Introduction and purpose: The impact of electronic devices on our daily lives is becoming increasingly significant. The contemporary generation of young people is growing up in a world where smartphones, tablets, computers, and other electronic devices are widely available and utilized. Scientists are contemplating the challenges posed by excessive exploitation of electronics on the health of young individuals. The aim of the article is to present the harmful effects of using electronic devices before sleep in young people, considering medical aspects such as sleep disorders and their influence on overall psychophysical health. Summary: Electronic devices negatively affect the sleep of young people by reducing sleep time and delaying the sleep onset phase. The main problem is the use of electronic devices without time limits. In the era of technology, it is significantly important to raise awareness among young people about the importance of sleep hygiene and how blue light emitted by electronic devices affects its quality.

Diabetes mellitus type 2 is a chronic metabolic disease that presents a growing global health challenge. Its long-term complications, including nephropathy, neuropathy, and retinopathy, significantly contribute to patient morbidity and the healthcare burden. Diabetic kidney disease, one of the significant complications, often progresses to end-stage renal failure, necessitating renal replacement therapy. This case report describes a 67-year-old man with longstanding type 2 diabetes mellitus and hypertension complicated by progressive chronic kidney disease, diabetic foot syndrome, and subsequent neurological and psychiatric manifestations. The patient was initially admitted to the nephrology department for predialysis assessment and optimization of anemia management. Over the following months, he experienced recurrent hospitalizations due to diabetic foot ulceration, phlegmon requiring surgical intervention, and episodes of psychotic syndrome related to metabolic and vascular factors. The final admission to the stroke unit revealed a left thalamic intracerebral hemorrhage associated with severe arterial hypertension and worsening disturbances of consciousness. A multidisciplinary approach was employed, including nephrological, surgical, psychiatric, and neurological care, along with complex polypharmacotherapy and insulin therapy. This case illustrates the intricate relationship between diabetes, chronic kidney disease, and cerebrovascular complications. It emphasizes the importance of early nephrological and metabolic monitoring, personalized treatment strategies, and ongoing interdisciplinary collaboration. Early recognition and management of diabetic complications can significantly improve prognosis and prevent life-threatening outcomes in patients with advanced type 2 diabetes mellitus.

Introduction and purpose: Juvenile idiopathic arthritis (JIA) is the most common chronic rheumatic disease in children, involving not only joints but also internal organs, skin, and eyes. It is diagnosed in children under the age of 16 when symptoms last longer than six weeks. The ILAR classification includes several subtypes such as oligoarticular, polyarticular (RF-positive and RF-negative), systemic (sJIA), psoriatic, and enthesitis-related arthritis. Systemic JIA is characterized by fever and rash, while the oligoarticular form often coexists with positive ANA antibodies and carries a high risk of chronic uveitis. New subtypes have been added in recent years, such as early-onset ANA-positive JIA. Imaging, including X-ray, MRI, and ultrasound, plays a crucial role in assessing disease progression, especially in the hip, knee, and temporomandibular joints. Treatment involves a multidisciplinary approach and includes NSAIDs, intra-articular and systemic glucocorticoids, non-biologic DMARDs (especially methotrexate), and biological therapies. Biologic agents include TNF inhibitors (adalimumab, etanercept, infliximab), IL-1 inhibitors (anakinra, canakinumab), IL-6 inhibitor (tocilizumab), T-cell inhibitor (abatacept), and B-cell therapy (rituximab). These targeted treatments improve disease control, reduce joint damage, and enhance quality of life, enabling many patients to achieve remission and prevent long-term disability.

Introduction and Objective: Lyme disease is an infection caused by Gram-negative,microaerophilic spirochetes of the Borrelia genus, transmitted to humans through the bite ofan infected tick, which serves as the vector of this disease. It is one of the most frequentlydiagnosed tick-borne illnesses worldwide, with a rising incidence rate. Notably, childrenrepresent an increasingly affected population, emphasizing the need for focused attention onpediatric manifestations and management.Brief Overview of Current Knowledge - Lyme disease progresses through three clinicalstages: early localized, early disseminated, and late stage. Each phase presents withcharacteristic clinical manifestations. The early localized stage typically features erythema migrans, most often appearing onthe scalp, neck, shoulders, legs, or lower back. The early disseminated stage is marked by flu-likesymptoms, lymphadenopathy, arthralgia, myalgia, cranial nerve palsies—mostfrequently involving the facial nerve (cranial nerve VII) —ocular involvement,and lymphocytic meningitis. The late stage is characterized predominantly by pauciarticular arthritis, affecting largejoints—especially the knees. In some cases, cardiac manifestations may occur, suchas conduction abnormalities, myocarditis, or pericarditis.This progression underscores the multisystemic nature of Lyme disease and highlights theimportance of early recognition and treatment to prevent long-term complications.

This article presents the case of a 39-year-old woman with a positive family history of breast cancer (her family member had left breast cancer, cT4N2M0, non-luminal human epidermal growth factor receptor 2 (HER2)-positive). During routine prophylactic ultrasonographic examination, a breast mass was detected, which, on further diagnostics, turned out to be an invasive ductal carcinoma of the left breast. The stage of the disease was determined as pT1cN1mic(sn), Nottingham Histologic Grade 3 (NHG 3). The patient was subjected to surgical treatment, which involved left mastectomy with simultaneous removal of the axillary sentinel lymph node. Subsequently, adjuvant chemotherapy was administered, including a "dose-dense" regimen with the use of doxorubicin and cyclophosphamide, followed by treatment with paclitaxel. During chemotherapy, complications related to the implantation of a vascular port occurred, which resulted in its removal before the completion of treatment. After the completion of chemotherapy, breast reconstruction was performed. During the entire treatment process, extended genetic diagnostics were performed, which did not demonstrate the presence of pathogenic gene mutations. The treatment was completed, and the patient remains under continuous care of the oncology outpatient clinic.

Introduction and Objective. Hidradenitis suppurativa (HS) is a chronic, recurrent inflammatory skin disease characterized by follicular occlusion, painful nodules, abscesses, sinus tract formation, and scarring, primarily affecting intertriginous areas. Although previously considered a disorder of the apocrine glands, HS is now recognized as a complex immunoinflammatory condition involving dysregulation of innate and adaptive immune pathways. This review aims to summarize current knowledge on the immunopathogenesis of HS, with particular emphasis on recent molecular and cellular insights relevant to targeted therapy. Brief Overview of Current Knowledge. The initiating event in HS is follicular hyperkeratosis, leading to follicular rupture and secondary inflammation. Disease progression is driven by persistent immune activation, dominated by Th1/Th17 polarization. Key mechanisms include increased expression of proinflammatory cytokines such as IL-17, IL-1β, TNF-α, and IFN-γ, activation of the complement system, especially C5a, and dysregulation of antimicrobial peptides. Aberrant interactions between keratinocytes, fibroblasts, plasma cells, innate lymphoid cells, and T-cell subsets contribute to chronic inflammation and tissue destruction. Summary. Hidradenitis suppurativa is a multifactorial immunoinflammatory disease in which follicular occlusion initiates a complex immune cascade. Identification of biomarkers and therapeutic targets, including IL-17-driven pathways, complement components, and CD2–CD58 signaling, supports the development of personalized, mechanism-based treatment strategies. Improved understanding of HS immunopathogenesis may enhance disease stratification and clinical outcomes.