Background: We present a case of a patient with the sequential development of clinical symptoms characteristic of multiple sclerosis, polymyositis, and malignant melanoma. Case presentation: Polymyositis occurred two years after the onset of multiple sclerosis. Clinical signs of melanoma were identified following the development of polymyositis. Treatment with corticosteroids and immunosuppressants positively affected the patient’s clinical manifestations of multiple sclerosis. It remains unclear whether there was an insidious progression of melanoma without clinical manifestations and whether the myositis developed in parallel with this melanoma. It is possible that polymyositis developed independently or preceded the onset of melanoma with lymph node metastases. Conclusion: The patient's clinical history demonstrates an overlap of demyelinating, systemic, and malignant diseases. Integrated treatment is essential for achieving clinical improvement in these patients.
Malignant melanoma is an aggressive skin tumor that accounts for 1% of all skin tumors. Immunotherapy is a new therapeutic approach for the treatment of melanoma neoplasms. Nivolumab is an immunotherapeutic product that belongs to the so-called checkpoint inhibitors. Nivolumab therapy has demonstrated a good effect in terms of overall survival and progression-free survival in patients with malignant melanoma. Nivolumab treatment is used both for therapy in patients in the metastatic stage and in the adjuvant aspect in patients with a high risk of disease recurrence. The interaction between the ligand of the programmed cell death receptor (PD-L1) and the programmed cell death receptor (PD-1) leads to suppression of autoimmune manifestations. Blocking this interaction carries a risk of various autoimmune reactions, which are expressed to varying degrees, and can sometimes be life-threatening and require prolonged immunosuppression or discontinuation of treatment with checkpoint inhibitors. Immune-related adverse reactions of varying degrees and severity have been described with the use of anti-PD-1 antibodies, such as pneumonitis, hepatitis, endocrinopathies, immune-mediated colitis, dermatitis, etc. Rheumatic immune-mediated complications such as myositis, myalgia, arthritis, arthralgia, vasculitis, scleroderma are rare with Nivolumab treatment. Most often, patients report arthritis that starts after several cycles of Nivolumab administration. The mechanism of occurrence of immune-mediated arthritis has not yet been established. A clinical case of an 84-year-old patient who developed immune-related arthritis after treatment with Nivolumab is presented. After treatment with corticosteroids and immunosuppressants led to the control of the immune-related arthritis, reinitiation of immunotherapy is being evaluated for the management of the oncological disease.
Systemic sclerosis (SSc) is a rare autoimmune connective tissue disease with multifaceted clinical manifestations, unclear etiology, and specific immunological phenomena that continue to be a challenge for modern science regarding their etiopathogenetic role in the onset and course of the disease. In SSc, different autoantibodies could be detected, and three are defined as diagnostic. They are considered potential biomarkers as they may eventually be used to distinguish distinct patient groups with specific clinical manifestations. Three specific autoantibodies and capillaroscopic abnormalities were included in the 2013 ACR/EULAR classification criteria for SSc. The autoantibodies defined as diagnostic in SSc are anti-centromere, anti-topoisomerase I, and anti-RNA polymerase III antibodies. Other SSc-associated antibodies are anti-Th/To, Ku, PDGFR, PM-Scl, etc. Growing evidence suggests an association between specific autoantibody profiles and distinct capillaroscopic patterns, indicating a link between immunological mechanisms and microvascular damage.
Background: Biosimilar infliximab agents are increasingly used in the management of axial spondyloarthritis (axSpA), primarily driven by cost considerations. While clinical outcomes after switching from originator infliximab (INF) to several biosimilars have been reported, real-world data regarding switching to Ixifi remain limited. Objectives: To evaluate clinical outcomes, treatment retention and safety following non-medical switching from originator INF to the biosimilar Ixifi in patients with axSpA. Methods: This single-center observational cohort study included adult patients with axSpA who were transitioned from originator INF to Ixifi for non-medical reasons. Clinical assessments and laboratory parameters were recorded at baseline and at 3 and 6 months after switching. Disease activity was evaluated using ASDAS, BASDAI and BASFI. Safety outcomes and treatment discontinuation were systematically recorded. Results: 72 patients were included. Inflammatory markers, including C-reactive protein and erythrocyte sedimentation rate, remained stable over 6 months (p>0.05 for all), as did ASDAS scores (p>0.05). In contrast, BASDAI and BASFI showed modest but statistically significant improvements at month 6 (p=0.008 and p=0.002, respectively). 2 serious infections (2.8%) and 2 infusion reactions (2.8%) were observed. Treatment discontinuation occurred in 13.9% of patients, exclusively due to loss of efficacy. The estimated 6-month treatment retention rate was 86.1%. Conclusion: In this real-world cohort, non-medical switching from originator infliximab to Ixifi in axSpA was associated with maintained short-term clinical stability, acceptable treatment retention and a favorable safety profile. However, the absence of a control group limits causal interpretation of these findings. Larger studies with longer follow-up are warranted to confirm long-term outcomes.
IgG4-related disease (IgG4-RD) has evolved from a series of organ-specific clusters into a recognized systemic fibroinflammatory disorder defined by a unique B-T cell axis. This review provides a comprehensive analysis of current diagnostic and therapeutic paradigms, emphasizing the pathogenic roles of CD4+ cytotoxic T lymphocytes and follicular helper T cells in driving storiform fibrosis. Despite the utility of the 2019 ACR/EULAR classification criteria, diagnostic challenges persist; notably, serum IgG4 remains a fallible biomarker, with a significant amount of patients maintaining normal concentrations during active disease. While glucocorticoids are the traditional first-line treatment, their long-term toxicity and high relapse rates have catalyzed a shift toward targeted B-cell depletion. Emerging evidence suggests that early intervention with biological agents can arrest and even reverse established fibrotic lesions, highlighting the dynamic nature of the immune-fibroblast interface. However, the current reliance on retrospective data and the lack of sensitive biomarkers for diagnosis and monitoring disease activity remain significant hurdles. This review underscores the necessity for precision-driven management and large-scale randomized trials to optimize long-term outcomes and minimize organ damage in this complex multi-organ condition.
