Insulin resistance is a condition of impaired tissue reactivity to insulin. This state is primarily associated with obesity and the lifestyle of modern Western societies, which favors abnormalities of glucose and lipid homeostasis. As a result, more and more people suffer from illnesses that develop because of the disturbed metabolic function of insulin, including type 2 diabetes, nonalcoholic fatty liver disease and polycystic ovarian syndrome. There are many studies describing the relationship between declining sensitivity to insulin and insufficient physical activity or unhealthy dietary habits. However, there is a vast number of other factors that may contribute to the development of this condition. In recent years, more attention has been paid to environmental pollutants as promoters of insulin resistance. As the overall grade of waste accumulation in the environment rises, factors like toxic metals, pesticides, dust, harmful gases and micro- or nanoplastics are starting to pose an increasingly serious threat in the context of metabolic disorder development. This review gathers data concerning the influence of the mentioned pollutants on the metabolic health of living organisms, with particular emphasis on the impact on carbohydrate processing, insulin resistance and molecular pathways associated with these processes.

Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by progressive joint destruction and immunometabolic complications, notably rheumatoid cachexia. This review article investigates the significance and efficacy of resistance exercise in mitigating myopenia, sarcopenic obesity, and systemic inflammation in RA patients. The objective is to elucidate the underlying molecular mechanotransduction pathways, the role of myokines, and the clinical outcomes of progressive resistance training (PRT). A comprehensive review of the current literature, including recent randomized controlled trials and meta-analyses, was conducted to evaluate clinical and physiological effects. The findings indicate that PRT effectively counteracts muscle atrophy by activating the mTORC1 pathway and exerts potent anti-inflammatory effects via the release of muscle-derived interleukin-6 (IL-6). Furthermore, PRT demonstrates synergistic potential with modern biological and targeted synthetic disease-modifying anti-rheumatic drugs (DMARDs). Clinically, properly dosed PRT improves functional capacity, reduces cardiovascular risk, and alleviates patient-reported outcomes such as fatigue and sleep disruption, without exacerbating synovial inflammation or radiographic progression in stable RA. We conclude that structured resistance training is a crucial, evidence-based non-pharmacological therapy for RA — warranting equal consideration alongside standard aerobic exercises — and provide structured dosing guidelines based on the FITT-VP framework.

Background: Neovascular age-related macular degeneration (nAMD) is a leading cause of irreversible central vision loss in older adults. Intravitreal anti-vascular endothelial growth factor (anti-VEGF) therapy has transformed disease management, but the expanding range of agents and evolving dosing strategies has complicated therapeutic decision-making. Objective: To summarize the anti-VEGF agents currently available for nAMD, compare their efficacy, safety and durability, and evaluate contemporary treatment strategies used to optimize long-term visual outcomes while minimizing treatment burden. Methods: A narrative literature review was conducted using PubMed and Google Scholar. Eligible publications included landmark randomized trials, real-world studies, systematic reviews, meta-analyses, consensus statements and international clinical guidelines addressing anti-VEGF pharmacotherapy and treatment regimens in nAMD, prioritizing high-quality evidence. Key Findings: Ranibizumab, aflibercept 2 mg, brolucizumab, faricimab, aflibercept 8 mg and the recently approved ophthalmic formulation bevacizumab-vikg all preserve or improve visual acuity. Functional outcomes are broadly comparable across agents, with meaningful differences confined to durability, anatomical fluid control and safety, most notably the intraocular inflammation signal associated with brolucizumab. Treat-and-extend dosing matched fixed dosing for visual acuity while requiring fewer injections and outperformed pro re nata regimens. Faricimab and aflibercept 8 mg maintained intervals of 12 weeks or longer in most patients, and switching agents improved anatomical outcomes in insufficiently responding eyes. Conclusions: Contemporary management of nAMD centers on individualized anti-VEGF therapy guided by disease activity, treatment response and patient-specific factors. Longer-acting agents and emerging approaches are expected to further improve disease control while reducing the burden of repeated intravitreal injections.

Traumatic triangular fibrocartilage complex (TFCC) tears are an important cause of ulnar-sided wrist pain, reduced grip strength, restricted forearm rotation, and distal radioulnar joint (DRUJ) instability. Their diagnosis and management remain challenging because morphological abnormalities do not always correlate with symptoms or functional impairment. This narrative review summarizes contemporary concepts in the diagnosis, treatment, and rehabilitation of traumatic TFCC tears, with particular emphasis on modern imaging and arthroscopic technologies. English-language publications were identified through PubMed without restrictions on publication year. The reviewed evidence indicates that diagnosis should integrate the mechanism of injury, physical examination, bilateral assessment of DRUJ stability, and imaging findings. Magnetic resonance imaging and magnetic resonance arthrography improve visualization of TFCC lesions, but incidental abnormalities and variable diagnostic performance limit their use as isolated decision-making tools. DRUJ stability appears to be a key factor in treatment selection. Structured non-operative management may provide satisfactory outcomes in patients with a stable DRUJ, whereas persistent symptoms, mechanically unstable tears, and foveal detachment may require surgical intervention. Contemporary arthroscopic options include all-inside repair, suture-anchor fixation, and transosseous techniques, although current evidence does not establish a single superior method. Postoperative rehabilitation protocols remain heterogeneous, and validated criteria for progression and return to work or sport are lacking. Future research should focus on standardized diagnostic pathways, comparative evaluation of repair techniques, objective functional monitoring, and patient-centered return-to-activity outcomes. Modern technologies should support, rather than replace, integrated clinical and functional assessment.

Acute peroneal tendon injuries are rare and often misdiagnosed due to their subtle nature, leading to delayed treatment and potential functional impairment. Among these, isolated ruptures of the peroneus longus (PL) tendon are particularly rare, complicating to a larger extent diagnosis and management. The primary surgical treatment methods for a PL tendon rupture include end-to-end suturing in acute cases, suturing to the peroneus brevis (PB) tendon, or tenodesis to the cuboid bone. This article presents the case of a 45-year-old male who sustained a complete distal rupture of the PL tendon during a sports activity. The diagnosis was based on a clinical examination and ultrasound (US) imaging. The described minimally invasive US-guided repair of the distal PL tendon rupture utilizes three small incisions, allowing for the restoration of the tendon’s native course, even in distal ruptures. Distally, sutures from the proximal stump are secured using a PushLock anchor after approximation to the distal stump, ensuring the anatomic restoration of tendon continuity. The presented case suggests that this technique provides an effective and minimally invasive alternative to conventional open surgical repair of PL tendon ruptures. Furthermore, the use of ultrasound imaging minimizes the extent of the surgical approach, thereby reducing trauma to surrounding structures.

Autoantibodies are commonly detected during or shortly after viral illness, sometimes in patients whose presentation already resembles a systemic or organ-specific autoimmune disorder. The difficulty is that the laboratory finding often arrives before the clinical meaning of that finding is clear. In acute parvovirus B19 and hepatitis E, ANA, RF or autoimmune liver serology may accompany the infection and then recede as the illness resolves. SARS-CoV-2 cohorts that include pre-infection samples show that genuine seroconversion can occur, but they also expose a separate problem: a newly detectable or persistent autoantibody is not the same endpoint as clinically defined autoimmune disease. HCV-associated cryoglobulinaemic vasculitis is different because infection, immune-complex formation and organ disease belong to the same pathogenic process. Across the other viral settings, interpretation is limited by referral bias, incomplete follow-up, assay heterogeneity and the frequent use of serological rather than clinical endpoints. Taken together, the recent literature supports post-viral autoreactivity far more consistently than it supports frequent progression to a new autoimmune disease. Diagnostic weight increases when the antibody is disease-concordant, persists beyond the acute infection and accompanies an objective phenotype that the infection no longer adequately explains.