Cystic fibrosis (CF) is a genetic disorder affecting multiple organs, primarily the lungs and digestive system. Over the years, advancements in medical care and treatments have significantly increased the life expectancy of individuals with CF. However, with this improved longevity, concerns about the potential risk of developing certain types of cancers have arisen. This narrative review aims to explore the relationship between CF, increased life expectancy, and the associated risk for cancers. We discuss the potential mechanisms underlying this risk, including chronic inflammation, immune system dysregulation, and genetic factors. Additionally, we review studies that have examined the incidence and types of cancers seen in CF patients, with a focus on gastrointestinal, breast, and respiratory malignancies. We also explore the impact of CFTR modulator therapies on cancer risk. In the gastrointestinal tract, CF patients have an elevated risk of developing colorectal cancer, pancreatic cancer, and possibly esophageal cancer. The underlying mechanisms contributing to these increased risks are not fully understood, but chronic inflammation, altered gut microbiota, and genetic factors are believed to play a role. Regular surveillance and colonoscopies are recommended for early detection and management of colorectal cancer in CF patients. Understanding the factors contributing to cancer development in CF patients is crucial for implementing appropriate surveillance strategies and improving long-term outcomes. Further research is needed to elucidate the molecular mechanisms involved and develop targeted interventions to mitigate cancer risk in individuals with CF.

Cystic fibrosis (CF), a genetic disorder characterized by mutations in the CFTR gene, has seen significant advances in treatment through cutting-edge approaches such as gene therapy and personalized medicine. This review examines the current and emerging strategies shaping CF care, focusing on novel therapies that target the root cause of CF and optimize patient outcomes. CFTR modulators have transformed cystic fibrosis management by enhancing protein function for specific mutations, leading to improved lung function and quality of life. Concurrently, gene therapy offers transformative potential by aiming to correct CFTR mutations using tools like CRISPR/Cas9 or prime editing, though challenges remain in delivery and long-term efficacy. The integration of precision medicine, facilitated by genomic and computational technologies, allows for personalized treatment plans that account for genetic variability and disease severity. Complementing these approaches, holistic management emphasizes the importance of psychological support and nutritional optimization, acknowledging CF’s multi-system impact. Future directions include exploring anti-inflammatory agents and microbiome modulation to further mitigate disease morbidity. However, global disparities in treatment access continue to challenge equitable healthcare delivery, underscoring the need for policy reform and international cooperation. By synthesizing these developments, this review highlights the transformative potential of modern CF treatments, advocating for continued innovation and global healthcare equity, with the ultimate goal of dramatically improving life expectancy and quality of life for individuals with CF.

Food allergy (FA) is a pathological immune response, potentially deadly, induced by exposure to an innocuous and specific food allergen. To date, there is no specific treatment for FAs; thus, dietary avoidance and symptomatic medications represent the standard treatment for managing them. Recently, several therapeutic strategies for FAs, such as sublingual and epicutaneous immunotherapy and monoclonal antibodies, have shown long-term safety and benefits in clinical practice. This review summarizes the current evidence on changes in treating FA, focusing on monoclonal antibodies, which have recently provided encouraging data as therapeutic weapons modifying the disease course.

The introduction of CFTR modulators has dramatically shifted the clinical management of cystic fibrosis (CF) from a life-limiting pediatric condition to a chronic disease with broader health implications. This review explores the impact of these advancements on lung immunology and the emerging spectrum of health challenges. While these modulators have reduced traditional pulmonary complications by mitigating inflammation and infection, they also introduce new considerations for long-term health management. As patients experience longer lives, issues such as the increased risk of certain cancers and other systemic complications like CF-related diabetes and liver disease are gaining attention. Understanding the interplay between CFTR modulators, immune response, and the development of these conditions is essential for optimizing patient outcomes. This review highlights the importance of integrated care strategies that address both the respiratory improvements and emerging health risks associated with longer life expectancy in CF patients. By fostering a comprehensive approach, we aim to enhance the overall quality of life and address the complex needs of individuals navigating CF in the modern therapeutic landscape.

Cystic fibrosis (CF) is a genetic disorder caused by mutations in the CFTR gene, leading to multi-system impairment. Sleep respiratory disorders (SRDs) are frequent in individuals with CF—even in those with normal or mildly impaired lung function—and may adversely affect overall health. The triple combination of elexacaftor, tezacaftor, and ivacaftor (ETI) has markedly improved clinical outcomes in CF; however, its long-term impact on SRDs remains unclear. This study aimed to assess the effects of ETI on nocturnal cardiorespiratory parameters in individuals with CF over a two-year period. Thirty-five clinically stable patients aged ≥13 years, eligible for ETI therapy, were enrolled. Nocturnal cardiorespiratory polygraphy and spirometry were performed at baseline (T0), one year (T1), and two years (T2) after ETI initiation. After one year, significant improvements were observed in mean oxygen saturation (mSpO₂), time with SpO₂ ≤ 90% (t ≤ 90%), and respiratory rate. Spirometric indices (FEV₁, FVC, FEF) also significantly increased (p < 0.05). Correlation analysis revealed positive associations between mSpO₂ and FEV₁ (ρ = 0.515, p = 0.002) and between FEV₁ and FVC (ρ = 0.894, p < 0.001), while t ≤ 90% negatively correlated with FEV₁ (ρ = −0.404, p = 0.016). No additional significant changes were found at T2. ETI therapy resulted in sustained improvements in nocturnal oxygenation and lung function, supporting the importance of nocturnal respiratory monitoring during follow-up.

Pediatric interstitial lung diseases (chILD) are a diverse and complex group of rare but impactful disorders characterized by heterogeneous etiologies and variable clinical courses. Traditional diagnosis-based management often delays targeted treatment, underscoring the need for a more precise therapeutic approach. The “treatable traits” framework, originally developed in adult respiratory medicine, offers a novel paradigm for personalized care by focusing on identifying and modifying discrete, clinically relevant features in each child. This narrative review synthesizes existing evidence and expert consensus to define key treatable traits in pediatric ILD, encompassing genetic and surfactant dysfunction, immune dysregulation, pulmonary hypertension, hypoxemia, aspiration, growth deficits, and environmental exposures. For each trait, we describe diagnostic pathways—including genetic testing, bronchoalveolar lavage, imaging, and functional assessments—and outline targeted management strategies. The implementation of a trait-based approach necessitates multidisciplinary collaboration, standardized protocols, and ongoing research to validate biomarkers and optimize therapies. By adopting this personalized strategy, clinicians can improve early diagnosis, tailor interventions, and potentially alter disease trajectories. Our discussion highlights the current limitations and future priorities, emphasizing the importance of pediatric-specific studies and international networks to fully realize the promise of precision medicine in pediatric ILD.