Background: Upper airway tract infections (UATIs) are among the most common infectious diseases worldwide, accounting for an estimated 12.8 billion episodes annually and more than 8 million disability-adjusted life years (DALYs). Despite their generally self-limiting nature, their cumulative clinical, socioeconomic, and public health burden remains substantial, particularly in children, older adults, and low- and middle-income countries (LMICs). Methods: We performed a structured narrative review of the peer-reviewed literature and reports from major international health organizations to summarize the current evidence on the epidemiology, etiology, clinical impact, socioeconomic burden, prevention strategies, and future challenges associated with UATIs. Particular attention was given to the influence of antimicrobial resistance, vaccination policies, and lessons learned from the COVID-19 pandemic. Results: UATIs remain one of the leading causes of healthcare utilization worldwide. Children experience the highest incidence, averaging 6–8 episodes annually, whereas vulnerable populations are at increased risk of complications and hospitalization. Marked geographical disparities persist, with LMICs experiencing a disproportionate burden due to limited healthcare access, lower vaccination coverage, and higher complication rates. Inappropriate antibiotic prescribing continues to accelerate antimicrobial resistance, while the COVID-19 pandemic profoundly altered the epidemiology of respiratory infections and demonstrated the effectiveness of non-pharmaceutical interventions. Advances in vaccination, antimicrobial stewardship, rapid diagnostics, and novel therapeutic strategies offer promising opportunities to reduce disease burden. Conclusions: Reducing the global burden of UATIs requires integrated public health strategies combining equitable vaccine access, effective antimicrobial stewardship, strengthened healthcare systems, and sustained surveillance. Lessons learned from the COVID-19 pandemic provide a unique opportunity to improve preparedness for future respiratory outbreaks while addressing persistent regional inequalities in prevention and care.

Chronic rhinosinusitis with nasal polyps (CRSwNP) is a type 2 inflammatory disease effectively treated with dupilumab, a monoclonal antibody that inhibits IL-4 and IL-13 signaling. Dupilumab is an effective treatment for type 2 inflammatory diseases such as CRSwNP. Although efficacy of dupilumab in controlling upper airway inflammation is well established, concerns have emerged regarding its potential cardiovascular effects. Emerging evidence suggests that IL-4/IL-13 signaling plays a protective role in post-myocardial infarction remodeling by promoting anti-inflammatory macrophage polarization, angiogenesis, and controlled fibrosis, especially during the early healing phase. Pharmacological blockade of the IL-4/IL-13 signaling pathway, such as that induced by dupilumab, may theoretically impair myocardial repair mechanisms, particularly in male patients who appear more responsive to these cytokines. Although rare, dupilumab-associated hypereosinophilia and myocarditis have been reported. In patients with pre-existing ischemic heart disease or heart failure, a multidisciplinary risk–benefit evaluation should be considered. Concomitant use of cardioprotective agents such as sacubitril/valsartan or SGLT2 inhibitors may help mitigate potential cardiac risks. Future studies are needed to clarify the safety and therapeutic implications of combining dupilumab with cardiovascular therapies in patients with coexisting CRSwNP and heart disease. This review critically evaluates emerging evidence of potential interference with post-infarction myocardial repair and highlights the importance of a multidisciplinary approach in managing patients with coexisting inflammatory and cardiovascular diseases. The aim of this review is to explore the available data on the cardiovascular impact of dupilumab and to provide possible future perspectives.

Background: Hearing loss is one of the most common yet often overlooked sensory deficits worldwide, with consequences extending well beyond auditory function. Mounting evidence highlights the complex interrelationships among hearing loss, cognitive decline, and psychosocial well-being. Neural mechanisms underlying this association include increased cognitive load, cortical reorganisation, and social isolation, which mediate the impact of auditory deprivation on the brain and mental health. Furthermore, hearing impairment is consistently associated with a higher risk of depression and anxiety, particularly when the duration of untreated deafness is prolonged. Methods: This narrative review summarises recent longitudinal and neuroimaging studies investigating the effects of hearing loss and the timing of intervention with hearing aids. The review focuses on evidence addressing cognitive, psychological, and neural outcomes in relation to early versus delayed amplification. Results: Across multiple studies, early adoption of hearing aids within a limited timeframe after diagnosis is linked to better cognitive performance, lower depressive symptom scores, and more preserved neural network integrity. Experimental evidence supports the existence of sensitive periods for auditory intervention, during which brain plasticity allows for optimal reorganisation and recovery of function. Conversely, delayed amplification may lead to irreversible cortical changes and persistent psychosocial distress. Despite this, several barriers—healthcare accessibility, patient attitudes, and economic constraints—continue to delay timely intervention. Conclusions: Early identification and management of hearing loss are critical to preserve cognitive and emotional health. An integrated approach addressing both hearing and cognitive well-being, supported by patient education and personalised care strategies, may maximise the benefits of amplification and improve overall quality of life.

Obstructive sleep apnea (OSA) is a highly prevalent disorder with far-reaching systemic consequences. While its cardiometabolic and neurocognitive impacts are well established, growing evidence highlights OSA as a contributor to infertility in both men and women. The pathophysiological mechanisms include intermittent hypoxia, oxidative stress, systemic inflammation, and endocrine disruption, all of which can impair spermatogenesis, reduce semen quality, alter gonadal hormone secretion, and compromise ovarian function. Clinical studies consistently demonstrate associations between OSA and impaired semen parameters, reduced testosterone, and erectile dysfunction in men. In women, OSA is frequently observed in those with polycystic ovary syndrome, is associated with ovulatory dysfunction, and negatively affects in vitro fertilization outcomes, pregnancy rates, and miscarriage risk. Despite these findings, infertility is not systematically included in global burden estimates of OSA, leading to the underestimation of its true health and socioeconomic impact. Therapeutic strategies such as weight loss, continuous positive airway pressure, and integrative approaches show promise, though robust evidence from randomized trials is still lacking. Integrating sleep health into reproductive medicine may provide a cost-effective and equitable pathway to improve fertility outcomes worldwide.

Background: Hearing loss is a widespread sensory disorder affecting over 1.5 billion people worldwide, with the number projected to exceed 700 million by 2050. It imposes social and economic burdens across all ages and regions. Approximately half of adult cases are preventable, but the underlying causes are complex, with 75–80% due to autosomal recessive genetic factors and key roles for mutations in genes such as GJB2. Advances in sequencing technologies have accelerated gene discovery, but challenges remain in interpreting variants. Epigenetic mechanisms such as DNA methylation and histone modifications are increasingly recognized as crucial in auditory biology and could offer new biomarkers and therapeutic targets. Integrating epidemiological, genetic, and epigenomic data is essential to developing targeted prevention and treatment strategies to reduce the global burden of hearing loss. Methods: This narrative review examines recent genomic and epigenomic advances in hearing loss, with particular emphasis on molecular mechanisms, emerging diagnostic applications, and translational therapeutic opportunities. A comprehensive review of current epidemiological data, genetic studies, and epigenomic research was conducted using the peer-reviewed literature from international databases. Key areas of interest include inheritance patterns, molecular pathways, and recent advances in omics technologies. Results: Epigenetic mechanisms, including DNA methylation and histone modifications, are increasingly recognized as important regulators of cochlear development and hair cell survival, although much of the current evidence remains preclinical. Studies suggest that peripheral epigenetic signatures may serve as biomarkers for early diagnosis and risk stratification. Conclusions: Integrating established screening pathways with epidemiological trends and molecular knowledge offers a promising path toward precision medicine in hearing care. Connecting these domains is essential to developing equitable and effective interventions and addressing persistent global disparities in hearing health. This review highlights the evolving landscape of auditory genetics and epigenetics and outlines future directions for translational research and personalized therapy.

Background and Objectives: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a heterogeneous inflammatory disease of the sinonasal mucosa characterized by persistent symptoms, high recurrence rates, and a significant impact on quality of life. Increasing evidence suggests that oxidative stress plays a role in its pathophysiology, although its precise contribution remains incompletely defined. Materials and Methods: A narrative review was conducted following SANRA recommendations. A structured literature search was performed using PubMed, Scopus, and Google Scholar to identify studies investigating oxidative stress, antioxidant systems, and molecular pathways in CRSwNP. Relevant articles published between January 2000 and March 2026 were included and critically appraised, distinguishing clinical from ex vivo, in vitro, and animal evidence. Results: Available evidence, derived mainly from small cross-sectional case–control studies, consistently associates CRSwNP with increased oxidative stress, characterized by elevated levels of reactive oxygen and nitrogen species, lipid peroxidation products, and DNA damage. Impaired antioxidant defenses accompany this imbalance, although findings for individual enzymes such as superoxide dismutase, catalase, and glutathione peroxidase are inconsistent across sample types and assays. At the molecular level, oxidative stress activates pro-inflammatory signalling pathways, including NF-κB and the NLRP3 inflammasome, and is linked to epithelial barrier dysfunction and type 2 immune responses. Oxidative signatures appear to differ between eosinophilic and non-eosinophilic endotypes. Furthermore, oxidative stress represents a plausible mechanistic link between CRSwNP, asthma, and allergic rhinitis, supporting the concept of united airways disease. Antioxidant strategies are supported almost exclusively by preclinical data. Conclusions: Oxidative stress is a consistent feature of CRSwNP and, on the basis of experimental data, a likely amplifier of chronic inflammation; however, a causal role in humans has not been established. Standardized, endotype-specific oxidative biomarkers, longitudinal studies, and randomized trials are needed before redox-targeted strategies can be integrated into clinical practice.