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.

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.

Autoimmune encephalitis is a rare immune-mediated neurological disorder characterized by brain inflammation associated with autoantibodies targeting neuronal surface or synaptic antigens. It frequently presents with rapidly progressive psychiatric symptoms, cognitive impairment, seizures, and autonomic instability, often mimicking primary psychiatric or infectious conditions. The disease course may be further complicated by concomitant endocrine dysfunction, requiring interdisciplinary management. We report the case of an 18-year-old woman with a history of autoimmune encephalitis and secondary hormonal abnormalities who developed recurrent psychotic decompensation. At the age of 15, she was hospitalized due to acute behavioral deterioration, hallucinations, confusion, and autonomic symptoms. Diagnostic evaluation revealed influenza A infection and inflammatory-demyelinating lesions in the corpus callosum and left cerebral hemisphere on MRI. Laboratory findings showed elevated antithyroid antibodies and hypothalamic amenorrhea, confirming endocrine involvement. Combined antiviral, immunomodulatory, and corticosteroid therapy resulted in significant clinical and radiological improvement. After two years of remission, the patient was readmitted with severe psychotic symptoms, including agitation, delusions, and behavioral disorganization. Neuroimaging demonstrated a stable post-inflammatory lesion without signs of active inflammation. Treatment required individualized polypharmacotherapy, with careful monitoring of extrapyramidal and endocrine adverse effects. This case highlights the complex interaction between autoimmune neuroinflammation, hormonal dysregulation, and psychiatric manifestations. Early recognition, comprehensive immunological and endocrine evaluation, and long-term multidisciplinary follow-up are essential to optimize outcomes and reduce relapse risk in autoimmune neuropsychiatric syndromes.

A case of a 64-year-old female patient diagnosed with left-sided inflammatory breast cancer at stage T4dN2aM0 was described. Histopathological examination revealed grade 3 invasive ductal carcinoma, negative for hormonal receptor expression (ER−, PR−), with HER2 overexpression (3+) and a high Ki-67 proliferation index (85%). Metastatic involvement of the axillary lymph nodes was present. Neoadjuvant therapy was administered, resulting in a partial clinical response. Subsequently, a modified radical mastectomy according to the Madden technique was performed. Postoperative histopathological assessment demonstrated no residual carcinoma within the breast (ypT0); however, metastatic involvement was confirmed in 5 lymph nodes (ypN2a). Adjuvant treatment included trastuzumab and radiotherapy. During follow-up, no evidence of local recurrence or distant metastases was observed. Extended genetic testing did not identify mutations associated with hereditary cancer predisposition.