Cystic fibrosis (CF) is a genetic disorder caused by mutations in the CFTR gene, leading to defective ion transport and impaired function of various organs. Chronic inflammation, oxidative stress, and microbial dysbiosis are key pathological features of CF patients, contributing to disease progression, lung damage, and an increased susceptibility to infections. Emerging evidence suggests that in CF patients these factors can promote cancer development, especially lung cancer. Chronic inflammation in CF, driven by immune cell dysfunction, results in the release of pro-inflammatory cytokines and reactive oxygen species (ROSs), fostering an environment conducive to cancer initiation. Oxidative stress can amplify cellular damage and hinder airway remodeling. ROSs not only damage cellular components such as lipids, proteins, and DNA but also disrupt lung homeostasis, creating a favorable environment for cancer development. Furthermore, the lung microbiome in CF patients is often dysbiotic, with a reduced diversity and the predominance of pathogenic bacteria such as Pseudomonas aeruginosa, which exacerbate inflammation and may contribute to carcinogenesis. This review explores the mechanisms linking CF to lung cancer, examining the potential clinical implications of these mechanisms for early detection, monitoring, and targeted therapies for lung cancer prevention in CF patients.

Chronic Obstructive Pulmonary Disease (COPD) is a multifactorial condition associated with significant systemic complications such as cardiovascular disease (CVD), metabolic disorders, muscle wasting, and sarcopenia. While Body Mass Index (BMI) is a well-established indicator of obesity and has prognostic value in COPD, its role in predicting disease outcomes is complex. Muscle wasting is prevalent in COPD patients and exacerbates disease severity, contributing to poor physical performance, reduced quality of life, and increased mortality. Additionally, COPD is linked to metabolic disorders, such as dyslipidemia and diabetes, which contribute to systemic inflammation and worse prognosis and, therefore, should be treated. The systemic inflammatory response plays a central role in the development of sarcopenia. In this review, we highlight the mixed efficacy of statins in managing dyslipidemia in COPD, considering side effects, including muscle toxicity in such a frail population. Alternative lipid-lowering therapies and nutraceuticals, in addition to standard treatment, have the potential to target hypercholesterolemia, which is a coexisting condition present in more than 50% of all COPD patients, without worsening muscle wasting. The interference between adipose tissue and lung, and particularly the potential protective role of adiponectin, an adipocytokine with anti-inflammatory properties, is also reviewed. Respiratory, metabolic and muscular health in COPD is comprehensively assessed. Identifying and managing dyslipidemia and paying attention to other relevant COPD comorbidities, such as sarcopenia and muscle wasting, is important to improve the quality of life and to reduce the clinical burden of COPD patients. Future research should focus on understanding the relationships between these intimate mechanisms to facilitate specific treatment for systemic involvement of COPD.

Benign endobronchial tumors are rare clinical entities characterized by considerable variability in etiology and clinical presentation. The authors report four cases of endobronchial hamartomas treated and followed up from 2018 to 2023. Three of these cases, with identical endobronchial localization in the right lower lobe, were radically treated in flexible bronchoscopy with only the use of biopsy forceps. Another case with a different localization in the left main bronchus was treated with a laser through rigid bronchoscopy. In addition, the authors outline the main interventional pulmonological strategies for the treatment of benign tumors with endobronchial growth based on the existing literature.

Alectinib is a highly selective tyrosine kinase inhibitor of anaplastic lymphoma kinase (ALK) that is approved as first-line treatment in adult patients with ALK-positive non-small cell lung cancer (NSCLC) and as second-line in patients previously treated with crizotinib, and has been shown in the literature to significantly prolong progression-free survival compared to chemotherapy in patients with advanced non-small cell lung cancer. The authors describe a clinical case of a 24-year-old woman with malignant massive pleural effusion caused by ALK rearranged pulmonary adenocarcinoma with pleural and pericardial metastasis, in which, despite a dramatic clinical debut, the correct and timely management of the diagnostic and therapeutic path allowed for extraordinary therapeutic success.

Inflammatory cytokine storm play a central role in disease progression of Covid-19. Many laboratory markers have been associated to an adverse outcome in COVID-19 patients. Lactate dehydrogenase enzyme (LDH) is a sensitive indicator of the cellular metabolic state, aerobic or anaerobic direction of glycolysis and cell injury. High lactate dehydrogenase level was significantly associated with severe COVID-19 pneumonia on admission.[1] Aim: to investigate if LDH, an easy laboratory test, could define the severity of Covid-19 pneumonia and guide physicians in their choice of therapeutic strategy. Methods: we analyzed laboratory tests to identify tissue damage and inflammatory status in 70 CoVID-19 patients (41 males and 29 females) admitted to Pneumology Department of Monaldi Hospital (Naples). We investigated the relationship between LDH values(normal range 80-300 U/L) and the type of therapeutic strategy (low and high flow oxigen therapy and non-invasive ventilation). Results: patients had a mean age of 67,28 years. Serum level of LDH was > 300 U/L in 71,42% of patients (first group) and <300 U/L in 28,58% of patients (second group). In the first group 44% of patients needed non invasive ventilation (CPAP/NIV), 38% needed high flow nasal cannulae oxygen therapy (HFNC) and 18% needed low flow oxigen therapy. In the second group 5% of patients needed CPAP/NIV, 40% needed HFNC and 55% needed low flow oxigen therapy. Conclusions: LDH seems to be related to severity of Covid-19 pneumonia and to the type of therapeutic strategy. Moreover could guide physicians in the choice of respiratory support such as non-invasive ventilation. [1] Li X et al. J Allergy Clin Immunol. 2020 Jul;10.1016/j.jaci.2020.04.006.

Background/Objectives: Skeletal muscle wasting is a frequent and clinically consequential comorbidity in COPD, affecting 15–50% of patients and predicting reduced exercise tolerance, impaired quality of life, hospitalization, and mortality. However, no consensus exists on the optimal diagnostic approach, and the role of nutritional assessment remains underemphasized despite its contribution to muscle depletion. Methods: This narrative review synthesizes evidence from original research, systematic reviews, and consensus statements on diagnostic methods for evaluating muscle mass, strength, physical performance, and nutritional status in COPD. Results: Computed tomography and magnetic resonance imaging offer accurate assessment of muscle mass but are limited by cost and accessibility. Dual-energy X-ray absorptiometry provides a low-radiation alternative but cannot assess muscle quality. Bioelectrical impedance analysis and ultrasound are portable and inexpensive, yet lack standardized COPD-specific cut-offs. Functional tests provide clinically meaningful performance data but do not directly measure muscle mass. In parallel, nutritional screening tools and dietary assessment can identify modifiable risk factors and are associated with sarcopenia prevalence and prognosis in COPD. The choice of diagnostic approach significantly influences prevalence estimates. Conclusions: Optimal assessment of muscle wasting in COPD requires a multimodal approach combining muscle mass quantification, strength measurement, physical performance evaluation, and nutritional assessment. Standardized COPD-specific diagnostic criteria are needed. A practical algorithm integrating simple screening tools with targeted confirmatory assessments, including nutritional evaluation, may help guide clinical practice.