis, thrombocytopenia, or elevated liver enzymes raised the incidence of liver fibrosis by 1.78 to 2.47 times. In these individuals, liver stiffness was negatively correlated with MCV, platelet count, and albumin concentration; GGTP activity and HbA1c percentage were positively correlated. The regression analysis results suggest that the concentration of albumin and the activity of GGTP are likely to have a substantial influence on the future management of liver fibrosis in patients with diabesity. The findings of this study can serve as the basis for subsequent investigations and actions focused on identifying potential therapeutic and diagnostic avenues.

Metabolic-associated fatty liver disease (MAFLD) has become a very significant health problem worldwide, characterized by hepatic steatosis and systemic metabolic disturbances. Grasping the complex interaction between the intestine and liver, referred to as the gut-liver axis, is crucial to decipher the pathogenesis of MAFLD and identify potential therapeutic targets. Probiotics, which are live microorganisms offering health benefits, have garnered attention for their potential in treating MAFLD. A literature search in PubMed and Google Scholar using "MAFLD," "NAFLD," "probiotics," and "gut microbiota" yielded 642 studies; 32 clinical trials met the inclusion criteria for the final analysis. This review encapsulates the current knowledge of MAFLD pathophysiology, emphasizing the role of the gut-liver axis, and assesses the clinical evidence supporting probiotic treatments for MAFLD. The mechanisms of action of probiotics are explored, including their ability to modulate gut microbiota composition, enhance epithelial barrier function, and influence the immune response. Various randomized controlled trials have shown that probiotics are effective in enhancing several aspects of MAFLD, such as liver enzymes, lipid profiles, body mass index, insulin sensitivity, or even histological efficacy. However, mixed results have been reported in some clinical trials, highlighting the need for further research to optimize probiotic interventions. Future investigations should focus on standardized protocols, personalized approaches and exploring synergistic combinations with other therapeutic modalities to maximize the potential of probiotics in the treatment of MAFLD.